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Boston AF Symposium

Boston AF Symposium – 2008

Boston AF Symposium, January 17-19, 2008

“Atrial Fibrillation: Mechanisms and New Directions in Therapy”

The annual international Boston A-Fib Symposium is one of the most important conferences on A-Fib in the world. It brings together researchers and doctors who share the latest information.  But if you haven’t read and understood most of A-Fib.com, it may be difficult reading.

OVERVIEW-HIGHLIGHTS

The 13th annual Boston A-Fib Symposium may mark the emergence of the Robotics Era in the treatment of A-Fib. Much attention was focused on the competing robotic ablation systems by Hansen and Stereotaxis. These systems are already changing the way doctors perform ablations, and will likely provide significant benefits to A-Fib patients.

Catheter Ablation Outside the Heart

In what may be a major medical breakthrough, two doctors announced that they had combined Endocardial ablation (ablating inside the heart) with Epicardial ablation (outside the heart) to more effectively ablate sources of A-Fib which are hard to reach.

Significantly Decreasing the Risk of Stroke

Clinical trials are underway of the Watchman device for closing off the Left Atrial Appendage, which may well be another major medical breakthrough. In a simple, very low risk procedure performed in as little as twenty minutes, the Watchman device is inserted via a catheter into the Left Atrial appendage to close it off. This simple procedure reduces the risk of stroke by as much as 95%. (The risk of A-Fib stroke risk is reduced to that of someone with a normal heart).

(The Watchman device may also help people with other risks of stroke.) (See Reddy, Novel Catheter Approaches to Thrombo-Prophylaxis.)

Eight-step Ablation Procedure for Treating Chronic A-Fib with a 93% Success Rate

The Italian Milan group announced an eight step ablation procedure for treating Chronic (all-the-time) A-Fib which is 93% successful. This is a significant improvement in the success rate for ablating Chronic A-Fib. (See also 95% success rate in curing Persistent A-Fib reported by the French Bordeaux group at the 2007 Boston A-Fib Symposium.) (Other centers like Massachusetts General are using similar procedures and are achieving similar success rates for curing Chronic A-Fib.) (See: Comparison of Dr. Pappone’s, Haïssaguerre’s, and Reddy’s Stepwise Approaches in Ablating for Chronic A-Fib)

Atrial-Esophageal Fistula

Though no cases of Atrial-Esophageal Fistula were reported since last year’s Boston A-Fib Symposium, there was still a  great deal of concern over this rare complication (a Fistula usually begins as an injury or lesion (Necrosis) of the Esophagus which then spreads to the Left Atrium creating a puncture).

Some centers use an esophageal temperature probe and stop ablating if the esophageal temperature rises 0.2 degrees. But research indicates that even this small increase in esophageal temperature may cause ulceration in the esophagus. This ulceration, however, is easily cured by administering Proton Pump Inhibitors (to limit gastric acid) and other meds. (Examples of Proton Pump Inhibitors are: Nexium, Prilosec, Prevacid, and Protonix.) (See Morady: Evaluating Strategies to Prevent Atrial-Esophageal Fistula. and Nakagawa: Improving the Safety of Catheter Ablation of Atrial Fibrillation: Prevention of Left Atrial-Esophageal Fistula)

(Doctors commented that they would now routinely use Proton Pump Inhibitors after Pulmonary Vein Ablation procedures to help prevent Atrial-Esophageal Fistula.)

Electrophysiologists and Surgeons Present Consensus Statement on Treating A-Fib 

In an inspiring example of collaboration and cooperative concern for A-Fib patients, EPs and Surgeons together developed a consensus statement on A-Fib ablation that is detailed, practical, far reaching, and addresses head-on many of the major issues of A-Fib ablation. (This document may have major implications for A-Fib patients not only from its content, but also because it demonstrates how effectively EPs and surgeons are now working together to cure A-Fib.) (See Calkins: Consensus Statement on A-Fib. For the complete text of the Consensus Statement,

In a major change from current medical guidelines, Catheter Ablation is approved as first line therapy for A-Fib patients.

Catheter Ablation Far Superior to Current Antiarrhythmic Meds in Treating A-Fib

Data from several research studies demonstrated that catheter ablation is significantly better at restoring and maintaining sinus rhythm than current antiarrhythmic (AA) drugs (one study showed a 64% difference).

These studies also compared complication rates for both treatment approaches. One-time complications for catheter ablation were relatively low, compared to the side effects and long time complication risk of antiarrhythmic drugs. In addition, the research showed that A-Fib patients on AA drugs run an additional risk of getting worse and developing Cardiomyopathy. (See Kottkamp: Is Catheter Ablation of Atrial Fibrillation Superior to Antiarrhythmic Drug Treatment for Rhythm Control?)

Live Satellite Demos of both Catheter and Surgical Ablation

This Symposium featured two live catheter ablations: one from the Un. of Austin using the Hansen robotics system, and the other from Massachusetts General using the Phillips ultrasound 3-D imaging which produces a real time 3-D image during the ablation. Also, for the first time at a Boston A-Fib Symposium, there was a live satellite surgical ablation case (from the Medical College of Virginia).

Danger of “Silent” A-Fib Strokes
Several disturbing studies indicated that A-Fib patients, without any apparent neurological symptoms, often had silent cerebral strokes (15%-26%) which showed up on computer tomography (CT) images of the brain. A-Fib patients with “silent” strokes are at much greater risk of a subsequent stroke. (If you’ve had A-Fib for a while, you might want to discuss with your doctor getting a computer tomography (CT) scan of your brain to see if you’ve had any “silent” strokes or TIAs [Transient Ischemic Attacks].) (See Camm: Oral Anticoagulation: A Critical Review of the Data But be aware of the possible long term dangers of too much exposure to radiation through CTs, X-rays, etc.)

Aspirin may not be Effective in Preventing A-Fib Stroke

Several studies were presented which cast doubt on the effectiveness of aspirin as an anticoagulant to prevent A-Fib stroke. According to Dr. John Camm of St. George’s Medical School, London, England, “there is little if any efficacy of aspirin…The evidence for aspirin (to prevent clotting) is marginal and at best modest.” (See Camm: Oral Anticoagulation: A Critical Review of the Data)

French Bordeaux Group Honored

Ten years ago in 1998 the French Bordeaux group published their groundbreaking article demonstrating how A-Fib is initiated by ectopic beats in the Pulmonary Veins. This article helped develop catheter ablation as it is performed today. Many patients have been cured of A-Fib thanks to their pioneering research.

In recognition of their work, Drs. Michel Haïssaguerre and Pierre Jaïs from the French Bordeaux group were presented with a Chelsea clock from Boston with the inscription: “In recognition of your pioneering contribution to the science of catheter ablation and to the care of patients with cardiac arrhythmias.”

(The author was surprised to find out that he was the first US patient to be cured of A-Fib by the French Bordeaux group back in 1998.)

PRESENTATIONS

TOPICS DOCTOR TITLE OF PRESENTATION
EPs & Surgeons’ Consensus Statement on A-Fib  Catheter Ablation Approved as First Line Treatment for A-Fib Calkins The HRS/EHRA/ECAS Expert Consensus Statement on A-Fib Ablation:Implications for Patient Care and Clinical Investigation
Blood Thinners & A-Fib Stroke, CHADS2-Risk Factors for Stroke Camm Oral Anticoagulation: A Review of the Data
Catheter Ablation Far Superior to Current Antiarrhythmic Drugs  Kottkamp Is Catheter Ablation of Atrial Fibrillation Superior to Antiarrhythmic Drug Treatment for Rhythm Control?
Evaluating Strategies to Prevent Atrial-Esophageal Fistula. The Un. of Michigan’s Individualized Ablation Approach.  Morady Lesions Learned: Providing Guidance for the Next (and Current) Generation of Ablationists
How to Prevent Atrial-Esophageal Fistula   Nakagawa Improving the Safety of Catheter Ablation of Atrial Fibrillation: Prevention of Left Atrial-Esophageal Fistula
Comparison of Dr. Pappone’s, Haïssaguerre’s, and Reddy’s Stepwise Approaches in Ablating for Chronic A-Fib  Pappone Biatrial Catheter Ablation for Chronic Atrial Fibrillation
The Watchman Device to Close off the Left Atrial Appendage  Reddy Novel Catheter Approaches to Thrombo-Prophylaxis
Problems with Warfarin, Future Alternatives  Waldo  Novel Approaches to Thrombo-Prophylaxis

Dr. John Camm of St. George’s Medical School, London, England, UK was part of a 3-person panel and discussion on Stroke Prophylaxis (Prevention) in the A-Fib Patient. His presentation was on “Oral Anticoagulation: A Critical Review of the Data.”

One of the most difficult challenges for A-Fib patients and doctors is to prevent A-Fib stroke. Oral anticoagulation with dose-adjusted warfarin remains the mainstream therapy for the prevention of A-Fib stroke.

So many people have A-Fib today (2.3 million in the US alone) that it’s considered an world-wide epidemic, affecting 1%-1.5% of people in developed countries.1Someone with A-Fib has a five times greater risk of stroke, and the A-Fib stroke is usually more severe, with a greater risk of death, permanent disability, and increased health care cost. An A-Fib stroke is twice as likely to be fatal. Nearly three-quarters of stroke victims with A-Fib require daily health care assistance, compared to about one-third with sinus rhythm, and are more likely to remain handicapped. (Poor stroke outcome may be due to a reduction in cerebral blood flow caused by A-Fib. Also, the clots that can form in the Left Atrial Appendage can be quite large and completely block blood vessels in the brain often resulting in death or severe neurologic damage. See the photographs at A-Fib Stroke.)

In A-Fib the atria don’t contract properly, which results in increased atrial pressure, atrial stretch, and dilation often leading to blood stagnation and clot formation. Atrial stretch also produces chemical changes in the atria (increased natriuretic peptide and decreased vasopressin) which can produce increased blood concentrations (often resembling a gelatinous, Jell-O-like substance), and increased platelet activity.

The left atrium and particularly the Left Atrial Appendage (LAA) produce 70-90% of A-Fib clots. The LAA is a long, closed-end pouch which acts as a decompression chamber in volume overload where blood can easily stagnate. It has many cavities, resembling a piece of coral. Even when A-Fib patients are effectively anticoagulated, 14% of patients are still found with clots. However, approximately 4 weeks of warfarin therapy dissolves these clots in 75% of cases.

According to Dr. Camm, patients today are generally being successfully managed with warfarin therapy to prevent thrombis (clotting), though there is room for improvement.

THE “CHADS2″ RISK MODEL

Doctors today use a risk-based approach to stroke prevention. Each individual’s stroke risk is calculated to identify those who are at higher risk, and who may benefit most from anticoagulant (warfarin) therapy. The CHADS2 is currently the recommended risk model to determine anticoagulant use.
CHADS2 refers to risk factors for stroke. If you have one of the risk factors, you have a risk score of 1. However, if you’ve had a stroke already, that counts as a risk score of 2 (“S2″):

“C” Congestive Heart Failure Score = 1
“H” Hypertension Score = 1
“A” Age over 75 Score = 1
“D” Diabetes Score = 1
“S2″ Previous Stroke or TIA Score = 2

 

 

 

 



For example, someone with a risk factor of 1 not receiving any anticoagulant therapy would have 1.9%-2.8% chance of having a stroke within a year, whereas someone with a score of 6 would have an 18.2% chance of having a stroke. Aspirin is recommended for A-Fib patients who have a low to intermediate risk of stroke, but aspirin only provides modest protection.2.

Dr. Camm pointed out that the CHADS2 risk score model doesn’t take into account other less predictive risk factors such as female gender, coronary artery disease, age 65-74, and thyrotoxicosis (overactive thyroid). (Editor’s Note: A-Fib by itself, such as Lone A-Fib with no other risk factors, is not part of the CHADS2 risk model for stroke. The chances of low-risk or intermediate-risk A-Fib patients getting an A-Fib stroke, according to the Center for Shared Decision Making, are:

Under age 65 with no history of hypertension, stroke, arterial embolism, left ventricular dysfunction, or TIA:
Chance of stroke in two years 2 out of 100
Taking daily coated aspirin 1.5 out of 100
Taking daily warfarin 1 out of 100)

Age 65-75 with no history of hypertension, stroke, arterial embolism, left ventricular dysfunction, or TIA:
Chance of stroke in two years 4 out of 100
Taking daily coated aspirin 3 out of 100
Taking daily warfarin 2 out of 1003

ASPIRIN VS. WARFARIN EFFECTIVENESS

Dr. Camm cited seven recent studies which together showed a 22% overall risk reduction effectiveness of aspirin in preventing A-Fib stroke. However, the range of these studies varied from 2% to 39% and was not consistent. “The evidence for aspirin thrombus prophylaxis (preventing clot formation) is marginal and at best modest.”

However, studies comparing warfarin to both a placebo and to aspirin demonstrated compelling, convincing evidence of the effectiveness of warfarin. “There can be no doubt that warfarin is superior to aspirin.” Warfarin had a 64% relative risk reduction in preventing A-Fib stroke vs. a questionable 22% for aspirin. “There is little if any efficacy for aspirin.”

WARFARIN UNDERUSED

Both the young (under 55) and the elderly tend to under use warfarin. The difficulty of maintaining the proper INR (International Normalized Ratio) is a factor. But also 40% of those at high risk of stroke, particularly the elderly, aren’t receiving warfarin therapy, often because of an assumed inherent risk of hemorrhagic stroke. (The risk of a hemorrhagic [bleeding] stroke increases when the INR level goes above 4. An ideal INR level is between 2-3, Below 2 one runs more of a risk of an A-Fib ischemic stroke.)

Even young Paroxysmal (Intermittent) A-Fib patients with a high risk of stroke aren’t being properly anticoagulated. But studies show that there is no difference in A-Fib stroke risk between Persistent and Paroxysmal A-Fib. Warfarin therapy should depend on one’s CHADS2 score, not on what type of A-Fib one has.

SILENT CEREBRAL STROKE

Dr. Camm cited several disturbing studies which showed that A-Fib patients, without any apparent neurological symptoms, often had silent cerebral strokes (15%-26%) which showed up on computer tomography images of the brain. A-Fib patients with these “silent” strokes are at much greater risk of a subsequent stroke. (If you’ve had A-Fib for a while, you might want to discuss with your doctor getting a computer tomography (CT) scan of your brain to see if you’ve had any “silent” strokes or TIAs [Transient Ischemic Attacks]. But be aware of the possible long term dangers of too much exposure to radiation through CTs, X-rays, etc.)

GENETIC WARFARIN THERAPY

Using genotypes to help determine warfarin dosage reduces the number of times an A-Fib patient is out of INR range, and the number of times INR has to be calculated. But it doesn’t seem to make a significant difference in keeping patients in the approved INR range. See: FDA Approves Genetic Testing Labeling For Coumadin

CONCLUSION

The prevention of A-Fib by improved medications, and/or by Pulmonary Vein Ablation procedures (which have a 75%-85% success rate) may reduce the prevalence of stroke by almost one-quarter in the general population, particularly in the elderly. (In this author’s opinion, one of the major advantages of a successful Pulmonary Vein Ablation procedure is the reduction of A-Fib stroke risk. Studies indicate that a successful catheter ablation does lower the risk of an A-Fib stroke without having to take warfarin. But see also the danger of stroke from “silent” A-Fib attacks after catheter ablation.)

The second presenter on the 3-person stroke prevention panel was Dr. Albert Waldo of University Hospitals of Cleveland, OH who talked about “Novel Medical Approaches to Thrombo-Prophylaxis”

Though warfarin (brand name Coumadin) is very effective and reduces the risk of A-Fib-related stroke by about 70%, doctors are very aware of its problems and wish there were better options for patients.

(Warfarin is what is called a Vitamin K Antagonist (VKA). A technical description of how VKAs work is the following: “they prevent the y-carboxylation of the vitamin K-dependent coagulation factor prothrombin and Factors VII, IX, and X.4 In layman’s terms warfarin works by affecting several steps in the anticoagulation pathway to prevent clotting.)

WARFARIN PROBLEMS

  1. Narrow therapeutic window. Insufficient anticoagulation (INR less than 2) may result in stroke. Over-anticoagulation (INR over 4) increases the risk of bleeding.
  2. Late onset and offset. A patient has to be taking warfarin for a while for it to reach a therapeutic level.
  3. Unpredictable dose response. Genetic and other factors may influence how individuals react to warfarin.
  4. Drug-drug interactions. Certain drugs (and some supplements) interfere with warfarin.
  5. Drug-food interactions. People taking warfarin must limit foods containing vitamin K (like broccoli or some leafy vegetables)
  6. Problematic monitoring. It’s very difficult for both doctors and patients to monitor INR levels. Patients may be required to visit a doctor’s office weekly in order to be adequately monitored.
  7. Slow reversibility. It’s difficult to reverse, for example, a too high INR level.

Dr. Waldo pointed out that this was only a partial list of the problems with warfarin.

FUTURE ALTERNATIVES TO WARFARIN

Dr. Waldo discussed ongoing research and clinical trials of alternatives to warfarin.
One of the most promising seems to be dabigatran, a direct thrombin inhibitor (affecting the last stage in the anticoagulation pathway). (A more technical description of how dabigatran works is: “In the final step of the coagulation pathway, thrombin converts fibrinogen to fibrin. Dabigatran binds directly to thrombin, blocking its interaction within substrates and thereby preventing fibrin formation, thrombin-mediated activation of Factors V, VIII, XI, and XIII, and thrombin-induced platelet aggregation.”4

Dabigatran is in Phase III clinical trials with 15,000 patients. (Phase III is usually the last phase before FDA approval.) Results are expected in 2010.

So far dabigatran seems to be as effective and safe as warfarin. It’s administered as a pill and doesn’t require frequent monitoring. It starts working right away and has a wide therapeutic window. Its effects are reliably predictable. It doesn’t seem to have many food and drug interactions, and can be administered in fixed doses. (The other direct thrombin inhibitor formerly in clinical trails, ximelagatran, was rejected by the FDA because of liver toxicity and heart problems. Dabigatran doesn’t seem to have those problems.)

Other possible future alternatives to warfarin are Factor Xa Inhibitors which work further up the anticoagulation pathway. They may cause fewer side effects, because they affect mainly coagulation and not other functions like thrombin. There are many different Factor Xa medicines in development, but they are not as far along in clinical trials as dabigatran.

Dr. Vivek Reddy of Massachusetts General in Boston, MA was the third speaker of the 3-person panel on Stroke Prophylaxis in the A-Fib Patient. His topic was “Novel Catheter Approaches to Thrombo-Prophylaxis (Prevention).”

(Editor’s Comment: Dr. Reddy’s presentation raised an important question: what if the threat of A-Fib stroke could be easily eliminated without having to take warfarin or other meds? This may be possible in the near future because of the Watchman device.)

Dr. Vivek Reddy described ongoing clinical trials of the Watchman device which closes off the Left Atrial Appendage (LAA) where most A-Fib clots originate. (The Watchman device was created by Atritech, Inc.,[now owned by Boston Scientific] Graphics courtesy of WATCHMAN®)

HOW THE WATCHMAN DEVICE WORKS

Once a patient’s Left Atrial Appendage is measured, a wide-sheathed catheter with a spline is used to insert the Watchman device which has a self-expanding Nitinol (a special metal) open-ended circular frame. The atrial surface of this frame is covered with a thin, permeable 160 μm (micron) pore filter made of polyester material (Polyethylene Terephthalate known as Dacron or PET). This filter allows blood to pass through while stopping clots. Little hooks or anchors called fixation barbs at the middle of the device make sure it is attached firmly to the LAA wall. The Watchman device comes in multiple sizes from 21mm to 33mm to accommodate the different sizes of LAAs.

Before the catheter is removed (which fixes the Watchman device in place), contrast agents are used to make sure the Watchman device is stable and entirely closes off the LAA opening. Over time heart tissue grows over the polyester (PET) material so that it completely closes off the LAA with smooth heart tissue similar to other heart surfaces. In this Occlusion slide, heart tissue has completely covered the Watchman device after only nine months.

Some doctors are inserting the Watchman device in as little as 20 minutes. It is a low risk procedure with no surgery or ablation involved.

Patients on Coumadin continue to take it for six weeks after the Watchman device is inserted. They are then examined using a TEE (Transesophageal Echocardiogram) to make sure there is complete closure of the LAA. At that time they are taken off of Coumadin.

CLOSING OFF THE LAA AND A-FIB STROKE

The theory behind the Watchman device is that most A-Fib clots are found in the Left Atrial Appendage (LAA). Dr. Reddy cited a study where 98% of A-Fib strokes came from the LAA.

Studies of the early Maze operations (in which the Left Atrial Appendage was routinely cut out and sewn shut) showed a major decrease in A-Fib strokes. After 11 1/2 years of following 265 patients, only one had a stroke. However, there was no way to determine if this stroke risk reduction was due to the elimination of A-Fib or to the excision of the LAA.

Dr. Reddy cited studies of current Mini-Maze operations which show a high percentage of incomplete closure of the LAA. Even though surgeons have direct vision of the LAA and can over-sew or re-staple, sutures have a less than 50% success rate, while staples have a success rate of around 72%. In addition, 20% of patients in these studies later had strokes.

Instead of sewing or using staples, surgeons are also researching the use of a fabric coated band which is placed as close to the base of the LAA as possible. This band draws shut and closes off the LAA in 16 weeks.

PRELIMINARY DATA ON THE WATCHMAN DEVICE

Preliminary non-randomized data from the Watchman device clinical trials has been very positive. Following some patients for up to 5 years, there have been no strokes, cardiovascular deaths, or systemic embolisms (there were concerns about possible air bubbles forming in the heart due to the large catheter sheath used to insert the Watchman device).

Of the people who applied to participate in the Watchman clinical trials, 80% were accepted. Patients had to have a CHADS2 score of at least 1. Also, patients with Vagal A-Fib were excluded (Dr. Reddy reported that some researchers suspect that Vagal A-Fib patients tend to have less clots originating in the LAA). (An acceptance rate of 80% for a clinical trial indicates that the Watchman device, if and/or when it receives FDA approval, will be available for many, if not most A-Fib patients.)

The Watchman device clinical trial is entitled “PROTECT-AF.” (The full title is: Watchman Left Atrial Appendage System for Embolic PROTECTion in Patients with Atrial Fibrillation.) It is a multi-center, prospective, randomized-controlled trial at 60 medical centers across the US comparing the Watchman device to drug therapy using warfarin (brand name Coumadin). It attempts to answer the question, “Can the Watchman device replace warfarin treatment in A-Fib patients?” (In the future a subset of these clinical trials will include patients who can not take Coumadin.)

It will also directly measure how important the Left Atrial Appendage is to the development of A-Fib stroke.

This clinical trial also examines if there are potential detrimental effects of closing off the Left Atrial Appendage.

Editor’s Comments:

Though some heart pumping dynamics and other functions of the LAA may be lost when the Watchman device closes off the LAA, this seems a small price to pay to be freed from the threat of an A-Fib stroke. 

FUTURE USE OF THE WATCHMAN DEVICE

If the Watchman device works as well as preliminary data indicate and if the FDA approves it, how will it be used? Will it be a stand-alone procedure, or will it be routinely inserted as part of an A-Fib ablation procedure? (The following opinions are speculative and depend on the results of the ongoing clinical trials.)

The Watchman device as a stand-alone procedure

Since A-Fib is so damaging to the heart and to one’s overall health, most A-Fib patients probably won’t be satisfied with just having their Left Atrial Appendage closed off by the Watchman device, even though this would lessen the threat of an A-Fib stroke.
People with other risks of stroke than A-Fib may opt for insertion of the Watchman device to prevent stroke.

If insertion of the Watchman device becomes routine and easy to do, someone newly diagnosed with A-Fib with a moderate to high risk of stroke may have the Watchman device insertion procedure right away, while waiting for a  catheter ablation to cure their A-Fib.

Asymptomatic A-Fib patients at risk of stroke but who don’t want to take warfarin may be prime candidates for the Watchman device.

Young people and athletes with A-Fib who do not have a high risk of stroke may not want the Watchman device, because of the potential damage to their heart’s dynamics from losing the Left Atrial Appendage.

The Watchman device as part of a catheter ablation procedure
If the Watchman device works as intended, it may become part of most catheter ablation procedures. If the catheter ablation procedure were unsuccessful or in case of silent A-Fib attacks after ablation, the patient would still be protected from A-Fib stroke by the closing off of the Left Atrial Appendage.

Dr. Carlo Pappone from Milan, Italy discussed “Biatrial Catheter Ablation for Chronic Atrial Fibrillation”

Dr. Pappone from the Italian Milan group announced an eight step ablation procedure for treating Chronic (all-the-time) A-Fib which is 93% successful. This is a significant improvement in the usual success rate for ablating Chronic A-Fib.

A table is presented comparing and contrasting the stepwise approaches for Chronic A-Fib of Dr. Pappone, Dr. Michel Haïssaguerre of the French Bordeaux group, and Dr. Vivek Reddy of Massachusetts General. (The author is indebted to his colleague Dick Inglis for this info and for his idea of comparing the Pappone/Bordeaux/Reddy approaches to ablating Chronic A-Fib.)

Pappone Haïssaguerre Reddy
Pulmonary Veins Pulmonary Veins & Left Atrial Appendage Pulmonary Veins
Pulmonary Vein-Mitral Valve Isthmus Line
Left Atrium Roof Left Atrium Roof CFAEs
Posterior Wall Left Atrium Roof
Coronary Sinus Coronary Sinus & Inferior left Atrium Mitral Isthmus Block Line
Septal Area Areas of Atrial Activity: Outer left Atrium, LAA, Septum, Posterior Left Atrium, Superior Vena Cava, Right Atrium Septum (CFAEs) Right Atrium-Cavotricuspid Isthmus (for Flutter)
Right Atrium-Cavotricuspid Isthmus (for Flutter) Mitral Isthmus Block Line-Mitral Annulus to Left Inferior PV Coronary Sinus
Accessory Pathways (between Left Atrium & Left Ventricle) Right Atrium-Cavotricuspid Isthmus (for Flutter)
CFAEs

(Editor’s Notes: All three of the above stepwise approaches seem similar and in general ablate the same areas of the heart, though not in the same order. For example, all the stepwise approaches start with the Pulmonary Vein openings and move to making a roof line linear ablation linking the Right Superior Pulmonary Vein with the Left Superior Pulmonary vein opening. The main difference is Dr. Haïssaguerre’s emphasis on ablating the Left Atrial Appendage as the first step [see 5-Step Ablation Treatment for Chronic A-Fib]. This is a new approach  and may become an important first step in ablating for Chronic A-Fib.)

Another important development in ablating for Chronic A-Fib is the first clinical trials focusing on ablation of Chronic A-Fib in the US. Dr. Fred Morady of the Un. of Michigan is associated with these trials. His stepwise approach starts with Wide Area PV Ablation, then moves to Ablation of Fractionated Electrograms in the Left Atrium (particularly the septum and roof of the heart), the Right Atrium, the Coronary sinus and Superior Vena Cava until A-Fib can not be induced by isoproteranol.

Questions for Future Research

Since the Left Atrial Appendage (LAA) is so important in Chronic A-Fib, would closing off the LAA by the Watchman Device also help cure A-Fib, in addition to helping prevent A-Fib stroke?

Dr. Fred Morady of the Un. of Michigan gave the following presentation at one of the working lunches/dinners at the Boston A-Fib Symposium: “Lessons Learned: Providing Guidance for the Next (and Current) Generation of Ablationists”

Dr. Morady’s talk is combined with:

Dr. Hiroshi Nakagawa of the Un. of Oklahoma discussed his research in “Improving the Safety of Catheter Ablation of Atrial Fibrillation: Preventing of Left Atrial-Esophageal Fistula”

(Though it occurs very rarely, an Atrial-Esophageal Fistula [where a hole forms between the Esophagus and the Left Atrium after a Pulmonary Vein Ablation] is a dreaded nightmare for both patients and doctors. Most medical centers are making continuing, determined efforts to avoid this problem. Dr. Morady and Dr. Nakagawa described how Atrial-Esophageal Fistulas occur and how they can be avoided.)

How Atrial-Esophageal Fistulas Develop

An Atrial-Esophageal Fistula typically occurs 3-10 days after an ablation, and begins as an injury, lesion, or ulcer (Necrosis) of the Esophagus which then spreads to the Left Atrium. An Atrial-Esophageal Fistula normally isn’t caused by an ablation catheter punching through the left Atrium into the Esophagus. Rather, the heat from an ablation catheter penetrates from the posterior Atrium wall to the Esophagus and causes the damage. The Esophagus lies directly behind the posterior left Atrium wall, usually near the Left Pulmonary Veins and Coronary Sinus. According to Dr. Nakagawa, Fistulas are associated with stomach acids [reflux] interacting with the damaged Esophagus. Stomach acids may reach the esophagus because of relaxation of the lower esophageal sphincter due to injury to the nerve system around the esophagus.

According to Dr. Morady, a patient with an Atrial-Esophageal Fistula experiences pain when swallowing, and fever. These symptoms are often accompanied by clinical signs of blood bacteria (Bacteremia), inflammation of the lining of the heart and valves (Endocarditis), and/or Emboli (bubbles).

Preventing Atrial-Esophageal Fistula

In a study using canine models by Dr. Hiroshi Nakagawa from the Un. of Oklahoma, preventive measures were employed during Pulmonary Vein Ablations such as using only 15-25 Watt power catheters for 30 seconds near the Esophagus, and an Esophageal temperature probe calibrated to stop the ablation if there was a temperature rise of just 0.2°C in the Esophagus. Even with these precautions, an inspection of the interior of the Esophagus the next day (an Endoscopy), revealed Esophageal lesions in 46% of subjects.  However, treatment with sucralfate (brand name Carafate—a medicine used to heal ulcers) and a Proton Pump Inhibitor omeprazole (brand name Prilosec) for two weeks prevented any Fistulas from forming.

(It is disturbing that, even when taking precautions, 46% of ablation patients developed Esophageal Lesions.

However, the major medical breakthrough news is that Esophageal Lesions were prevented from developing into Fistulas by a simple two-week treatment with Carafate and a Proton Pump Inhibitor. This treatment works possibly because it prevents stomach acids from irritating the damaged Esophagus. But be advised, this data is new, preliminary and experimental, and has not been extensively studied.

If you are going to have a Pulmonary Vein Ablation, you may want to check with your doctor if he/she provides this or similar treatment after an ablation. Though Atrial-Esophageal Fistula is a very rare occurrence, it may be preventable by a very simple treatment.)

Evaluating Current Strategies to Prevent Atrial-Esophageal Fistula

Dr. Morady listed all the current techniques to prevent Atrial-Esophageal Fistula indicating which ones lacked in effectiveness:

TECHNIQUE EFFECTIVENESS EXPLANATION
Avoid RF Near the Esophagus Not Effective Especially in complicated cases of A-Fib, it’s often necessary to ablate near the Esophagus
Low Power for only 5-10 seconds near the Esophagus Not Effective Uncertainty about what is the maximum safe power
Probe to Monitor Esophageal Temperature Not Effective Even with a small rise in temperature, there are still lesions
Monitor for Bubbles with ICE Not Effective Not viable
Monitor for Pain Not Effective Sedation may mask pain, or the patient may not feel any pain
Displace (move) the Esophagus Away from the Spots to be Ablated Not Effective Not yet practicable
Cryoablation (freezing) for Sites Near the Esophagus Effective
Post-Ablation Carafate/Proton Pump Inhibitor 2-Week Program Effective

(From this patient’s perspective, the only sure fire way to prevent Atrial-Esophageal Fistula is to use Cryo Ablation (Freezing) for sites near the Esophagus, and to follow a treatment program of Carafate/Proton Pump Inhibitor for two weeks post-ablation.)

What to do in case of Atrial-Esophageal Fistula

Dr. Morady discussed what treatments to use if someone develops Atrial-Esophageal Fistula.

  • Perform a CT scan with water soluble contrast by mouth, looking for: In the chest, air in the space between the lung sacks (the Mediastinum), and for Fistulous tracts.
  • Do not use TEE (Transesophageal Echocardiogram) or Endoscopy, because they might damage or irritate the Fistula.
  • ASAP Esophageal Isolation Surgery (to allow the Esophagus to heal and to not be affected by stomach acids), and a Gastrotomy (a surgical incision into the stomach for food)

Current “Tailored” Approach Used at the Un. of Michigan

What’s the best ablation technique for curing A-Fib? Dr. Morady described how and why he and his colleagues back in 2006  changed from the Circumferential PV Ablation approach to a more tailored, individualized segmental treatment of A-Fib patients. (For a more detailed explanation, see Morady Boston A-Fib Symposium 2006).

After two years of experience with the “tailored” approach, he illustrated the different ablation strategies.  (Note how the high-wattage “Drop-and-Drag” ablation lines in the left have been replaced by segmental, targeted lesions on the right with significantly less damage to the heart tissue.) 

Dr. Hans Kottkamp from the Clinic Hislanden-Heart Center in Zurich, Switzerland discussed “Is Catheter Ablation of Atrial Fibrillation Superior to Antiarrhythmic Drug Treatment for Rhythm Control?”

While medical guidelines recommend that A-Fib patients try one or two antiarrhythmic drugs before they can receive a Pulmonary Vein Ablation (Isolation) procedure, several studies indicate that ablation is far superior to current antiarrhythmic meds.

Current Antiarrhythmic Drugs Not Very Effective
Dr. Kottkamp described a study which compared the drugs quinidine plus verapamil and sotalol to a placebo. Patients were followed for a year with a very high quality protocol using daily Tele-EKGs (telephone transmission of EKG signals). The antiarrhythmic meds were better than the placebo, but not by much. Even studies of the new experimental antiarrhythmic drug Dronedarone indicate it is only 10-15% better than a placebo.

Recent Studies Comparing the Effectiveness of Antiarrhythmic Drugs vs. Catheter Ablation
Dr. Kottkamp described three studies which used the same type of high quality follow-up as described above. Patients were randomly assigned either an Antiarrhythmic drug (such as amiodarone, flecainide or sotalol) or a Pulmonary Vein Catheter Ablation (Isolation) procedure. They were followed for a year with 7-day EKGs or Tele-EKGs. Any recurrence of A-Fib over 30 seconds was considered a failure.6

For example, in the third study by Dr. Pappone, the drugs amiodarone, flecainide, and sotalol had an effectiveness ranging from 20%-30%; whereas Catheter Ablation had a success rate of 86%. (That’s a 64% difference in effectiveness!) The other two studies had similar results.

Complications of Antiarrhythmic Drugs vs. Catheter Ablation
From a patient’s perspective, the complications from taking antiarrhythmic drugs are dissimilar and unequal to those arising from a Catheter Ablation.
Antiarrhythmics may produce a long-time complication risk. Drugs such as amiodarone may cause thyroid or other toxic problems, flecainide can lead to Ventricular Tachycardia or Atrial Flutter, sotalol may cause sexual impairment. In the three studies cited above, these antiarrhythmic drugs caused 23% of patients to withdraw from the studies.

Another serious complication of antiarrhythmic drugs is the A-Fib patient’s risk of “remodeling” in which the heart is stretched, develops more Fibrosis, and progresses to Cardiomyopathy.  Dr. Kottkamp showed a disturbing visual of a patient’s heart tissue in sinus rhythm with 5% Fibrosis, a Paroxysmal patient with 14% Fibrosis, and a Persistent patient with 35% Fibrosis. Fibrosis is generally considered irreversible. Currently we do not know how fast the heart progresses through the different stages of A-Fib Fibrosis.

Catheter Ablation, however, produces a 1-time complication risk of around 4% which ranges from mild to somewhat serious though treatable. (None of the above three studies had an Esophageal Fistula complication which is increasingly rare.)

Editor’s Comments:

Catheter Ablation is far superior to antiarrhythmic drugs for most A-Fib patients, as these randomized studies with very rigorous follow-up show. Catheter Ablation is both more effective and has less worrisome risks of complications. (For example, bruising in the groin which usually goes away in a couple of weeks is a 1-time complication of Catheter Ablation. This bruising is, from a patient’s perspective, of much less concern than the long-term risk of destroying one’s thyroid from being on amiodarone.)

As Dr. Jeremy Ruskin of Massachusetts General pointed out in a talk at Cardiostim 2008, “…we certainly know that ablation makes people feel better.”Anyone who has been cured of A-Fib by a Catheter Ablation (as this author was in 1998) can testify to how wonderful it feels to have a heart that beats normally again.

In addition, as Dr. Kottkamp pointed out, a successful Catheter Ablation, seems to improve overall heart health, even in patients with heart failure and Fibrosis.

Current Guidelines Don’t Work

Though current guidelines recommend trying two antiarrhythmic drugs before one can get a Catheter Ablation, this policy seems outdated and not in the best interest of most A-Fib patients.

If you ask, most doctors (though not necessarily insurance companies) will allow you to have a Catheter Ablation without having tried antiarrhythmic drugs. But it’s currently up to you to ask. (But see Calkins: Catheter Ablation Approved as First Line Therapy for A-Fib Patients.)

Dr. Hugh Calkins from Johns Hopkins discussed “The HRS/EHRA/ECAS Expert Consensus Statement of AFib Ablation7

Implications for Patient Care and Clinical Investigation.”

(Editor’s Comments: the consensus statement demonstrates that Electrophysiologists and Surgeons have moved from an attitude of competition to one of collaboration and cooperation in treating A-Fib patients. The consensus statement addresses issues with major implications for A-Fib-ers.)

The consensus statement is intended to provide a foundation of techniques, definitions and guidelines for Catheter and Surgical A-Fib ablation. Here are excerpts from the consensus document and its goals.  (Many medical organizations participated in developing this consensus statement. They are listed on the References page.8The complete text can be found at Consensus Statement for A-Fib.

1. Standardize procedures and terminology. The three types of A-Fib are defined:
“Paroxysmal A-Fib”: recurrent A-Fib that terminates spontaneously within 7 days

  • “Persistent A-Fib”: A-Fib which is sustained beyond 7 days, or lasting less than 7 days but necessitating pharmacologic and/or electrical cardioversion
  • “Longstanding Persistent A-Fib”: continuous A-Fib of greater than one-year duration (the terms
  • Permanent” or “Chronic” aren’t appropriate any more, because patients with Longstanding Persistent A-Fib can now be effectively treated by ablation)

2. Identify the symptoms and clinical situations where catheter and surgical ablation is appropriate.
Catheter Ablation

In a major change from current medical guidelines, catheter ablation is approved as first line therapy for A-Fib patients. “In rare clinical situations, it may be appropriate to perform A-Fib ablation as first line therapy.” (Recognizing what is a common practice in many centers, this new guideline no longer requires patients to have tried and failed antiarrhythmics meds before getting an ablation. In addition, insurance companies no longer have a basis to deny coverage to patients based on medical guidelines. The guidelines have changed. See also Kottkamp: Catheter Ablation Far Superior to Antiarrhythmic Drugs.)

3. Surgical Ablation
Surgical ablation is appropriate for:

  • Patients undergoing other cardiac surgery
  • “Patients who prefer a surgical approach, have failed one or more attempts at catheter ablation, or are not candidates for catheter ablation” such as those allergic to anticoagulants, or who have a thrombus (clot) in their heart. Surgery may also work better for severely obese people.

4. Recommend ablation techniques.

  • The importance of Pulmonary Vein Isolation and linear lesions is recognized. “In patients with long standing persistent A-Fib, PV Isolation alone may not be sufficient (linear lesions and other ablation techniques may be necessary).”

5. Determine procedural “end points”—situations where an ablation would be considered a success or failure.

  • A blanking period (time to allow the heart to heal from the ablations) of three months should be allowed before monitoring for reoccurrence of A-Fib, A-Flutter and/or Tachycardia; and repeat procedures should be delayed for at least three months.
  • An episode 30 seconds or longer should be considered a reoccurrence, but may under represent the true benefit of the ablation. (An ablated patient may feel healthy and improved, may return to normal life, even with occasional short episodes of A-Fib or while needing to take antiarrhythmic meds.)

6. Help decide anticoagulation strategies.

  • Warfarin (Coumadin) is recommended for all patients for at least two months following ablation
  • Warfarin therapy should be continued in patients with a CHADS2 score of 2 or more.

7. Establish requirements for physician training and competencies.  (A-Fib ablations require specialized equipment and special technical training and skills.)

  • Doctors in clinical training should have performed a minimum of 30-50 ablation procedures, though “this number underestimates the experience required for a high degree of proficiency.”
  • Outcomes are better at centers that have performed more than 100 procedures.
  • Electrophysiologists should perform several A-Fib ablation procedures per month if they intend to remain active in this area.

8. Specify patient follow-up criteria.

  • Patients should be seen in follow-up at a minimum of three months following the ablation procedure and then every six months for at least two years.
  • 24-hour Holter monitoring is recommended at three to six month intervals for one to two years following ablation.
  • For patients who complain of palpitations during follow-up, an event monitor should be used to screen for recurrent A-Fib, A-Flutter, and Tachycardia.

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Last updated: Friday, January 1, 2016

References    (↵ returns to text)
  1. Camm, “Stroke in atrial fibrillation: Update on pathology, new antithrombotic therapies, and evolution of procedures and devices.” Annals of Medicine, 39:5, 371-391, 2007
  2. Turpie, “New oral anticoagulants in atrial fibrillation.” European Heart Journal advanced publication 12/19/07
  3. The Center for Shared Decision Making. http://www.dartmouth-hitchcock.org/medical-information/decision_making_help.html
  4. Turpie, “New oral anticoagulants in atrial fibrillation.” European Heart Journal advanced publication 12/19/07
  5. Turpie, “New oral anticoagulants in atrial fibrillation.” European Heart Journal advanced publication 12/19/07
  6. Wazni OM et al: JAMA 2005; 293:2634-2400.Stabile G et al: European Heart Journal 2006; 27:216-221,Pappone C et al: J Am Coll Cardiol  2006; 48: 2340-47.
  7. Calkins H, Brugada J, Packer DL et al. HRS/EHRA/ECAS expert consensus statement on catheter and surgical ablation of atrial fibrillation: recommendations for personnel, policy, procedures, and follow-up. Heart Rhythm Society 2007 Scientific Sessions; May 9, 2007: Denver, CO. DOI: 10.1016/j.hrthm.2007.04.005
  8. A report of the Heart Rhythm Society (HRS) Task Force on Catheter and Surgical Ablation of Atrial Fibrillation.
    Developed in partnership with the European Heart Rhythm Association (EHRA) and the European Cardiac Arrhythmia Society (ECAS); in collaboration with the American College of Cardiology (ACC), American Heart Association (AHA), and the Society of Thoracic Surgeons (STS). Endorsed and Approved by the governing bodies of the American College of Cardiology, the American Heart Association, the European Cardiac Arrhythmia Society, the European Heart Rhythm Association, the Society of Thoracic Surgeons, and the Heart Rhythm Society.

2015 AF Symposium by Steve S. Ryan, A-Fib.com

Steve Ryan at the 2015 AF Symposium

Steve Ryan 2015 AF Symposium

20th Annual AF Symposium

Mechanisms and New Directions in Therapy, January 8-10, 2015, Orlando, FL

My AF Symposium reports are in three parts (click title to go to that page):

Part 1: News & Views from the 2015 AF Symposium (below)
Part 2:  My Brief Reports
Part 3:  My In-depth Reports Written for Patients

Looking for other AF Symposium reports? see Steve’s AF Symposiums Summaries By Year

The annual AF Symposium (formerly called the Boston AF Symposium) is an intensive and highly focused three-day scientific forum that brings together the world’s leading medical scientists, researchers and cardiologists to share the most recent advances in the treatment of atrial fibrillation.

I attend in order to offer A-Fib.com readers the most up-to-date A-Fib research findings and developments that may impact the treatment choices of patients who are seeking their A-Fib cure (or best outcome).

News & Views From the 2015 AF Symposium

Orlando Mariott slide

One of four water slides at the Orlando World Center Marriott.

by Steve S. Ryan, PhD

The Symposium was held at the Orlando World Center Marriott, the largest Marriott hotel in the world which is a tourist attraction in itself. With 2,009 rooms, all 1,000+ Symposium attendees could stay at the same hotel (unlike when the Symposium was held in Boston when going outside was a necessity rather than an option.)

The grounds were relaxing as well as beautiful and a fun walk after spending 10-11-hour days concentrating on heavy-duty, content-rich talks.

I was surprised at how crazy the air conditioning was at the Marriott. In the morning in the large meeting room you’d be freezing and need a heavy jacket. Then in the afternoon sometimes they’d shut off the AC and you’d be sweltering and stinky and need a shower before the next meeting.

As a journalist, my registration fee was waived, but all my other costs were out-of-pocket. So, I stayed at the Motel 6 down the road for $30+ a night (with AARP discount) and drove a Payless rental car from the Orlando airport for $13.00/day plus taxes (I brought my own GPS for the car). But the Marriott did get me for $18.00/day to park in their garage.

About the 2016 AF Symposium

Dr. Jeremy Ruskin, Director of the Symposium, announced that next year the AF Symposium hotel location will move to the Orlando Hyatt Regency and will be scheduled a week later in the month, January 14-16, 2016. The later date will help avoid the mad dash right after the New Year holiday to get organized, make travel plans, etc.

Celebrating the 20th Anniversary of the AF Symposium: A Nostalgic Look Back

David Keane MD Ireland

David Keane

Dr. David Keane of St. Vincent’s University Hospital in Dublin, Ireland, gave a heart-warming, nostalgic presentation about how the Boston/Orlando AF Symposium has developed and evolved over 20 years.

He found a wealth of old photos starting when the Symposium was only a one-day meeting for local doctors. He showed an ‘excited’ Dr. Jeremy Ruskin back in 1995 initiating the first AF Symposium in Boston.

Jeremy Ruskin, MD

J N Ruskin

Dr. Keane related how Dr. Jeremy Ruskin would spend his summers inviting speakers, developing topics, constantly planning and improving the content of the AF Symposium. “You have no idea just how much effort Jeremy Ruskin puts into these meetings.”

One of the most surprising slides was of a draft of a proposed schedule by Symposium Director, Jeremy N. Ruskin. It read “JNR Draft 58”!

[The next day I happened to be walking down the hallway with Dr. Ruskin. He mentioned that this year’s Symposium only took 70 drafts! His own talk was the first to go on the chopping block to make room for another speaker.]

Dr. Ruskin said he has probably put in about 10,000 hours over 20 years planning the Symposiums! Many speakers offered their heartfelt thanks to Dr. Ruskin for his incredible efforts.Steve Ryan

Steve S. Ryan photo: another surprising slide was one of me! I was so shocked I can’t tell you what was said. I think it was something about patients who attend the AF Symposium. (I’ve been writing reports on the AF Symposiums since 2003―twelve years!)

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Live via Satellite—Seven Catheter Ablation Cases-2014 Boston AF Symposium

Boston AF Symposium

What is the ‘Boston AF Symposium’ and Why its Important to Patients

2014 Boston AF Symposium

Live via Satellite—Seven Catheter Ablation Cases: Impressive Educational and Technical Achievement

By Steve S. Ryan, PhD The most impressive technical achievement of the Symposium was seven live satellite ablation cases including one from Siberia. The satellite cases alone were worth the price of admission.

In previous Symposia two or three satellite cases would be interspersed with pre-recorded videos. But this time they scheduled seven live cases back to back and for some events, even intercut between locations. Note: Throughout the Symposium doctors would often describe a particular device but not name it or the company which produced it. They probably wanted to avoid any conflict of interest or didn’t want to appear to favor one device or procedure over another. But I did research after the presentations and for the most part, I have identified and noted the name and manufacturer of particular devices that were demonstrated. GFX TV set Lights Camera Action

GFX TV set THE NETHERLANDS 150 pix by 96 resHYBRID THORASCOPIC SURGICAL AND CATHETER ABLATION OF PERSISTENT AF (The netherlands)

Drs. Mark La Meir and Laurent Pison of Maastricht University Medical Center in the Netherlands performed live a hybrid surgical and catheter ablation The patient was a very large man with significant body mass, exactly the type of patient often referred for surgery by EPs. It’s difficult for current ablation mapping technologies such as fluoroscopy to see clearly through significant body mass.  Several ports were cut in between the rib openings on one side of the chest. (I neglected to count how many and apologize for this oversight.) 

The robotic camera and operating instruments were inserted through the various ports. With this system the patient did not have to go on bypass. His heart was still beating when the surgical lesions (RF burns) were made. He did have to have one side of his lungs deflated and re-inflated in order to fit the AtriCure bipolar RF clamp around the pulmonary veins. This same procedure was repeated on the other side of the chest after the live presentation.

The images transmitted by the robotic camera were remarkably clear and vibrant. The clamp was inserted around each vein. 5-6 burns at a median output of 10 to 15 W were made on each vein to ensure transmurality. A roof line was also made. [I apologize for not being able to follow what additional lesions or burn patterns were made.] It was remarkable how big the patient’s Left Atrial Appendage was and how active and rapidly it pumped into the ventricle along with the left atrium. It was fascinating to watch the surgeons position the AtriClamp on the LAA and close it off.

[After the LAA is closed off, I’m told it eventually shrivels up like a dried grape. Partially because his LAA was so large and active, this patient will likely experience a significant loss of pumping volume in his left atrium after closing off his LAA. But he probably wasn’t very active any way and may not even notice the change.] They did not perform ablation of the ganglionated plexi areas. “There is until now too little evidence to advocate a systematic ganglionated plexi ablation strategy.”1

GFX TV set SIBERIA RUSSIA150 pix by 96 resRenal Denervation and Pulmonary Vein Isolation for PAF (siberia, russia)

Probably one of the most technically difficult cases to schedule and coordinate was a live presentation from Siberia. (One can only imagine the effort it must have taken to pull this off!)  Dr. Evgeny Pokushalov and his colleagues at the State Research Institute of Circulation Pathology in Novosibirsk, Russia worked on a 55-year-old female patients who had high blood pressure that couldn’t be lowered by drugs or other methods and who had A-Fib. She had a moderately enlarged left atrium (5.2mm) and a CHA2DS2-VASc score of 2. (Hypertension  [high blood pressure] is a well-recognized trigger or cause of A-Fib, probably because of the extra pressure and stress it puts on the Pulmonary Veins where most A-Fib develops. This patient’s A-Fib probably was caused and sustained by high blood pressure.)

Dr. Pokushalov and his colleagues first did a normal PVI checking for Entrance and Exit Block and waiting 40 minutes to see if recurrence occurred before completing the PVI. They then mapped and developed a 3-D image of the artery and its branches leading to the kidneys just as EPs do when mapping and doing an ablation of the heart’s left and right atria. They made ablation burns within the artery branches leading to the kidneys (renal denervation) at 10 Watts for 6 seconds thereby reducing Sympathetic Tone (the functioning of the Sympathetic Nervous system). They made four burns in each artery branch, but they acknowledged that this field is so new they don’t know if this is the best technique. “What is a clear end point? How many burns are enough?” It’s not like doing a PVI catheter ablation where one can see the patient return to sinus rhythm.

They said they’ve done over 100 of these renal denervations with no complications. They use the same catheter as for PVI ablations. They said they need to use more sedation than with a normal Paroxysmal PVI ablation. (Research has shown that when one partially ablates the nerves going to the kidneys, this can significantly reduce blood pressure in people who can’t otherwise lower their hypertension. It also seems to diminish A-Fib attacks. These four burns in each artery branch didn’t seem to affect the integrity of the arteries.)

Later in the Symposium different presenters discussed the just released findings of the Medtronic Symplicity HTN-3 trial which basically found that Medtronic’s system – though safe – was no better than a sham procedure for reducing office systolic blood pressure through six months.  What this means is that renal denervation, although performed frequently in Europe and in other parts of the world, will not be approved in the U.S. in the foreseeable future. (The clinical trials Symplicity 1 and 2 seemed to produce good results and had a clear therapeutic effect. Other data have shown that renal denervation reduces blood pressure in animal models and in smaller human trials. One doctor speculated that the artery nerves are very deep and that in the Symplicity 3 trial the energy level used may not have been high enough to penetrate to the nerves.)

Attendees seemed shocked and disappointed at this news.

Everyone, both doctors and patients, expected and hoped renal denervation would work. For some patients, who had tried everything else, it was their only hope to reduce their high blood pressure. There are many other methods being tested to denervate the renal arteries. But because of this news, one company has already announced it’s halting its trial. Until the data from Symplicity HTN-3 can be more thoroughly examined, renal denervation may be dead in the water.

Editor’s comments: This ultimately may not be a bad thing. It points out the importance of well-performed trials to prevent the premature adaption of therapies [whether procedures or drugs] until they are thoroughly studied. It’s difficult when the expected benefits of renal denervation are so high, when patients know about it and request it, and when the procedure is recognized as safe. But in spite of its promise and the data coming from Europe, preliminary findings from the Symplicity HTN-3 study indicates that renal denervation doesn’t work.

GFX TV set THE NETHERLANDS 150 pix by 96 resThen back to the Netherlands and the Hybrid

They then cut back to the Netherlands to show the catheter ablation part of the operation. The EP used a Lasso catheter inside the heart to confirm that the pulmonary veins were indeed isolated.

The EP basically continued the lines inside the heart that the surgeon had created outside the heart. The EP also ablated the right atrium for Flutter which current surgical approaches can’t do. The EP also ablated the Coronary Sinus. They mentioned that if someone has been in Persistent A-Fib for over three years, the success rate drops by 25%. If someone has had a previous heart operation, they generally can’t undergo this Hybrid Operation. Their goal is to return a patient to sinus rhythm during the operation. If they have to cardiovert someone to return them to sinus rhythm, the operation isn’t as successful.

They talked about making a box set of lesions in the posterior left atrium to “debulk” that area, to stop A-Fib signals from propagating through the left atrium substrate which is often necessary in cases of persistent A-Fib.

GFX TV set BORDEAUX FRANCE 150 pix by 96 resCatheter Ablation of Persistent AF Guided By Noninvasive Mapping (Bordeaux, France)

Dr. Mélèze Hocini of the Centre Hospitalier Universitaire De Bordeaux was introduced with her arms poking through arm holes in what looked like a Plexiglas type of shield, undoubtedly to protect her from radiation during the ablation.

In the beginning Dr. Hocini couldn’t hear Dr. Ruskin and Dr. Mansour in Orlando. But that problem was soon resolved. (She was very poorly lit with low production values.) Dr. Hocini’s 61-year-old male patient had been in Persistent A-Fib for four months. Such cases are generally the hardest to cure. Someone in Persistent A-Fib has usually been in A-Fib for a long time and has often developed many A-Fib producing spots throughout the left and right atria. In this type of case, a simple Pulmonary Vein Isolation Ablation (PVI) usually won’t terminate A-Fib.

The patient also had a huge left atrium (59mm) and a lot of fibrosis (22%). In the MRI fibrosis scale he would have been classified as a Utah 3. All the attendees recognized that this was a difficult case.

This was a truly ground-breaking presentation and historically an important milestone in the treatment of A-Fib.

For the first time the world saw the ECGI (body surface) imaging and mapping system in action and in practical, day-to-day use. Instead of having to spend a great deal of time and effort [and radiation exposure] mapping and hunting down the multiple A-Fib-producing spots in the heart, this was all done beforehand for Dr. Hocini using ECGI.

The day before his ablation, the patient simply laid down with a special vest on his chest like having an ECG exam with 256 electrodes rather than just twelve. These electrodes, imaged on the patient by a CT scan, produced an exact 3-D image of his heart and, what was most innovative, identified and labeled the location of all the spots producing A-Fib signals. This 3-D rendering of the left and right atrium with CT scan showed many different foci and rotors in the patient’s heart, but they seemed to cluster in three distinct areas. ECGI established a hierarchy of where to ablate. One starts where the most foci and rotors are.

Fibrosis doesn’t guide the procedure or change this hierarchy at the present time. Rotors are generally found next to or bordering areas of fibrosis in preliminary data. We then saw Dr. Hocini ablating the areas that showed up on the ECGI. For an extensive discussion of ECGI, see my reports under the 2013 Boston A-Fib Symposium.

GFX TV set MILAN ITALY150 pix by 96 resLEFT ATRIAL APPENDAGE CLOSURE (Milan, Italy)

From Milan, Italy. Drs. Claudio Tondo, Gaetano Fassini and Antonio Bartorelli of the Centro Cardiologico Monzino, University of Milan, Italy did a live insertion of a new Left Atrial Appendage (LAA) closure device available in Europe but not currently approved in the US. The patient receiving the device was a 72-year-old man in Chronic A-Fib who had a history of intestinal and cerebral bleeding. He also had a stroke risk score of four which meant he needed to be on anticoagulants and protected from having an A-Fib stroke.

Coherex AFIB Wavecrest occlusion GFX - after placement the catheter is withdrawn - used with permission

Coherex AFIB Wavecrest occlusion GFX – after placement the catheter is withdrawn – graphic used with permission

The Coherex WaveCrest occluder they installed looked like a piece of white foam with little barbs or hooks which attached the device to the LAA but were small enough that they wouldn’t puncture it. The device collapsed so that it fit on the end of a catheter which they maneuvered into the left atrium and into the LAA using fluoroscopy (X-ray) imaging and ICE (Intracardiac Echo).

They had different sizes and shapes of these occluders to fit patients’ different LAA openings. Once inside the LAA they opened up the device, like opening up an umbrella, and attached the hooks. They weren’t happy with their first two tries and re-collapsed the device and repositioned it in the LAA a third time.

To check that they had good contact and closure, they injected dye from the tip of the catheter to see if any would flow past the device into the left atrium. Then they simply withdrew the catheter, leaving the occluder in place in the LAA. This whole procedure seemed really simple to perform, though these doctors developed this facility only after years of study and experience. And it didn’t take long to do. (I know an EP in Los Angeles who installs the Watchman device in an average time of 20 minutes.) Anyone thinking of having a LAA occluder device installed could benefit from seeing this Left atrial appendage (LAA) Animation by Coherex. It’s reassuring to see how apparently easy it is to install.

Editor’s comments: Regarding A-Fib Stroke Risk, Blood Thinners and Occlusion Devices
One of the most difficult tasks of a Cardiologist/Electrophysiologist (EP) is to determine, along with the patient, whether or not someone in A-Fib has a real need to be on anticoagulants. Blood thinners are not benign drugs. They’re not like taking vitamins. Current anticoagulants have their own set of risks and, in spite of the ads you see on TV, they are not to be taken lightly.
This 72-year-old man had a high A-Fib stroke risk score and certainly needed protection from an A-Fib stroke which can be a fate worse than death. In A-fib the upper part of your heart (the left atrium) doesn’t pump out properly but instead fibrillates. Large clots can form usually in the Left Atrial Appendage (LAA) where 90%-95% of A-Fib clots come from. These clots are usually much larger than a “normal” clot. When they break loose and are transported to the rest of the body, they can completely close off a vein branch and cause a lot of damage.
But when this 72-year old man took blood thinners, he suffered intestinal bleeding and cerebral hemorrhaging. This unfortunately happens all too often when one has to take anticoagulants especially as one gets older, and is part of the risk/reward ratio doctors and patients have to agonize over. Since he couldn’t tolerate blood thinners, this 72-year-old man decided to have his LAA closed off, where 90%-95% of A-Fib clots come from. It’s not an absolute guarantee he will never have an A-Fib stroke. There’s still that 5%-10% chance. But it’s probably his best option.
If you can’t tolerate blood thinners or just don’t want to take them, you may want to check out LAA occlusion devices like the Watchman, Lariat II or AtriClip. Your doctor can discuss with you the strengths and weaknesses of each device. The Watchman is still in clinical trials in the US, but was recently approved by an FDA advisory panel.
LAA occlusion devices do reduce blood flow in your heart which may be a concern if you are young and exercise regularly. But if you’re in your 70s or 80s and/or aren’t very active, this probably isn’t something to worry about.

GFX TV set BORDEAUX FRANCE 150 pix by 96 resBack to Bordeaux, france Again

Dr. Hocini in France and Drs. Michele Haissaguerre and Pierre Jais in Orlando pointed out that many foci in persistent A-Fib patients are found in the left and right atrial appendages. This patient’s inferior left atrium, as is often the case, had the highest number of rotors.

They discussed the fact that rotors do seem to drift somewhat. But they can be broken up or stopped from rotating by cross hatch ablations or other techniques such as using the newer circular wide area ablation catheters to encircle and block off the rotor areas. Thanks to ECGI this procedure used much less RF energy and needed much less RF burns than the old five-step protocol, which was good both for the patient and for the operating doctor. Later in the day Dr. Ruskin announced that this patient’s persistent A-Fib was eventually terminated and that he was in normal sinus rhythm.

GFX TV set Frankurt 150 by 96 - revisedNew CryoBalloon Ablation (FrankfUrt, Germany)

Arctic Cryoballoon Catheter

Arctic Cryoballoon Catheter

They then cut to Frankfurt, Germany. Drs. Boris Schmidt and KR Julian Chun of the Cardioangiologisches Centrum Bethanien performed a CryoBalloon ablation (“ICE T concept”) using the new, second-generation Arctic Front Advance Cardiac Cryo Ablation catheter (Medtronic) with eight cooling ports instead of four.

The patient was a 61-year-old female in Paroxysmal A-Fib for two years. They used a temperature probe in the esophagus (as in RF ablation) The temperature in the esophagus should not go cooler than +12°C. Therefore they stop the freeze at +15°C. In contrast, if the CryoBalloon temperature goes beyond -60°C, they stop the freeze rather than complete the ablation. In Germany they have been using the CryoBalloon catheter for years before it was approved by the FDA for use in the US. Their results have been very good. The process of making the CryoBalloon ablations seemed amazingly fast.

GFX TV set MI USA 150 pix by 96 resThermal Balloon Ablation (Michigan, USA)

We then were transported to Royal Oaks, Michigan. Dr. David Haines of William Beaumont Hospital performed a thermal balloon ablation for paroxysmal A-Fib. The Toray Satake Hot Balloon Catheter is named after its inventor Dr. Shutaro Satake of the Hayama Heart Center in Japan who was with Dr. Haines.

The balloon is filled with a solution of saline. When radio frequency energy is applied through a coil electrode in the balloon, this heats the saline. Dr. Haines maneuvered the balloon into a pulmonary vein opening. When he pressed the balloon into the PV opening, the compliant material of the balloon seemed to mold itself to the shape of the opening. He would apply heat to the PV opening for around 2½ minutes and heat it to 70 degrees Celsius. He used an esophageal probe to measure heat and a special cooling system in the esophagus. He also paced the phrenic nerve to make sure it wasn’t damaged by the heat.

Dr. Satake has performed over 500 ablations in Japan using this Hot Balloon catheter. One would expect applying this much heat to an extensive area of the PV openings would carry an increased risk of stenosis, a swelling of the pulmonary vein opening restricting blood flow. But Dr. Haines says this has not been the case. (For a detailed description of the thermal balloon catheter, see the subheading “Radiofrequency ‘Hot’ Balloon” in the article, “Balloon Catheters for Ablation“.) In an interesting juxtaposition during Dr. Haines’ presentation, the satellite program cut back to the Frankfurt group who were doing CryoBalloon ablations. They had completely isolated all four pulmonary veins in 60 minutes. That’s a very short time to do a catheter ablation PVI.

They then cut back to Dr. Haines who finished his ablations with the Hot Balloon catheter. NOTE: Dr. Haines and three other centers are recruiting patients for preliminary clinical trials of the Hot Balloon Catheter. The other centers are Mount Sinai in New York (Dr. Vivek Reddy), Texas Cardiac Arrhythmia Institute in Austin (Dr. Andrea Natale), and the Medical University of South Carolina in Charleston (Dr. J Marcus Wharton).

Editor’s comments: As a patient you may be asking which of these different catheter balloon strategies would be the best for me. It’s far too early to tell with the Thermal Balloon until it gets further along in clinical trials. But from what I’ve seen, I’m willing to speculate. Because the thermal Balloon is more compliant and flexible than the CryoBalloon, when it’s pushed up into a pulmonary vein, it probably burns higher up into the vein than the CryoBalloon. This combined with the RF heat would seem to be more apt to produce stenosis than the CryoBalloon. And stenosis is something patients need to avoid if at all possible. Unlike most other catheter ablation complications which are temporary and fixable, stenosis is permanent and usually irreversible. If you develop stenosis, your life is wrecked.   
CryoBalloon catheters are more rigid than the Thermal Balloon and, when sized properly, usually only freeze on the outside edges of a pulmonary vein. Because pulmonary vein openings aren’t perfectly round, it may take two or three CryoBalloon placements and freezes to completely isolate around a vein. But this is relatively easy to do.
Freezing creates a different kind of ablation than thermal RF. One advantage of Cryo is that, if the Balloon is improperly positioned, the preliminary freezing can be stopped and the area allowed to defrost and return to normal. This isn’t possible with thermal RF.
A freezing ablation looks different than a thermal RF ablation. There is no burn scarring. Frozen ablated heart tissue looks very similar and seems to have an integrity similar to that of normal heart tissue.
When the CryoBalloon is positioned against a vein opening, the preliminary freezing action sticks the balloon to the opening (like a kid sticking his tongue to a frozen lamp post). It’s harder for flowing blood to push the CryoBalloon away from the vein opening or create gaps.
Someone asked me why most of the world leaders in A-Fib ablation haven’t moved to CryoBalloon ablation, since it seems to be easier, faster and safer for patients than regular RF ablation. Most likely because they are so experienced and skillful with RF point-by-point ablation and get such good results, that for them RF ablation is as easy and fast as CryoBalloon ablation. And they generally work in the antrum and don’t get near the pulmonary vein openings. But this is definitely a question I need to ask these A-Fib leaders. Right now I don’t have the answer.

GFX TV set BOSTON USA 150 pix by 96 resRadiation Reduction Strategies (BOSTON, USA)

The last live case was from Massachusetts General in Boston with Drs. Kevin Heist and Moussa Mansour. The title of their presentation was “Radiation Reduction Strategies During Catheter Ablation of AF.” The patient was a 61-year-old female with a history of persistent Flutter. She also had three right veins instead of the normal two. (I have the same unusual anatomy.) The doctors used an innovative Electromagnetic Navigational System integrated with fluoroscopy (X-Ray). (Mediguide system, with NavX mapping, an externally irrigated ablation catheter and a pent array mapping catheter.)

It produced 3-D color images of the left and right atrium. You could see in real time the catheter electrode making burns. The doctors explained how this system used only 2-3 minutes of fluoroscopy compared to a normal ablation which could produce 38 minutes of radiation exposure. This was most welcome news for the attendees doing catheter ablations.

Editor’s comment: Radiation Reduction is a concern not just for patients, but especially for doctors, nurses and staff in the cath lab during ablations. I was recently in a cath lab and observed several ablation procedures. I and everyone there had to wear a leaded waist belt, vest and thyroid protector. The doctor doing the procedure wore special anti-radiation glasses to protect him from retinal radiation damage. These leaded protectors are not light. The floor is padded to make it easier for the EP to stand with all this weight. Doctors may do 3-4 ablations a day and are exposed to a lot of fluoroscopic radiation. Doctors and others in the cath lab worry about being exposed to so much radiation and its long-term effects. Anything that will lower exposure to radiation in the cath lab is important both to patients and particularly to doctors.

SUMMARY OF THE SATELLITE EVENTS

GFX TV set THATS A WRAP 150 pix by 96 resThese live satelite events were extremely informative and educational. And as a five-and-a-half hour event, quite an accomplishment. Having worked in broadcast television and on several Live TV events (i.e.; the live EMMY Awards Presentation show, broadcasting of the 1984 Los Angeles Olympics and numerous sporting events for NBC), I know this was an incredibly complex event.

The staging teams had to coordinate and intercut between multiple satellite and trans-oceanic optical fiber video feeds. But before that, the planning teams had to schedule and coordinate multiple locations, with multiple cameras, audio and lighting personnel and equipment in order to video the numerous doctors working in their respective operating rooms and EP labs. (Not to mention dealing with the multiple languages spoken by the doctors and their staff).

Frankly I doubted they could pull it off, especially since the Symposium was held at a new conference site. But, WOW! From the audiences’ perspective the presentations were seamless and, except for some audio problems, the presentations came off perfectly. (Though I’m sure the behind-the-scenes people were pulling out their hair trying to make everything work.)

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Last updated: Wednesday, September 2, 2015 

References    (↵ returns to text)
  1. Pison, L. et al. Hybrid Thoracoscopic Surgical and Transvenous Catheter Ablation of Atrial Fibrillation. Journal of the American College of Cardiology, Volume 60, Issue 1, July 2012. http://content.onlinejacc.org/article.aspx?articleid=1208681

About the Annual AF Symposium (formerly the Boston AF Symposium)

What is the Annual ‘AF Symposium’ and Why it’s Important to Patients

by Steve S. Ryan, PhD

Introduction

The past two decades have witnessed dramatic advances in all areas of A-Fib research with major progress in our understanding of atrial fibrillation and the development of safer and more effective strategies for the treating and curing of atrial fibrillation.

The annual international AF Symposium (formerly called the Boston AF Symposium) is one of the most important conferences on A-Fib in the world. The Symposium is a major scientific forum at which health care professionals have a unique opportunity to learn about advances in research and therapeutics directly from many of the most eminent investigators in the field. This intensive and highly focused three-day symposium brings together the world’s leading medical scientists to share the most recent advances in the field of atrial fibrillation.

Why I attend the Symposium

Each year I attend the Symposium to learn and ‘absorb’ the presentations and research findings. Attending the annual AF Symposium gives me a thorough and practical view of the current state of the art in the field of A-Fib. I then apply this newly acquired knowledge and understanding to the publishing of A-Fib.com.

What this means to You

On the plane ride home I start writing summaries of significant presentations and important research findings that are relevant to A-Fib patients and their families. I strive to ‘translate’ as much of the medical jargon into everyday language. I add my own comments and insights to help interpret the information for A-Fib.com readers.

In the months following the Symposium, I write and post three or four reports each month usually ending up with about 15–20 articles. (Why does it take so long? I send each of my summaries to the presenter inviting their feedback, so it takes some time to get each article written, reviewed, and posted.) I announce each posting on the A-Fib News page with a link to each article.

For the readers of A-Fib.com, my goal is to offer the most up-to-date A-Fib research findings and developments that may impact the treatment choices of patients seeking their A-Fib cure.

Be warned: If you haven’t read and understood most of the articles on A-Fib.com, it may be difficult reading. (Hint: our Glossary of Terms may be helpful.)

Read: 2015 AF Symposium Reports by Steve S. Ryan, PhD

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Last updated: Saturday, February 14, 2015

2013 Boston AF Symposium

18th Annual Boston AF Symposium, January 17-19, 2013, Mechanisms and New Directions in Therapy

by Steve S. Ryan, PhD

Steve at entrance to BAFS 2013 exhibits Jan 17, 2013.

Steve at BAFS 2013 exhibits Jan 17, 2013.

INTRODUCTION

The annual international Boston A-Fib Symposium (BAFS) is one of the most important conferences on A-Fib in the world. It brings together researchers and doctors who share the latest information.

Each year I attend the Symposium to learn, and ‘absorb’ the presentations and findings. On the plane ride home I start writing summaries of significant presentations and important research findings as it applies to A-Fib patients seeking their A-Fib cure. I add my own comments to help interpret the information for A-Fib.com (non-medical) readers.

Over the next months, I will be posting my summaries. (FYI: I send each of my summaries to the presenter for their feedback before posting, so it takes time to get all my summaries written, reviewed, and posted.) I’ll announce each addition on the A-Fib News page with a link to each report.

Be warned: If you haven’t read and understood most of the technical articles on A-Fib.com, it may be difficult reading. (Hint: Our Glossary of Terms may be helpful.)

Over the three days of the 2013 BAFS, there were 43 presentations, eight Live and Pre-Recorded Case Presentations, and two 2-hour-long panel discussions.

By far and away the most innovative, important and groundbreaking presentations dealt with ECGI (Noninvasive Electrocardiographic Imaging) which the author predicts will revolutionize the way A-Fib is mapped and ablated. See my in-depth article: “Noninvasive Electrocardiographic Imaging“.

My reports on the 2013 Boston Atrial Fibrillation Symposium are divided into three parts (click title to jump to topic or open new browser window):

 Part 1:  BAFS Overview (below)
 Part 2:  Highlights of Symposium Presentations
 Part 3:  Steve’s In-Depth Reports

BAFS OVERVIEW

Surprise Announcement: AF Symposium will be moving to Orlando, FL in 2014

TBAFS 2014 Moving to Orlando FLhe 18th annual Boston A-Fib Symposium opened with a surprise announcement—the AF Symposium will be moving to Orlando, FL in 2014. It wasn’t just because of the January snow and cold in Boston. The Orlando World Center Marriott is a 200 acre resort that can house the entire Symposium meeting in one place.

The dominant mood of this year’s Boston A-Fib Symposium seemed to be impending change and a bitter-sweet nostalgia. The Symposium had been at the Seaport World Trade Center for 15 years, ever since the hotel opened. In Dr. Ruskin’s words, “we’re certainly going to miss them and this place.”

On a Personal NoteBeat Your A-Fib formats: eBook and print

I presented speakers with an autographed copy of our new book ”Beat Your A-Fib: The Essential Guide to Finding Your Cure. Most of the speakers are mentioned in the book’s Acknowledgements as a resource and support in writing the book. It is available both as a print book (see Amazon.com for reviews) and in a .PDF version. Visit our book site at www.BeatYourA-Fib.com for more info.

Over three days there were 43 different short presentations, eight Live and Pre-Recorded Case Presentations, and two 2-hour-long panel discussions—the first on Difficult Cases in AF Management, the second on Challenging Cases in AF Ablation. The most discussed subject was Persistent A-Fib with six different speakers.

Format: Speaker + Open Discussion

Most of the presentations were structured so that each speaker would have time to answer a few questions. Then after the last speaker’s presentation on, for example, ‘Persistent A-Fib’, each six speakers would then move to the elevated head table for a no-holds-bared discussion with the audience. Often these audience and speaker interaction discussions produced remarkably insightful comments and thinking. See for example “Difficult Cases in AF Management” below. (One featured speaker, who is one of the most experienced and knowledgeable doctors in A-Fib, said that the Boston A-Fib Symposium is the only conference where he attends all sessions.) Not only are the presentations excellent and provide new, important information, but the discussions after presentations are unique opportunities for the best minds in the A-Fib field to exchange ideas and viewpoints, argue, and expand their thinking about the major issues and challenges in A-Fib.

Speaker-Audience Interactivity Via Remote

As in previous years, each audience member had a remote clicker on which they could select choices. A presenter might ask, for example, which of the following five treatments would you recommend or choose in your practice? Within seconds the percentage of audience members selecting a choice would be flashed on the screen. This resulted in much more involvement and interaction of the audience with the presenters. It was also a learning experience for audience members to see how their colleagues’ choices compared to theirs.

Note: I am indebted to the writers and publisher of “The Boston AF Symposium News” (MediFore) for their daily news publication with many detailed reports.

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Last updated: Sunday, February 15, 2015

Boston AF Symposium – 2006

Boston AF Symposium, January 13-14, 2006

The annual international Boston A-Fib Symposium is one of the most important conferences on A-Fib in the world. It brings together researchers and doctors who share the latest information. Unlike other heart related conferences, it concentrates only on A-Fib. But if you haven’t read and understood most of A-Fib.com, it may be difficult reading.

Overview

The dominant tone of the 2006 Boston A-Fib Symposium seemed to be one of caution.

The first warning was about the re-occurrence of “silent” A-Fib in patients considered “cured’ of their A-Fib. Dr. Hans Kottkamp of the University of Leipzig, Germany described the use of a seven-day ECG to monitor patients after they were “cured” of their A-Fib by catheter ablation. Over a twelve month period 50% to 60% of cured patients experienced reoccurrences of their A-Fib. 70% of the reoccurrences were silent (asymptomatic) A-Fib. (See Kottkamp.)

A similar alarm was sounded by Dr. Hugh Calkins of Johns Hopkins Hospital who reported results using a seven-day Holter monitor. Over a six month period 31% of “cured” A-Fib patients experienced re-occurrences of their A-Fib, but 82% of these re-occurrences were silent (asymptomatic) A-Fib. (See Calkins.)
Silent A-Fib can be just as harmful as symptomatic A-Fib, according to Dr. John Camm of St. George’s Medical School in London, England. (See Dr. Camm’s presentation on Silent A-Fib in the Boston A-Fib Symposium 2004.)

Caveat: for those of us who have been “cured” of our A-Fib by a catheter ablation procedure, we may still have re-occurrences of silent A-Fib which could be dangerous. It would be a good idea to discuss monitoring for silent A-Fib with your doctor.

A common concern of many of the speakers was the recent deaths and traumatic events due to “atrial-esophageal fistula” where an unintended hole forms between the atrium and the esophagus. This may be due to using high wattage catheters in the back of the atrium near the esophagus. As one speaker put it, “There are only two kinds of Electrophysiologists—those who have not experienced a fistula (hole) in the esophagus and those who have!”

To minimize the danger of esophageal fistula (holes), Dr. Andre d’Avila of Massachusetts General described an Esophageal Temperature Monitoring device that is inserted in the esophagus next to the heart to monitor whenever the esophagus increases in temperature due to ablation in the heart. But this device is not yet a guarantee of not harming the esophagus. (See d’Avila.)

Another precautionary technique is to use a barium paste which the patient swallows to show where the esophagus lies in order to avoid making ablations near the esophagus. This was suggested by Dr. Fred Morady of the University of Michigan. (A possible danger of using barium paste in the esophagus is that barium might be breathed into the lungs and damage them.)

Dr. Morady completely reversed his position of two years ago when he was a proponent of the Pappone high wattage catheter “Anatomically Based Circumferential PV Ablation” method. He has abandoned this ablation method in favor of a procedure which identifies spiking A-Fib signals and ablates only them. (See Morady.) It is this author’s opinion that the Pappone high wattage catheter ablation procedure may pose serious dangers for patients and may be responsible for the recent deaths and traumatic events from atrio-esophageal fistula (holes).  1Another possible complication from the high-wattage catheter is damage to the Phrenic nerve in the Pericardium around the heart which may result in breathing difficulties.

A major, groundbreaking discovery was presented by Dr. Jose Jalife of SUNY Upstate Medical University in Syracuse, NY. He found that there are sites of high-frequency activity within a heart in A-Fib. When these sites are ablated, A-Fib can be terminated. (See Jalife.)

How to detect “Complex Fractionated Atrial Electrograms,” a new type of heart electrical signal, was discussed by the discoverer Dr. Koonlawee Nademanee of the Pacific Rim EP Research Institute in Inglewood, CA. “CFAE”s, when ablated, can eliminate A-Fib. (See Nademanee.)

The Bordeaux group’s newest procedures for curing Chronic A-Fib were discussed by Dr. Pierre Jaïs. He reported a success rate of 87% (which is remarkable considering how hard it is to cure Chronic A-Fib). (In a later follow-up study a success rate of 95% was reported using a second ablation procedure. Because of the importance of thi sarticle, the complete abstract is cited in the referance section.

In this author’s opinion, this is a major medical breakthrough in the A-Fib field.) He also identified several areas of the heart besides the Pulmonary Veins which produce A-Fib signals, including areas producing Dr. Nademanee’s “Complex Fractionated Atrial Electrograms.” (See Jaïs)

(It seemed to this author that several leading doctors in A-Fib were moving to a more individualized approach to curing patients, rather than using a one-size-fits-all procedure. See the presentations of Dr.Jaïs, Dr. Morady, and Dr. Marchlinski.)

Dr. Waldo’s data and conclusions cast doubt on aspirin’s effectiveness in preventing stroke from A-Fib. (See Waldo.)

The Symposium also featured two demonstrations of catheter ablation viewed live via satellite. In France Dr. Michel Haïssaguerre of the Bordeaux group performed an ablation of a woman with Chronic A-Fib. Dr. Vivek Reddy from Massachusetts General Hospital in Boston performed an ablation demonstrating the use of an experimental Cryoablation balloon catheter.

Also included is an update/summary of the 2006 Boston A-Fib Symposium by Drs. David Keane, Vivek Reddy and Jeremy Ruskin. Though written for the 2007 Symposium, it is included here—Update on Mechanisms and Therapy for A-Fib from the 11th Annual Boston A-Fib Symposium 2006. (This update is written by doctors for doctors and may be somewhat difficult to read. However, it is an excellent summary not only of the main points of the 2006 Symposium but of all the issues of concern to A-Fib patients today.)

Each presentation is listed by both the last name and by the topic of the presenter. If a doctor made more than one presentation, they are listed as (1) and (2). You can access a presentation either by the doctor’s name or by the topic. (Due to inadequacies of the author, all presentations are not currently summarized.)

 

TOPIC(S)
DOCTOR
TITLE OF PRESENTATION
Some “Cured” Patients in Silent A-Fib. Current Catheters Not FDA Approved. Calkins Defining Successful A-Fib Ablation
Esophageal Temperature Monitoring to Prevent Damaging the Esophagus  d’Avila Esophageal Temperature Monitoring During A-Fib Ablation
Should Drug Therapy or Catheter Ablation be Tried First Debate: Natale vs. Prystowsky Should Catheter Ablation Be First Line Therapy in Selected Patients with A-Fib?
Current Pacing Techniques Don’t “Cure” or Prevent A-Fib Gold Pacing to Prevent A-Fib and CHF—the Role of Lead Position and Pacing Algorithms
Location and Importance of Autonomic Ganglionated Plexi Jackman Relationship Between Locations of Autonomic Ganglionated Plexi and Sites of Complex Fractionated Atrial Electrograms During A-Fib
95% Cure Rate for Chronic A-Fib After Two Ablations Jaïs Ablation of Long-Lasting A-Fib
Mapping Sites of High-Frequency Activity (Dominant Frequency) to Ablate A-Fib Jalife The Relationship Between High-Frequency Fractionated Electrograms and Reentrant A-Fib Drivers in the Posterior Left Atrium
Overview of the 2006 Boston A-Fib Symposium Keane, Reddy, Ruskin Update on Mechanisms and Therapy for A-Fib from the 11th Annual Boston A-Fib Symposium 2006
High Rate of Silent A-Fib in “Cured” Patients Kottkamp Silent A-Fib after Catheter Ablation
New Drugs in Clinical Trials: Dronedarone, Atrial-Selectives, Fish Oil, Replacements for Coumadin Kowey Future Directions in Antiarrhythmic Drug Therapy
Cox Maze Operation, Radial Maze, Wolf Bipolar RF Mini-Maze, Saltman Microwave Mini-Maze Kress Advances in Surgical Therapy for A-Fib
42% of A-Fib Patients Have Unusual, Atypical Left Atrium Structure & Need Special Care Mansour Three Dimensional Left Atrial Anatomy: Implications for Catheter Ablation
Un. of Pennsylvania Method of Ablating A-Fib Patients Marchlinski Non-PV Triggers for A-Fib: Provocation, Recognition, Location, and Relationship to Chronicity of A-Fib
Individualized, Stepwise Approach to Catheter Ablation for A-Fib Morady An Individualized Approach to Catheter Ablation for Atrial Fibrillation
Complex Fractionated Atrial Electrograms (CFAEs) Nademanee Automating the Detection of Complex Fractionated Atrial Electrograms
Dangers Of A-Fib Stroke Decreased by Removing or Closing Left Atrial Appendage. No Insurance Coverage If On Coumadin. Packer Surgical & Catheter-Based Strategies for Stroke Prevention in A-Fib
Current Strategies for Ablating Paroxysmal, Persistent & Chronic A-Fib Panel Discussion How We Approach Catheter Ablation for A-Fib Today
Stereotaxis Robotic Magnetic Navigation in Catheter Ablation Pappone The Use of Remote Magnetic Navigation in Catheter Ablation for A-Fib
Remote Robotic Navigation in Catheter Ablation Reddy The Use of Remote Robotic Navigation in Catheter Ablation for A-Fib
Guidelines for Blood Thinners to Prevent A-Fib Stroke. Odds of Getting an A-Fib Stroke. Waldo Guidelines for Anticoagulation of A-Fib
Right and Left Atrium Flutter Wharton Atypical Atrial Flutter During and After A-Fib Ablation: Incidence, Physiology, and Management
Some Remodeling Effects of A-Fib Improve after Ablation. But Ablation May Decrease Atrial Function. Wilber Left Atrial Function and Remodeling Before and After Catheter Ablation or Surgery for A-Fib

Dr. Pierre Jaïs, Hôpital Cardiologique du Haut-Lévêque, Bordeaux-Pessac, France discussed Strategies for Catheter Ablation of Long-Lasting Persistent Atrial Fibrillation

Isolation of the Pulmonary Veins is effective in curing many patients with Paroxysmal (occasional) A-Fib. But this strategy isn’t as effective in patients with long-lasting (Persistent and Chronic) A-Fib.

For patients with long-lasting A-Fib a four-step procedure is used:

  1. Isolation (ablation) of the Pulmonary Veins.
  2. Isolation (ablation) of the inferior left atrium and Coronary Sinus.
  3. Ablation of other atrial tissue with rapid or different electrical signals such as Continuous Fractionalized Electrograms (see Nademanee).
  4. Linear ablation of the left atrial roof and mitral isthmus.

Cycle Length (how fast the A-Fib beats) was found to be very important. As the ablations continued the A-Fib cycles became longer, until the A-Fib stopped. People with the fastest A-Fib cycles were less likely to be cured.

Continuous Fractionalized Electrograms were found throughout the heart and therefore couldn’t be used to predict where to ablate. “Rapid or fractionalized electrograms were ubiquitous in both atria, and their interpretation could not be refined in terms of specificity and predictive value for ablation.”

In a later presentation of the results of the live Chronic A-Fib ablation, Dr. Jaïs identified the following sites in the heart that led to conversion from A-Fib to normal sinus rhythm:

  • Pulmonary Veins 21%
  • Coronary Sinus & Inferior Left Atrium 19%
  • Left Atrial Appendage 17%
  • Roof Line 12%
  • Septum 11%
  • Mitral Isthmus Line 10%
  • Posterior Left Atrium 4%
    Superior Vena Cava 4%
  • Mid Anterior Left Atrium 2%

In two patients A-Fib ended when the right atrial septum was ablated. In patients who weren’t cured, the right atrium had the most rapid A-Fib cycles, suggesting the both the left and right atria may be involved in maintaining A-Fib. (See http://www.medscape.com/viewarticle/515974)

87% of patients in this study were cured of their long-lasting A-Fib. (In a later follow-up study a success rate of 95% was reported using a second ablation procedure.In this author’s opinion, this is a major medical breakthrough in the A-Fib field. Before this study, curing Persistent/Chronic A-Fib was considered much more difficult and had a much lower success rate than for Paroxysmal (occasional) A-Fib)

Identifying other areas of the heart (other than the Pulmonary Veins) and different electrical signals responsible for A-Fib may eventually help doctors find a way to achieve 100% success in curing A-Fib.

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Dr. Hans Kottkamp, University Leipzig – Heart Center, Dept. of Electrophysiology, Leipzig, Germany discussed The Frequency and Significance of Asymptomatic A-Fib After Catheter Ablation.

Dr. Kottkamp warned that patients “cured” of their A-Fib may have “silent” A-Fib reoccurrences. In his study 144 patients with A-Fib were treated by a combination of circumferential and linear lines (ablation lesions). 84% had occasional (Paroxysmal) A-Fib. A 7-day ECG was used before the ablation procedure, after the procedure, and at 3, 6 and 12 months after the procedure. Patients also kept a symptom log.

Over a twelve month period 50% to 60% of “cured” patients experienced reoccurrences of their A-Fib. 70% of the reoccurrences were silent (asymptomatic) A-Fib.
Though reoccurrence rates may vary, what is alarming about Dr. Kottkamp’s study is the high rate of silent A-Fib in “cured” patients.

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Dr. Hugh Calkins, Johns Hopkins Medical Institutions, Baltimore, MD talked about Defining Success Following A-Fib Ablation.

Dr. Calkins’ study concerned the reoccurrence of “silent” A-Fib in patients previously considered “cured” by a catheter ablation procedure, and reinforced Dr. Kottkamp’s findings. In a six-month long study “cured” patients wore a 5-day Mobil Cardiac Outpatient Telemetry (MCOT) monitor which recorded their symptoms five days a month. They also kept a log of their symptoms. They telephoned in their monitored heart signals four times a day, and also whenever they had symptoms.

“Cured” patients were found to be in A-Fib 31% of the time. 82% of these A-Fib attacks were silent (asymptomatic). (In this study 57% of patients who thought they were  experiencing A-Fib symptoms were actually in normal sinus rhythm. Symptoms of shortness of breath and chest discomfort were good predictors of being in A-Fib, whereas skipped beats was a poor predictor.)

Dr. Calkins suggested a different way of defining success after AF Ablation which he called “reducing the A-Fib Burden,” rather than complete elimination of A-Fib symptoms. For example, after a “successful” A-Fib Ablation a patient may go from constant (Chronic) A-Fib to occasional (Paroxysmal) A-Fib which is a “reduction of their A-Fib burden.”

Dr. Calkins discussed a common concern of the Symposium participants, that no current ablation catheters in use today are FDA approved for treating A-Fib. They are “off-label” which means they have been approved for other heart uses but not for treating A-Fib. (This is not unusual in the US medical field. Roughly half of today’s current medical devices are used “off-label.”)

Current FDA guidelines for clinical studies of catheters say, “It is most appropriate to evaluate ablation therapy as a palliative therapy and select end points (results) that have the potential to clearly demonstrate a reduction in symptoms caused by A-Fib… For primary effectiveness end point the FDA recommends the relatively unambiguous end point of freedom from symptomatic A-Fib at one year. A blanking (healing) period may be reasonable of at least four weeks.”

Dr. Calkins suggested that being A-Fib symptom free for a year may be an unreasonably high bar to reach. If someone, for example, has a 15-minute A-Fib episode in month eleven, he/she fails the test and isn’t considered cured. He recommended a “definition of success other than freedom from all A-Fib episodes.”

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Dr. Peter Kowey of Lankenau Hospital in Wynnewood, PA talked about Future Directions in Antiarrhythmic Drug Therapy.

He discussed 10 areas of current research and clinical trials. (Most of the drugs mentioned below are still in clinical trials and have not been approved by the FDA.)

1. Carvedilol is a Beta Blocker that is also a Sodium Channel Blocker (Class I) and a Potassium Channel Blocker (Class III). It appears to prevent A-Fib in patients who’ve had a heart attack. (It has been approved by the FDA, but not for A-Fib.)

2. Azimilide Dihydrochlorid blocks both rapid and slow potassium channels in the heart (Class III). Though not very potent for A-Fib, it does seem to prevent shock from implantable defibrillators.

3. Dronedarone is a “congener” (a drug similar to) amiodarone which is currently the most effective antiarrhythmic drug, but also one with the most side effects. Dronedarone seems to have no thyroid or lung toxicity. It appears to work best in young people, and shouldn’t be used in cases of heart or renal failure. (This is perhaps the drug of most interest to A-Fib patients. To have a drug with the effectiveness of amiodarone, but without its side effects would be a major help to many A-Fib patients.)

4. Atrial Selective drugs such as RSD-1235 (only as an IV drug) and AVE 0118. These drugs are intended to affect the potassium current only in the atria and not the ventricles. (All current antiarrhythmic drugs tend to have an adverse effect on the ventricles.) RSD-1235 had an effectiveness of 55%-65% in clinical trials (this is a higher success rate then most antiarrhythmic drugs)(Atrial Selective drugs represent a potential major new development in treating A-Fib.) 

5. Atrial Repolarizing Delaying Agents (ARDA) affect potassium and fast sodium currents. They seem to work well after cardioversion to prevent A-Fib from recurring.

6. Gap Junction Modulators. These work on the theory that loss of cell contact in the gap junction may contribute to developing A-Fib. (A gap junction is a junction between cell-types that allows different molecules and ions to pass freely between cells. In the heart, the signal to contract is passed through the gap junctions, allowing the heart muscle cells to contract in tandem.)
7. ACE-I/ARB (Angiotensin Converting Enzyme Inhibitor and Angiotensin Receptor Blocker) may be primary therapy for A-Fib in patients with Congestive Heart Failure and Hypertension. These tend to produce dilation and stretch-induced A-Fib which the ACE inhibitors decrease.

8. Anti-Inflammatory Statins may prevent A-Fib recurrence after cardioversion. Studies have shown that inflammation may be important in the development of A-Fib.
9. Fish oil consumption (from baked or broiled fish, not from fried fish) has shown a decrease in the risk of A-Fib. (This is an important finding for A-Fib patients. Fish oil, a natural remedy, may decrease the risk of getting A-Fib.)

10. Oral Anticoagulants to replace Coumadin. Ximelagatran, which many hoped would replace Coumadin, was rejected by the FDA because of liver toxicity. But there are many other drugs being investigated to replace Coumadin such as Dabigetran which is the furthest along in clinical trials. According to Dr. Kowey, maintaining proper anticoagulant levels “is the most important thing we do for patients.”

In addition Dr. Kowey answered a question from the audience on home monitoring systems for Coumadin (warfarin). Currently they aren’t well accepted by patients and by insurers who are reluctant to pay for them, and they require a lot of maintenance. The need for monitoring is the single biggest impediment to using Coumadin, especially for young people. But, Dr. Kowey emphasized, if someone is motivated, home monitoring systems can be effective.

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Dr. Andre d’Avila of Massachusetts General Hospital in Boston, MA discussed the Role of Esophageal Temperature Monitoring During A-Fib Ablation.

Esophageal Temperature Monitoring is one of the methods currently being investigated to prevent Atrial Esophageal Fistula from an A-Fib ablation (a Fistula usually begins as an injury or lesion (Necrosis) of the Esophagus which then spreads to the Left Atrium creating a puncture).

Monitoring the position of the esophagus is important since its position varies from patient to patient and sometimes throughout the ablation process. But Dr. d’Avila stressed that only monitoring the position of the esophagus may be misleading. It may create a false sense of security and/or prevent important RF pulses from being delivered for fear of potential damage.

It was thought that the presence of micro bubbles at the ablation site would indicate a high esophageal temperature reading. But Dr. d’Avila’s study showed very little correlation between micro bubbles and high esophageal temperature. “Despite the presence or absence of type 1 micro bubbles, you can have very high esophageal temperatures at very low power.”

35 Watts can not be used as a cutoff for safety when one approaches the exterior wall (of the esophagus). Even at 15-30 Watts it is possible to record esophageal temperatures as high as 41 degrees.

Dr. d’Avila stated his conclusions about the possibility of creating fistulas during the A-Fib procedure:

  1. It doesn’t matter how experienced a doctor is doing ablations
  2. 2.  It doesn’t matter what particular ablation technique is used (It seems to this author there is more of a chance of fistula using the Pappone high wattage drop and drag technique than with other methods.1
  3. You can’t rely on the thickness of the left atrial tissue to decide whether or not you will be delivering a safe pulse.
  4. Using low power may be helpful in avoiding fistula when ablating at the left atrial posterior wall, but may be misleading. You can have very high esophageal temperatures even at 20 Watts.
  5. Short ablation times doesn’t seem to be very helpful. You can reach very high temperatures at only 20-30 seconds.
  6. Dr. d’Avila advocated using PVI guided by esophageal monitoring. But he pointed out the following limitations to this strategy:
  7. It depends on contact between the probe and the esophageal wall. The exterior wall of the esophagus may experience a higher temperature than registered by the esophageal monitor depending on the proximity of the probe to the esophageal wall. “The problem is when you don’t have high esophageal temperatures and you are very close to the esophagus. In that situation esophageal monitoring depends on contact and may create a false sense of security when normal temperatures are recorded during ablation.”
  8. General Anesthesia is needed to insert the esophageal probe.
  9. There is no animal model to prove this strategy.

Dr. d’Avila concluded that:

  1. 80% of current procedures may produce high esophageal temperatures
  2. Monitoring of esophageal temperatures allows for the isolation of all Pulmonary Veins despite the proximity of the esophagus, since pulses may be delivered which do not result in high esophageal temperatures.
  3. “High esophageal temperatures indicate some sort of esophageal damage.”
  4. Dr. Morady was formerly a proponent of the Pappone high wattage “Anatomically Based Circumferential PV Ablation” method. But after two episodes of esophageal fistula (holes in the esophagus), he now uses a variety of approaches depending on the individual patient. Dr. Morady’s reasons for this individualized approach are:
  5. A one-size-fits-all approach does not fit all patients. There is “a vast variability and differences between patients with A-Fib.”
  6. An individualized approach requires less ablation of heart tissue which is better for patients. (Dr. Morady’s patients average about 32 minutes of ablation burn time, compared to 46 minutes with Circumferential PV Ablation.)
  7. An individualized approach can identify important drivers and triggers of A-Fib in patients, and thereby provide insights into the actual mechanisms of A-Fib.
  8. With this individualized approach, eliminating a patient’s A-Fib can be reliably demonstrated, (when a high dose of isoproterenol does not induce A-Fib).

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Dr. Fred Morady of The University of Michigan discussed “An Individualized Approach to Catheter Ablation for Atrial Fibrillation.”

Before starting the ablation procedure, he uses a barium paste in the esophagus to avoid ablating near the esophagus. (Author’s note: A possible danger of using barium paste in the esophagus is that barium might be breathed into the lungs and damage them. The author has no hard data to support this warning, only anecdotal reports.) Then he uses a lasso catheter to map the Pulmonary Veins.

In the ablation procedure he first tries to eliminate Pulmonary Vein A-Fib triggers by Ostial PV Isolation. (He found in some patients that none of the Pulmonary Veins have A-Fib triggers.) If the patient’s A-Fib has not been eliminated by the PV ablation, he may use the following:

  • Wide Area PV Ablation
  • Linear Ablation
  • Superior Vena Cava Isolation
  • Ablation of Fractionated Electrograms in the Left Atrium (particularly the septum and roof of the heart), the Right Atrium, and the Coronary Sinus
  • Ablation of Ganglionated Plexi

Answering a question from the audience Dr. Morady said he uses an irrigated catheter with 20 second bursts of RF energy at 25-35 Watts.

His success rate for Paroxysmal (occasional) A-Fib patients is 84% with an 18% redo rate.

(To this author Dr. Morady’s individualized approach seems more promising for patients and safer. Dr. Morady gave many examples of the vast variability of patients with A-Fib, how a one-size-fits-all approach would not have eliminated many non-PV drivers. His individualized approach, like that of Dr. Jaïs and the Bordeaux group, may lead to finding more elusive A-Fib triggers and a higher success rate for A-Fib ablation.)

(In the 2008 Boston A-Fib Symposium Dr. Morady presented a slidewhich illustrated how he and his colleagues changed from the Circumferential PV Ablation approach to a more tailored, individualized segmental treatment of A-Fib patients. Note how the high-wattage “Drop-and-Drag” ablation lines in the left have been replaced by segmental, targeted lesions on the right.)

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Dr. David C. Kress of the Midwest Heart Surgery Institute talked about “Advances in Surgical Therapy for A-Fib.”

Dr. Kress briefly discussed the classic Cox Maze 3 (open heart surgery in which the heart is cut and sewn back together to eliminate A-Fib) and the Radial Incision approach (Radial Maze). The Radial Maze produces better left atrial activation and better left atrial transport function (the left atrium pumps blood better). Though the Cox Maze 3 has a good success rate (97%), it is performed relatively infrequently because it is so traumatic for the patient.
Dr. Cox also developed what he called a Mini Maze operation that involved fewer incisions in the heart and chest (a similar operation is the “Quarter 3”). But this operation still involved cardiopulmonary bypass, and the cutting and sewing of the heart. He also added a PV encircling lesion, left atrial isthmus lesion with coronary sinus lesion, and a right atrial isthmus lesion.

A European version adds connecting lesions from the isolated PVs across the dome of the heart roof and over to the Mitral Valve.

(Currently the term “Mini Maze” more often refers to the minimally invasive operations described below.)

Dr. Kress mainly focused on minimally invasive surgery which does not involve open heart surgery. He explained that there are essentially two concepts for minimally invasive operations:

Concept 1. Bilateral PV Isolation Using Bipolar RF (the Wolf Mini Maze), also called “Thorascopic Bipolar Isolation with EP Testing” by Dr. Randall K. Wolf. In the Wolf Mini Maze the surgeon cuts openings between the ribs, then uses a probe to punch through the pericardium (a sack around the heart) to access the heart (scissors or scalpels are not used). To encircle the PVs and heart, the lungs have to be alternately deflated and re-inflated. Using a bipolar RF clamp the surgeon makes transmural lesions (lesions that go through the wall of the heart) around the pulmonary veins and heart. The left atrial appendage is also cut and removed, and the opening of the left atrial appendage is stapled closed. The pericardium is then sewn back together. A patient can leave the hospital after only one or two days and can return to normal activities within a short time. (A video of this operation is found at http://www.or-live.com/healthalliance/1217/.)

(The left atrial appendage is removed because clots are more likely to form in that area. There is some controversy about whether removal of the left atrial appendage is justified if the patient is no longer in A-Fib.)

(The Journal of Thoracic and Cardiovascular Surgery has admonished a Un. of Cincinnati surgeon (Dr. Wolf) for failing to disclose financial ties to AtriCure, the West Chester, (Ohio) maker of heart-surgery equipment he and other researchers evaluated in a published study.3

Concept 2. Box Lesions around all four Pulmonary Veins using a Microwave Antenna (Saltman—the “Microwave MiniMaze”). Instead of bipolar RF clamps, the Microwave MiniMaze uses guide catheters to position microwave antennas around the Pulmonary Veins. Microwave energy is delivered at 65 Watts for 90 seconds. Also, a lesion is created from the left atrium appendage into the transverse sinus, connecting it to the Pulmonary Vein “box” lesion. The left atrial appendage is not removed but is usually stapled closed.

Preliminary results are very positive. In a study by Dr. Wolf involving 27 patients, 91% were free of A-Fib after three months. According to Dr. Kress, “We can probably substitute the bipolar RF clamp operation (the Wolf Mini Maze) for the cut-and-sew portion of the Cox Maze 3.” Dr. Kress also mentioned that there have been some instances of esophageal fistula in the early days of some of the Mini Maze operations.

Dr. Cox wrote this comment on the minimally invasive operations. “None of the present energy sources…are capable of creating the left atrial isthmus lesion from the epicardial (outside the heart) surface, because of the necessity of penetrating through the circumflex coronary artery to reach the left atrial wall near the posterior mitral annulus.”4

Dr. Kress also mentioned the work of Dr. Mack in Dallas who uses Argon Cryoablation in his Mini Maze operations. He reported a 90% success rate.

Answering a question from the audience, Dr. Kress said that in the future surgeons and electrophysiologists might work together to identify conduction block and the presence of ganglia that produce A-Fib signals. Dr. Wolf (University of Cincinnati) and Dr. Jackman (Oklahoma University) are conducting a multi-center study involving this sort of collaboration.

When asked why some patients required pacemakers after a Mini Maze, he hypothesized that the Mini Maze lesions may affect the blood supply to the sinus node which may result in Sick Sinus Syndrome.

(From this patient’s perspective, operations such as the Wolf Mini Maze are no longer “experimental.” These minimally invasive operations represent a new option for the treatment of A-Fib. The Mini Maze is probably a very important option for someone who can not tolerate anticoagulants. But a word of caution—these are surgical operations with the potential risks and complications of surgery.) 

aThe Radial Maze was developed by Dr. Cox as a refinement of his Maze operation. He found that in patients after the Maze operation, “left atrial transport function was significantly less than in normal control subjects.” He hypothesized this was because:

1. the incisions isolating the pulmonary veins also eliminate approximately 29% of the left atrium from contributing to the transport function.

2.  because of the complexity of the incisions, they may inhibit the activation and contraction of nearby atrial segments.

3. the incisions may prolong atrial activation time, thereby desynchronizing the atria and ventricles.

4. some of the Maze incisions may interrupt the atrial coronary arteries, impairing heart circulation.

Whereas in the Radial Maze operation the incisions parallel the direction of the atrium’s activation and the direction of the blood supply. No part of the atrium is electronically or mechanically isolated. This produces better left atrial activation and better left atrial transport function.

Annals of Thoracic Surgery 1999;67:27-35.

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Dr. Koonlawee Nademanee of the Pacific Rim EP Research Institute in Inglewood, CA discussed Automating the Detection of Complex Fractionated Atrial Electrograms (CFAEs).

Dr. Nademanee is the discoverer of CFAEs, a new tool to help doctors identify sources of A-Fib signals in the heart.

Dr. Nademanee defined Complex Fractionated Atrial Electrograms as follows: (an electrogram is a picture of the electrical activity of the heart as sensed by a pacemaker or catheter in the heart).

“a) atrial electrograms that have fractionated (divided) electrograms composed of two deflections (turns or bends) or more, and/or have a perturbation (disturbance) of the baseline with continuous deflection of a prolonged activation complex (a long A-Fib signal),
b) atrial electrograms with a very short cycle length (< 120 ms).

In general, CFAEs are usually low voltage multiple potential signals between 0.05-0.25 mV (milleVolts).”

These low voltage signals are close to the levels of background noise found in heart monitoring systems, and require operator experience and expertise to manually identify them. “…identifying and tagging CFAEs…is subjective and heavily dependent on operator experience.”

Manual mapping of the CFAEs is always done while the patient is in A-Fib. If the patient is in normal sinus rhythm, A-Fib is induced by giving the patient isoproterenol or through atrial pacing (using an electrical signal to stimulate the heart). Once the CFAEs are located during CARTO mapping (a mapping system that uses a special catheter to generate 3-D maps of the heart), the CFAEs are ablated. If the A-Fib or Atrial Flutter continues, the remaining sources of A-Fib signals are identified and ablated. If the A-Fib and/or Atrial Flutter are not successfully terminated, external cardioversion is performed.

(Dr. Nademanee’s approach differs from other doctors in that he first identifies and ablated CFAEs, then he looks for other sources of A-Fib signals in the heart. Whereas Dr.Jaïs and Dr. Morady, for example, first try to identify and ablate sources of A-Fib in the Pulmonary Vein openings before identifying and ablating other sources of A-Fib such as CFAEs.)

Dr. Nademanee described new software that identifies the CFAEs and displays them in a CARTO map. The CFAEs are color coded according to the degree of fractionated signals and their cycle lengths. This software provides better accuracy and considerably shortens the time of mapping. However, manual evaluation and editing of the resulting map is necessary, “because the (current) software has inherent weakness in detecting noise and also precisely recognizing the beginning and end of the complex.”

(From this patient’s perspective, CFAEs and the software used to identify them may prove to be an important tool to help find and ablate the more elusive sources of A-Fib in the heart.)

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Dr. Warren Jackman of the University of Oklahoma discussed the Relationship Between Locations of Autonomic Ganglionated Plexi and Sites of Complex Fractionated Atrial Electrograms and/or High Frequency Electrograms During A-Fib.

Dr. Jackman discussed the location and importance of Autonomic Ganglionated Plexi. (The Autonomic Nervous System controls the heart and smooth muscle tissue and involuntary actions.) (Ganglionated Plexi are areas of the atria containing clusters of nerve cells.) There are seven areas of Autonomic Ganglionated Plexi in the atria, four in the left atrium, three in the right. These Ganglionated Plexi areas are located near but not in the Pulmonary Veins, and may be involved in producing Complex Fractionated Atrial Electrograms and A-Fib.

In experimental studies using dog models, it was found that areas of Fractionated Atrial Potentials are close to and are “located primarily in the regions surrounding Ganglionated Plexi.” (“Fractionated Atrial Potentials” is the name Dr. Jackman uses for Dr. Nademanee’s “Complex Fractionated Atrial Electrograms.”) According to Dr. Jackman, “There is a distinct relationship or requirement for some degree of stimulation from the Ganglionated Plexi in order to have Fractionated Electrograms.”

He also hypothesized that stimulating the Ganglionated Plexi increases calcium loading and calcium release which may trigger Fractionated Electrograms (“Calcium Transient Triggered Firing Hypothesis”).

(Dr. Jackman’s studies may make it easier to identify and locate Complex Fractionated Atrial Electrograms since they are located primarily in the Ganglionated Plexi areas. They may also show how Fractionated Electrograms and A-Fib are generated.)

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Dr. Frank Marchlinski of the University of Pennsylvania discussed “Non-Pulmonary Vein Triggers for A-Fib: Provocation, Recognition, Location, and Relationship to Chronicity of A-Fib.”

Dr. Marchlinski described the protocol for ablating patients with A-Fib that he and his colleagues use:

He begins by using programmed stimulation to screen for Accessory Pathway/AVNRT (Atrioventricular Node Reentry Tachycardia). In AVNRT the AV Node develops two pathways instead of one, allowing a signal to go down one pathway, then back up the other pathway to the atrium (Reentrant Circuit) resulting in Supraventricular Tachycardia (speeding up the heart beat). He found that 4% of his patients who had A-Fib actually had AVNRT instead, and could be cured without having to go through a regular Pulmonary Vein Ablation (Isolation) procedure.

  • Both before and after PV isolation he initiates PV and non-PV triggers for A-Fib:
    If a patient is in Persistent/Permanent A-Fib, he first cardioverts them, then identifies areas of early reoccurrence of A-Fib.
  • If a patient is in sinus rhythm, he gives them isoproterenol in increments of 3, 6, 12, 20 mcg/minute to stimulate them into A-Fib (with a Median dose of 12 mcg/minute).
  • If the spontaneous triggers still haven’t been provoked, he induces A-Fib by burst pacing. He cardioverts the patient, then identifies areas of early reoccurrence of A-Fib.

He then repeats this initiation of A-Fib while administering low dose isoproterenol.

  • This protocol adds about 1/2 hour to the ablation procedure time.
    Dr. Marchlinski and his colleagues found that 15% of their patients had non-Pulmonary Vein A-Fib triggers (113 out of 761 patients), and 3% had only non-PV triggers. These non-PV triggers were found in the following areas of the heart:
  • Right Atrial Appendage
  • Superior Vena Cava
  • Crista Terminalis
  • Tricuspid Valve Annulus
  • Eustachian Ridge
  • Fossa Vallis
  • Septum
  • Posterior Wall of Left Atrium
  • Mitral Annulus
  • Epicardial Coronary Sinus
  • Preliminary data suggest that such factors as gender, race and type of A-Fib may influence where non-PV triggers are found.
  • Women have more only non-PV triggers than men;
  • Race seems to affect where non-PV triggers are found in the heart;
  • Patients with Persistent/Permanent A-Fib seem to have more non-PV triggers.

In addition, Dr. Marchlinski found that patients with only non-PV triggers had a higher success rate of being cured of A-Fib than other patients (91%).

Dr. Marchlinski and his colleagues’ work seems to be very promising for patients.

By limiting ablation only to identified trigger sites, he decreases the amount of burn lesions in the heart versus one-size-fits-all procedures. This lowers the risk of ablation proarrhythmia [where the ablation process may stimulate arrhythmias], and decreased atrial circulation and transport [blood doesn’t circulate in the heart walls as well and the heart doesn’t pump as well because of ablation lesions].

By identifying patients with AVNRT and with only non-PV A-Fib triggers, he seems to increase their chances of being cured of A-Fib. Whereas with a one-size-fits-all approach, many non-PV triggers may not be ablated or isolated.

By adding to our knowledge of non-PV A-Fib trigger sites, he increases our understanding of the physiology and anatomy of A-Fib. His work seems related to and moving in the same direction as that of Dr. Jaïs and Dr. Morady.)

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Dr. David Wilber of Loyola University Medical Center discussed “Left Atrial Function & Remodeling Before and After Catheter Ablation or Surgery for A-Fib”

Dr. Wilber’s presentation focused on the structural and mechanical changes that affect the heart in A-Fib, and whether any of these remodeling effects can be reversed by eliminating patients’ A-Fib. Some of the remodeling effects associated with A-Fib are:
a) Increased left atrial size

b) Decreased left atrial contractual and reservoir function (reservoir function refers to the capacity of the left atrium to expand and accept blood flow)

c) Pulmonary Vein expansion

d) Atrial fibrosis (the formation of fibrous tissue) and scarring

e) Increase in Left Ventricle size, decrease in LV Systolic and Diastolic function.
When a patient is restored to normal sinus rhythm (after an ablation procedure or after surgery), how much of this remodeling effect is reversed? Dr. Wilber discussed several surgical and catheter ablation studies that addressed this question.

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RADIAL MAZE SURGERY STUDIES

In one study, after patients were restored to normal sinus rhythm, left atrial size declined and contractual function improved, but they didn’t return to normal. “In every surgical study, (left atrial) function, even though it returned, it remained at dramatically reduced levels.” Most of the improvement occurred in the first month.

A second provocative surgical study investigated whether the Radial Maze linear lesions operation impaired atrial function even though it cured the patients’ A-Fib. After two years, cured patients in the treatment group still had an abnormal, stiff left atrium. Also, their left atrium volume was 30% more than normal, and their atrial function was still reduced. Whereas, in the control group who were cured by cardioversion, the left atrium returned almost back to normal. (This study may be particularly important for young people or athletes with A-Fib who are considering a catheter ablation procedure or surgery. A successful cardioversion may be better at restoring normal heart function after A-Fib than surgery or extensive catheter ablation procedures.)

CATHETER ABLATION STUDIES

After successful ablation, Dr. Pappone found a 15-20% reduction in size of the left atrium, and some improvement in atrial function. A Dr. Chen study and a Dr. Hopkins study, using the less destructive Segmental Ostial ablation procedure, found a decrease in volume both in the left atrium and the pulmonary vein openings. A Netherlands study using a more extensive procedure with circumferential ablation and linear lesions, also found a reduction in size of the left atrium. A Un. of Michigan study using circumferential ablation and linear lesions found a decrease in left atrium size, but also the Ejection Fraction (how well the atrium pumps) fell even further than before the successful A-Fib ablation.

A Bordeaux group study using Pulmonary Vein Isolation (Segmental) and Linear Lesions with an average follow-up of eleven months showed that left atrial volumes fell, but also that left atrial contractual and filling function almost returned to normal for Paroxysmal patients. For Chronic patients, left atrial contraction was low after ablation, but after eleven months it improved considerably. The study also showed improvements in ventricular, diastolic and systolic function. This improvement occurred even if patients had reoccurrences of A-Fib. According to Dr. Wilber, this data is somewhat at odds with other studies of catheter ablation.

CONCLUSION

Dr. Wilber concluded that most of the data showed that after successful A-Fib ablation:
1. There is a moderate decrease in size of the left atrium, but it doesn’t return to normal.

2. Left Atrial contractual and reservoir functions remain abnormal.

(Perhaps the most important point Dr. Wilber raised concerned, “…the potential deleterious (bad) effects of (catheter) ablation procedures on contractual and reservoir functions (of the left atrium)… Can we design a procedure that will optimize recovery?” Particularly for young people and athletes, years down the road how will their left atrial dysfunction affect their quality of life, exercise tolerance, performance, etc?

Another very important point he raised was that the more extensive ablation procedures may be related to or cause decreased atrial function.)

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Dr. Douglas Packer of the Mayo Clinic in Rochester, MN discussed “Surgical and Catheter-Based Strategies for Stroke Prevention in A-Fib”

One of the major dangers of having A-Fib is the risk of stroke. Dr. Packer cited some sobering statistics concerning A-Fib related strokes:

  • Of the 500,000 strokes per year in the U.S., 25% are caused by or are related to A-Fib.
  • 70% of A-Fib related stroke patients die or develop severe neurological problems.
  • Patients with A-Fib have 5 to 6 times greater probability of having a stroke and 18 times greater probability of an embolic event (a clot that doesn’t cause a stroke).
  • 35% of A-Fib patients who are not treated with anticoagulants will have a stroke in their lifetime.
  • Strokes are age dependent. For A-Fib patients over 80 years old, 30-35% of strokes are attributed to A-Fib.

Dr. Packer pointed out that most strokes come from the Left Atrial Appendage (91%) which is a very complicated structure with often more than one lobe. In A-Fib the flow of blood from the Left Atrial Appendage is particularly poor. Clots can easily form and cause stroke.

REMOVING THE LEFT ATRIAL APPENDAGE

He cited a surgical study in which 25% of patients undergoing open heart surgery had their Left Atrial Appendage cut out. In the follow-up study patients who did not have a stroke were usually the ones who had had their Left Atrial Appendage removed. Though there is controversy about this because of bleeding and partial ligations (sewing up the cut heart).5

Dr. Packer discussed whether catheter based procedures can close off the Left Atrial Appendage (LAA) without the risks of surgery. Catheter based Occlusion Devices (PLATTO, Watchman) are currently in clinical trials. In this procedure a catheter guide sheath with the Occlusion Device is positioned inside the Left Atrial Appendage, then the sheath is withdrawn and the device expanded to tighten in place and close off the LAA. This procedure takes about one hour. Preliminary results seem promising.

(Dr. Packer raised an important question of who would receive or need these Occlusion Devices. When and if these Occlusion Devices are approved, should a doctor doing a catheter ablation procedure routinely close off the Left Atrial appendage in case a patient’s A-Fib isn’t completely cured? Or should an Occlusion Device only be used for patients who need to be off of anticoagulants?

Dr. Packer raised another very important point both for doctors and for patients. He read a letter from a major insurance company which rejected a patient for coverage based on the patient being on Coumadin, “…because of the many unforeseen complications and side effects which may result from the continued use of Coumadin.” It’s very alarming that insurance companies would take over the role of the doctor and dictate what meds a doctor and patient can use. It would be a major crisis for A-Fib patients if people taking Coumadin were routinely denied health insurance. However, pragmatic reality could one day dictate the use of Occlusion Devices, so that someone with A-Fib wouldn’t have to take Coumadin and could be covered by medical insurance.)

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Dr. Carlo Pappone of San Raffaele University Hospital in Milan, Italy discussed “The Use of Remote Magnetic Navigation in Catheter Ablation for A-Fib.”

Dr. Pappone showed a video of a Stereotaxis robotic navigation system which uses a computer and magnetic fields to image the heart and control the ablation catheter. The system synchronizes fluoroscopic and CARTO mapping to create a 3-D real time image of the heart. This system produces perfect ablation lines and uses a maximum of only 4 grams of pressure on the heart wall. Soon the system will be able to do automatic ablations and remote robotic ablations just by moving a mouse. Dr. Pappone thinks this robotic navigation technique will be the most important application for A-Fib in the next two years.

Dr. Pappone said that he averages only 45 minutes doing a Circumferential Pulmonary Vein Ablation (he can do seven ablations a day). (See  Pappone and the Pappone Method.) He now uses an irrigated catheter with a 4mm tip at a maximum of 65° at 70 Watts.

Dr. Pappone also talked about a new refinement of his Circumferential Pulmonary Vein Ablation procedure. He found that ablating the vagal ganglia (areas of the heart where vagal reflex can be stimulated) significantly reduces recurrence of A-Fib after 12 months.

In another study Dr. Pappone compared A-Fib patients who had a Circumferential Pulmonary Vein Ablation procedure with patients who received antiarrhythmic drug therapy. After a median follow-up of 900 days, survival for ablated patients was longer than among patients treated medically, and the same as healthy persons. Ablated patients’ “Quality of Life” reached normal levels at six months and remained unchanged after one year. This differed from patients receiving medical therapy. “Pulmonary vein ablation improves mortality, morbidity, and quality of life as compared with medical (drug) therapy.”

Dr. Pappone discussed that catheter ablation is difficult to do on A-Fib patients who have an artificial Mitral Valve, because of the increased risk of damage to it. But he found that Circumferential Pulmonary Vein Ablation is feasible for patients with an prosthetic Mitral Valve, with outcomes similar to those of standard patients.

(Author’s Note: Dr. Pappone’s Circumferential Pulmonary Vein Ablation procedure may become the ablation procedure used by most doctors and medical centers, because it is more cost effective, easier to learn, and is less dependent on operator skill than other procedures. However, there are currently some criticisms of this procedure that patients should be aware of:

  • The use of high wattage catheters may lead to damage of the esophagus [see d’Avila] and Atrial Esophageal Fistula—a hole in the atrium and esophagus which often results in death.
  • The extensive scarring of the atrium in Dr. Pappone’s procedure may possibly lead to impaired functioning of the left atrium [see Wilber].)
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Dr. Vivek Reddy of Massachusetts General Hospital in Boston, Massachusetts discussed “The Use of Remote Robotic Navigation in Catheter Ablation for A-Fib.”

Dr. Reddy described a system that uses a robotic arm catheter (“Steerable Guide Catheter”) with a deflectable sheath that can bend in multiple levels and directions.  This “sheath-within-a-sheath” system uses both an internal guide sheath and an outer sheath (which bend and move independently) to remotely navigate and ablate within the heart.

This robotic catheter system is combined with electroanatomical mapping and 3-D Computed Tomography (similar to a CAT Scan). The physician, using a 3-D joystick, sees both a cartoon rendering of what the system estimates the catheter is doing, and real time fluoroscopic (X-ray) images. The system software combines the images. Any standard ablation catheter can be used with this system. Dr. Reddy described how in going through the transseptal wall, for example, one operator uses the joystick while another is at the operating table to advance the needle and dilator through the transseptal wall.

In discussing safety issues Dr. Reddy said this robotic catheter system maintained firm contact with heart tissue to produce better lesions, but that there might be a potential for perforation. Future systems should have “contact sensing strategies” to identify the degree of contact or pressure of the catheter on the heart tissue. “This is probably the future for all catheter ablation procedures.”

Dr. Reddy mentioned that Dr. Natale at the Cleveland Clinic and Drs. Haïssaguerre and Jaïs in Bordeaux, France have also used this system, but only around 30 patients have been treated so far.

Dr. Reddy described how using this system cured a patient in Chronic A-Fib which is harder to cure than other types. After ablating the Pulmonary Veins, he made roof and Mitral isthmus lines. Then he made several lesions near the base of the Left Atrial Appendage, along the anterior Septum, and in areas of Fractionated Potentials. At this point, the A-Fib rhythm organized into Atrial Flutter, a more organized arrhythmia. He then went into the right atrium and made a Cavotricuspid isthmus lesion line which put the patient into sinus rhythm.

Dr. Reddy said he believes that remote navigation for catheter ablation, whether magnetic (see Pappone) or robotic, will change the field of catheter ablation for A-Fib.

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Dr. Moussa Mansour of Massachusetts General Hospital in Boston, MA discussed “Three Dimensional Left Atrial Anatomy: Implications for Catheter Ablation.”

Dr. Mansour presented data that 42% of A-Fib patients have an atypical, unusual left atrium structure. This complex anatomy of the left atrium must be understood in order to perform a safe and effective ablation procedure. Some of the non-normal anatomical structures often found in the left atrium are:

  1. Instead of the normal four Pulmonary Veins, 16-26% of patients have a fifth vein between the right superior and right inferior Pulmonary Veins.  Instead of isolating (ablating) around each of the right PVs, all three Pulmonary Veins must be isolated as a single group.
  2. Approximately 3% of patients have a third Pulmonary Vein above the right superior PV. A normal circular ablation (isolation) around the right superior PV might damage and/or close this third PV. The encircling ablation lesions must be made wider to include this third vein.
  3. In 16-32% of patients the left superior and left inferior Pulmonary Veins have a common opening which can be quite large. Normal circular mapping catheters are too small to adequately map this opening, and ablation catheters can mistakenly ablate within this opening and damage it. Imaging techniques such as Intracardiac Ultrasound (Echo) can be used to identify and isolate this large vein opening.
  4. Many patients have ridges in their atrium, particularly between the Left Atrial appendage and the Left Superior Pulmonary Vein. It’s hard to position an ablation catheter over these ridges. An ablation line must instead be made at the base of the Left Atrial Appendage.
  5. The Mitral Valve Isthmus is often very long and may extend beyond the Coronary Sinus. Ablation of the Mitral Isthmus can be challenging. Creation of an incomplete line can leave gaps which can result in atypical flutter after PV Isolation. Completion of this line requires ablation within the Coronary Sinus in 50% of patients.
  6. Pulmonary Vein openings are often not circular but can be oval and irregular, requiring careful placement of the isolating ablation lines.

Dr. Mansour also pointed out that both the Cardiac Cycle (the beating of the heart) and the Respiratory (breathing) Cycle change the location of the Pulmonary Veins. Any imaging technology must record images of the inside of the heart at the same place in the Cardiac and Respiratory Cycles.

Dr. Mansour concluded that pre-procedure imaging and mapping is essential for patients having an A-Fib ablation procedure, in order to determine whether the patient has a typical or atypical atrium.

(Author’s Note: A one-size-fits-all ablation strategy may not work for the many patients who have an atypical atrium structure.) 

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Dr. Marcus Wharton of the Medical University of South Carolina in Charleston, SC discussed “Atypical Atrial Flutter During and After A-Fib Ablation: Incidence, Physiology, and Management.”

After an A-Fib ablation procedure, some patients develop Atrial Flutter. Conditions that contribute to developing Flutter are:

  • Chronic or Persistent A-Fib
  • A past history of Flutter
  • Atrial disease, scarring, and/or previous heart surgery
  • An enlarged left atrium

In addition, patients undergoing a Wide Area Circumferential Ablation procedure have a 3-35% chance of developing flutter in the long term.

TYPICAL ATRIAL FLUTTER

Dr. Wharton described Typical Atrial Flutter as Flutter originating in the Right Atrium. During an A-Fib ablation procedure, he routinely ablates the Cavotricuspid Isthmus (the area between the Tricuspid Valve Annulus and the Inferior Vena Cava in the right atrium) to prevent Right Atrial Flutter. If this Cavotricuspid Isthmus is not ablated, 10-15% of patients will develop Typical Atrial Flutter.

ATYPICAL ATRIAL FLUTTER

He described Atypical Atrial Flutter as coming from the Left Atrium. The mechanisms or patterns of Left Atrial Flutter are:

1. Macroreentry around the Pulmonary Veins (“Macroreentry” refers to  abnormal Flutter electrical circuits circling around the atrium)

2. Macroreentry through gaps in linear lesions

3. Macroreentry in the Pulmonary Veins

4. Focal Flutter signal sources within the Pulmonary Veins

5. Focal Flutter signal sources other than within the Pulmonary Veins.

Within the first two months after catheter ablation to cure A-Fib, 9% of patients will develop Atypical Atrial Flutter. But most of these patients can be cardioverted and will return to normal sinus rhythm. However, 2-3% may remain in Atrial Flutter.

Approaches to cure Flutter in these patients are:

1. Re-isolate the Pulmonary Veins and non-PV focal sources to eliminate the triggers for Flutter.

2. Make Mitral Isthmus and Left Atrial Roof lesion lines to cut off Macroreentry circuits around the Pulmonary Veins and Mitral Annulus. Dr. Wharton pointed out that it’s difficult to achieve complete block when making these line lesions. And any gap may actually be “proarrhythmic” (may increase Macroreentry Flutter circuits). “If we can’t achieve complete isolation, we potentially may be creating more harm than good with these lesions.” He also pointed out that in two-thirds of his patients, in order to achieve complete block, the Mitral Isthmus line lesion had to be extended to ablate within the Coronary Sinus (which can be risky).

CONCLUSION

Dr. Wharton concluded that Mitral Isthmus and left Atrial Roof lesion lines may improve success rates in curing/preventing Atrial Flutter in all varieties of A-Fib. He also suggested that ablating Complex Fractionated Atrial Electrograms and Autonomic Denervation (ablating sites or ganglia of the Autonomic nervous system) may also help cure Atrial Flutter.

(For someone considering a Right Atrium Ablation procedure to cure Flutter, some Flutter may originate from the left atrium. Consequently, a Right Atrium Ablation procedure might not cure Atrial Flutter.)

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Dr. Michael R. Gold of the Medical University of South Carolina in Charleston discussed “Pacing to Prevent A-Fib and CHF (Congestive Heart Failure)—the Role of Lead Position and Pacing Algorithms.”

Older A-Fib patients often have Bradycardia (slow heart rate) from sick sinus syndrome. Pacing (the insertion of a  pacemaker) helps these patients, but is of no benefit to A-Fib patients who don’t have Bradycardia.

Dr. Gold stated that pacing “…is not curative therapy” for A-Fib. Though atrial pacing may reduce A-Fib, the improvement is modest. “Pacing should be used primarily in (A-Fib) patients who need pacing for other reasons.” Dr. Gold pointed out that earlier retrospective (after the fact) studies had shown a marked reduction of A-Fib with atrial based pacing compared with ventricular pacing alone (VVI mode). But more recent prospective randomized studies have shown a more modest benefit.

Discussing the various pacing methods for A-Fib, Dr. Gold stated that Atrial Pacing (AAI mode) is more effective than Right Ventricular Pacing (DDD mode) which may actually increase A-Fib.

Other pacing methods and factors that improve A-Fib are:

  • Cardiac Resynchronization pacing (CRT), a biventricular pacing mode.
  • Dynamic Atrial Overdrive pacing where the atria are paced 100% of the time.
  • Placing the pacemaker leads in the high Septum area works better than placing the leads in non-Septum areas.

Ablation of the AV Node and insertion of a permanent pacemaker was a common A-Fib treatment. However, it is now used less frequently in the era of ablation procedures which cure A-Fib. There is a small risk of sudden death following AV Node ablation, which can be minimized with higher pacing rates in the first several months following ablation.
Answering a question from the audience about Implantable Defibrillators, Dr. Gold saw no role for them unless a patient needed ventricular defibrillation.

(At one time it was hoped that atrial pacing therapy might one day become a cure for A-Fib. Recent research cited by Dr. Gold shows that pacing modestly improves A-Fib but doesn’t cure or prevent it. Pacing should be used primarily for A-Fib patients who need pacing for other reasons.)

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Dr. Jose Jalife of SUNY Upstate Medical University in Syracuse, NY discussed “The Relationship Between High-Frequency Fractionated Electrograms and Reentrant A-Fib Drivers in the Posterior Left Atrium.”

(Dr. Jalife described what may be a major new discovery in the treatment of A-Fib.) He found that there are sites of high-frequency activity (Dominant Frequencies) within a heart in A-Fib. When these sites are ablated, A-Fib can be terminated.
He used spectral analysis and dominant frequency mapping to produce 3-D color coded images of the heart with the lower frequencies in red and the higher in purple.

He found that patients with Paroxysmal (occasional) A-Fib had high (Dominant) Frequencies mostly in the Pulmonary Vein openings, whereas Persistent or Chronic patients had sites of Dominant Frequencies more scattered throughout the left atrium. Also, Persistent/Chronic patients had higher Dominant Frequencies. This may be do to the remodeling effect of A-Fib which over time changes the substrate (structure) of the heart.
He hypothesized that ablating areas of high (dominant) frequency may become an alternative to making linear lesions in the atrium which are hard to make, are associated with an increased procedural risk, and may be proarrhythmic (may increase A-Fib).
He also related his work to that of Dr. Nademanee’s Complex Fractionated Atrial Electrograms (CFAEs). “Unlike what Nademanee suggests, CFAEs do not correspond to the highest dominant frequency sources. Our results strongly suggest that the region harboring the A-Fib source shows the highest dominant frequency and the highest degree of organization, but is surrounded by complex fractionated activity. Therefore, CFAEs may point to the location of adjacent high frequency sources.”

(In this author’s opinion Dr. Jalife’s discovery of High (Dominant) Frequencies and their role in A-Fib is a major breakthrough in catheter ablation for A-Fib.)

Dr. Jalife also presented an analysis of the previous year’s Boston A-Fib Symposium (2005). Four different approaches to catheter ablation for A-Fib are emerging; 6

  1. Isolation of triggers and reentrant circuits in the Pulmonary Veins (Dr. Haïssaguerre).
  2. Disruption of the substrate for perpetuating rotors in the Antra of the Pulmonary Veins and the posterior left atrium (Dr. Pappone).
  3. Targeted ablation of Ganglionated Autonomic Plexi in the Epicardial Fat Pads (Dr. Jackman).
  4. Disruption of putative dominant rotors in the atria as recognized by High Frequency Complex Fractionated Electrograms during mapping of atrial fibrillation (Dr. Nademanee).
  5. (Dr. Jalife may have discovered a fifth approach—the use of High (Dominant) Frequencies to identify and ablate A-Fib signals in the heart

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Dr. Patrick Ellinor of Massachusetts General Hospital in Boston, MA discussed “Advances in the Genetics of Atrial Fibrillation.”

Dr. Ellinor discussed whether there were “phenotypes” or genetic predictors for A-Fib. In his study at MGH he found that 30% of Lone A-Fib patients had a family history of A-Fib. Some studies have identified chromosome 10 and the genes KCNQ1 and KCNJ2 as related to A-Fib. But current research hasn’t been able to identify the dominant genes or gene mutations that may predict A-Fib.

Dr. Ellinor welcomes individuals with a family history of A-Fib (generally 3 or more members of a family) to participate in the study to identify genes for A-Fib. You can contact him directly to learn more about the study.

Patrick T. Ellinor, MD, PhD
Cardiac Arrhythmia Service
Massachusetts General Hospital
55 Fruit St., GRB 109
Boston, MA 02114
617-726-5067
Fax: 617-726-2155

E-mail: pellinor at partners dot org (Dr. Ellinor’s E-mail address is spelled out to prevent automatic search engines from flooding him with advertisements.)

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Dr. Albert Waldo of University Hospitals of Cleveland Cardiology/Case Western Reserve Un. discussed “2006 ACC/AHA/ESC Guidelines for the Treatment of A-Fib – Update and Critique: Impact of A-Fib Guidelines on Clinical Practice.”

One of the major problems facing both patients with A-Fib and doctors who treat them is how to prevent stroke. Current medical guidelinesfor A-Fib patients with risk factors for stroke recommend using an oral “vitamin K antagonist” such as warfarin (an antagonist works against the coagulation vitamin K). Risk factors for stroke are: prior ischemic (clotting) stroke, transient ischemic attack or systemic embolism (blood clot), being over 75 years old, impaired left ventricular systolic function, hypertension, and diabetes mellitus.

A-Fib patients 65-75 years old, even without any risk factors for stroke, are at intermediate risk of stroke and should be on warfarin. “The relative risk of ischemic stroke increases by 1.4 per decade beginning at age 65 years.” (A 1.4 increased risk means someone is 1.4 times more likely to have a stroke than a normal person.) According to Dr. Waldo, “aspirin only may not be an appropriate recommendation for patients between 65-74.”
If an A-Fib patient is younger than 65 years old with no heart disease, guidelines recommend aspirin (325 mg/d) or no therapy. If there is heart disease with no risk factors for stroke, aspirin (325 mg/d) is recommended.

Doubts About Aspirin Therapy

Dr. Waldo raised concerns about aspirin therapy. Citing several studies Dr. Waldo indicated that, “warfarin is far superior to aspirin in diminishing the risk of stroke.”7 Also, should a stroke occur on aspirin, it is usually more severe and has a significantly higher mortality when compared with warfarin therapy (with the INR maintained in the therapeutic range of 2.0-3.0). (“INR” stands for International Normalized Ratio and is a means of measuring the level of warfarin in the blood stream.) Dr. Waldo recommended that, “the use of aspirin really needs to be reconsidered or at least more seriously tested.”  “…if one needs protection against stroke, one needs a vitamin K antagonist (warfarin).”

Bleeding Risk From Warfarin

Dr. Waldo addressed concerns about bleeding risk (cerebral hemorrhage stroke) in patients taking vitamin K antagonists (warfarin). The relative risk of ischemic (clotting) stroke increases with age, as does the risk of a hemorrhagic stroke when taking warfarin. But “the risk of ischemic stroke (in an A-Fib patient not taking warfarin) is considerably greater than the risk of intracranial bleeding.”8 Dr. Waldo also pointed out that an increased risk of hemorrhagic stroke does not occur until a patient’s INR reaches 3.9-4.0 (a normal therapeutic warfarin INR range is 2.0-3.0).

Should Warfarin Be Stopped After A Successful A-Fib Ablation?

Common practice today is to terminate oral anticoagulation therapy 3-6 months following an apparently successful cure. But recent studies indicating reoccurrences of often silent A-Fib after ablation raise some doubts about this practice (see Kottkamp and Calkins). In his practice Dr. Waldo  keeps “cured” A-Fib patients with risk factors for stroke on warfarin.

Warfarin Under-Prescribed

In a study of hospitals treating A-Fib patients, 20% of high risk patients didn’t receive any anticoagulation therapy, and 24.7% only received aspirin when according to the guidelines they should have received warfarin. “The patients who need (warfarin) the most seem to be getting it the least.”

(Author’s Note: Dr. Waldo’s data and recommendations against aspirin and in favor or warfarin are very important for A-Fib patients. As Dr. Waldo put it, “Stroke is a fate worse than death.” Since aspirin is far less effective than warfarin in preventing stroke, A-Fib patients with risk factors for stroke on aspirin therapy should seriously consider changing to warfarin.)

(Added August 14, 2007: The Center for Shared Decision Making gives somewhat controversial odds of getting an A-Fib stroke depending on one’s overall heart health:

Under age 65 with no history of hypertension, stroke, arterial embolism, left ventricular dysfunction, or TIA:

Chance of stroke in two years 2 out of 100

Taking daily coated aspirin 1.5 out of 100

Taking daily warfarin 1 out of 100

Age 65-75 with no history of hypertension, stroke, arterial embolism, left ventricular dysfunction, or TIA:

Chance of stroke in two years 4 out of 100

Taking daily coated aspirin 3 out of 100

Taking daily warfarin 2 out of 100

Over age 75, or under age 75 with history of hypertension or left ventricular dysfunction:

Chance of stroke in two years 12 out of 100

Taking daily coated aspirin 9 out of 100

Taking daily warfarin 4 out of 100

Any age with a history of TIA, stroke or arterial embolism, or over age 75 with a history of hypertension or left ventricular dysfunction:

Chance of stroke 20 out of 100

Taking daily coated aspirin 16 out of 100

Taking daily warfarin 7 out of 100

aThere are two main sets of guidelines for the use of anticoagulants for A-Fib patients: the American College of Chest Physicians (ACCP) guidelines published in October 2004, and the American College of Cardiology (ACC), the American Heart Association (AHA), and the European Society of Cardiology (ESC) guidelines published in September 2001 (currently under revision). Both sets of guidelines are generally compatible with each other, but there are differences. For example, the ACC/AHA/ESC guidelines use age 60 as a cut off for some considerations, whereas the ACCP uses age 65.

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Debate and Discussion: “Catheter Ablation Should Be First Line Therapy in Selected Patients with A-Fib.” Pro: Dr. Andrea Natale, The Cleveland Clinic Cleveland, OH. Con: Dr. Eric Prystowsky, The Care Group, Indianapolis, IN.

The debate addressed a question that is very important to A-Fib patients: should drug therapy be tried first, or should a catheter ablation procedure be the first choice? Most current guidelines for treating A-Fib state that drug therapy should be tried first.

MEDICATION THERAPY

Both Dr. Natale and Dr. Prystowsky were in general agreement that current drug therapies have limited effectiveness and can have dangerous side effects.

Dr. Natale discussed the role of Rate Control (using medicines to control the heart rate, but leave the heart in A-Fib) and Rhythm Control (using antiarrhythmic medicines to try to stop A-Fib) in treating A-Fib. The AFFIRM clinical studies found no mortality difference between Rate Control and Rhythm Control. However, Dr. Natale pointed out that the AFFIRM study did not compare patients in Rate Controlled A-Fib with patients in normal sinus rhythm (the goal of catheter ablation). In fact, the AFFIRM investigators concluded, “the presence of sinus rhythm was one of the most powerful independent predictors of survival, along with the use of warfarin… Patients in sinus rhythm were almost half as likely to die compared with those with A-Fib.”

Dr. Natale pointed out that the AFFIRM study was not really an endorsement of Rate Control drugs. Rather it illustrated how ineffective and dangerous current antiarrhythmic drugs can be. “…data from several trials have demonstrated that the success of antiarrhythmic medications (AAMs) in maintaining sinus rhythm is borderline, at best, with increasing failure rates over time… AAMs clearly do not cure A-Fib; at best, they are a palliative treatment used to reduce the burden of A-Fib as opposed to eliminating it altogether. …in our experience rhythm control is not only ineffective and poorly tolerated, but only delays an inevitable ablation.”

In addition, AAMs frequently cause debilitating side effects. Amiodarone, possibly the most effective AAM, is associated with the most dangerous side effects: intolerable skin discoloration, pulmonary fibrosis, damaged thyroid, and neurological or ophthalmic problems. Also, AAMs may increase mortality. “Both cardiac mortality and arrhythmic death were significantly increased, particularly in patients with heart failure.”
Dr. Prystowsky concurred with Dr. Natale about “the limited long-term efficacy and high incidence of side effects for antiarrhythmic medications.”

CATHETER ABLATION (PVI) THERAPY

Both doctors’ PRO and CON arguments on using catheter ablation as a first-line therapy far treating A-Fib are listed in the following table.

PRO (Dr. Natale)
CON (Dr. Prystowsky)
Catheter Ablation is a lasting cure The long-term success of catheter ablation procedures is not known
Success rates are high (80%) in recent multi-center studies Success rates are operator dependent and are not consistent
Complication rates are low Complication rates may be greater and more serious than reported

Dr. Natale argued that, in contrast to Rate Control and Antiarrhythmic drug therapies, catheter ablation (PVI) offers the possibility of a lasting cure. Citing recent studies from several different medical centers, an overall success rate of over 80% is currently being achieved, which is 2- to 3-times better than anything achievable with AAMs. In all these centers there was a very low incidence of complications.

In a controlled, long-term study, patients who underwent A-Fib ablation had significantly improved survival compared to patients who received antiarrhythmic medications, suggesting that A-Fib ablation might be considered as a first-line strategy. Also, in the RAAFT study (Radiofrequency Ablation for Atrial Fibrillation Trial) comparing A-Fib ablation as first-line therapy to AAMs, A-Fib recurred in 65% of AAM patients compared to only 13% of ablation patients.

Dr. Prystowsky indicated that the long-term efficacy of A-Fib ablation isn’t definitely known. Perhaps, “…pulmonary vein isolation procedures may not result in long-term clinical success after initial clinical success.”

He also stated that with regards to A-Fib patients at high risk for stroke, “there is no long-term follow-up showing a reduction in stroke risk in patients apparently cured of A-Fib with catheter ablation.” Such patients may need constant long-term monitoring with, for example, an implanted loop recorder.

There is also a significant variance of success among medical centers using similar techniques of ablation. “Because the procedures are technically challenging and highly operator dependent,” the safety and efficacy of catheter ablation varies by doctor and medical center. Only 8% of medical centers worldwide do more than 300 A-Fib ablations a year.

He also thought the Complications Rate after A-Fib ablations may be under-reported due to publication bias. He was particularly concerned about Atrial-Esophageal Fistula. “Risk factors for this potentially fatal complication have not been established.” He mentioned that catheter ablation may sometimes damage the vagal nerve system with unknown long-term consequences. He expressed concern about the recent studies indicating “silent” A-Fib recurrences after ablation which would lower the reported success rate (see Kottkamp and Calkins).

SHOULD PATIENTS RECEIVE A-FIB ABLATION AS A FIRST CHOICE?

Both doctors basically agreed that A-Fib ablation should be offered as a first-line therapy to some patients, but not to all. They differed slightly when describing the patients who should be offered A-Fib ablation as first-line therapy.

According to Dr. Natale, at the present time A-Fib ablation as first-line therapy should not be offered to all patients with A-Fib. Large-scale, comparative clinical trials need to be performed before recommending ablation as a first choice for a very broad population of A-Fib patients.

Ablation should be offered as a first-line therapy to highly symptomatic patients with recurrent A-Fib (not related to other, curable causes), who have already failed drug therapy, with minimal or moderate structural heart disease.  Also, ablation may particularly benefit younger patients with lone A-Fib for whom very-long-term antiarrhythmic and anticoagulation pose higher risks and lifestyle costs.

However, Dr. Natale predicted that in the near future A-Fib ablation can be offered as first-line therapy to a broader A-Fib population. He cited data showing that good success rates are already being achieved in A-Fib patients with impaired left ventricular function, previous cardiac surgery or valvular heart disease, and advanced age. The only group that seems destined to fail ablation is that with extensive, preexistent scarring (atrial myopathy).

Dr. Prystowsky stated that catheter ablation might be considered as an initial therapy in the following cases:

  • patients with very symptomatic A-Fib who refuse antiarrhythmic medications,
  • patients in whom the only antiarrhythmic choice is long-term amiodarone,
  • possibly patients at high risk of stroke who refuse or cannot take long-term warfarin therapy,
  • young patients with paroxysmal A-Fib and sinus node dysfunction who may not tolerate antiarrhythmic medications without a permanent pacemaker.
THE IMPORTANCE OF EXPERIENCED DOCTORS AND CENTERS

Both doctors recognized that operator experience, skill and use of advanced technology affect the success rates of  A-Fib Ablation. Dr. Natale stated that only centers with considerable experience in performing A-Fib ablation should consider offering ablation as first-line therapy, because currently success is highly operator dependent.

Answering a question from the audience, Dr. Prystowsky reported that Wellpoint Inc. has a policy of not paying for a PVI unless a patient has failed two antiarrhythmic drugs. (This appears to be another disturbing example of insurance companies making decisions that should be left to the doctor and patient.)

(Editor’s Note: From this patient’s perspective, catheter ablation should be considered as first-line therapy for many A-Fib patients. According to Dr. Natale, “The lack of efficacy and known harm of alternative pharmacological therapy for A-Fib cannot be underestimated.” Whereas catheter ablation has a high success rate, is most likely a permanent cure, and is a low risk procedure. However, for best results a patient may need to go to centers with considerable experience in performing catheter ablations for A-Fib [over 300/year].)

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Panel and Audience Discussion: How We Approach Catheter Ablation for A-Fib Today: Tailoring Procedures to Individual Clinical Scenarios and Optimizing Safety and Effectiveness. Moderator: Dr. Jeremy Ruskin. Panelists: Dr. Warren Jackman, Dr. Pierre Jaïs, Dr. Steven Kalbfleisch, Dr. Karl Heinz Kuck, Dr. Francis Marchlinski, Dr. Andrea Natale, Dr. Douglas Packer, Dr. Carlo Pappone, Dr. Vivek Reddy, Dr. David Wilber

The panel moderator, Dr. Jeremy Ruskin of Massachusetts General, pointed out that catheter ablation, while still considered “new,” has been used to cure A-Fib patients for eleven years. He asked the panelists to describe their current strategies for Paroxysmal (occasional), Persistent (lasting over 24 hours but can be cardioverted) and Chronic (permanent) A-Fib patients.

Dr. David Wilber, Loyola Un. Medical Center, Chicago

Paroxysmal:

Pulmonary Vein (PV) Isolation is the cornerstone of our approach. We use electrograms to confirm isolation.

Then we use an individualized approach. If there is scarring and/or fibrous tissue in the atrium and we can still induce A-Fib, we ablate areas of low voltage (less than 0.5mV) and areas of Complex Fractionated Atrial Electrograms (CFAEs). If A-Fib can still be induced, we use linear lesions. But this rarely happens with Paroxysmal patients. At the end we use high dose isoproterenol (20 micrograms/min.) to try to induce A-Fib to make sure there are no focal drivers anywhere else. Because we regularly use anesthesia, we wake up patients at the end of the procedure. We are concerned about sedation suppressing some of the A-Fib drivers.

Persistent and/or Chronic:

We again begin by ablating (isolating) the Pulmonary Vein (PV) openings. Then we ablate CFAEs. Then we look at the right atrium, particularly the Coronary Sinus and Superior Vena Cava. Then we use linear lesions. Our ideal end point is non-inducibility of A-Fib. But with Chronic patients this may not be a realistic goal. For Chronic patients we are happy if we can maintain sinus rhythm, ablate CFAEs, and have good lesion sets.

Dr. Karl Heinz Kuck, St. George Hospital, Hamburg, Germany.

We spend a lot of time creating the true anatomy of the heart by imaging techniques. What some people call the outside of the Pulmonary Vein Ostia (openings), we would call the inside.

Paroxysmal/Persistent:

We use Circumferential Isolation outside the ostia and make sure the isolation is permanent.

Chronic:

The Circumferential Isolation procedure works for approximately 50% of Chronic patients. We don’t know yet which strategy is better than that. There are so many CFAEs in the heart. Is 115 burns enough? We need more experience.

Dr. Douglas Packer, The Mayo Clinic, Rochester, MN.

Paroxysmal:

We start with PV Circumferential Ablation, then move to non-PV foci (A-Fib trigger sources), then make linear lesions, making sure there are no gaps in the lesion lines.

Persistent/Chronic:

We start with a wider area Circumferential Ablation of the PVs, then ablate areas of CFAEs. We have been discouraged by ablation of CFAEs alone, which don’t terminate Chronic A-Fib. We then ablate in the Coronary Sinus, Posterior Mitral Annulus and Septum using linear lesions.

Dr. Warren Jackman, Un. of Oklahoma, Oklahoma City, OK.

Paroxysmal:

We start by mapping the left atrium and PVs using ICE to mark key landmarks. We identify and ablate the four Ganglionated Plexi areas in the left atrium. If A-Fib continues, and it usually does, we will cardiovert the patient to terminate the A-Fib. Then we will look for areas of spontaneous firing and do a complete Antrum PV Isolation. If we can still induce microreentry tachycardias by 4 micrograms/min of Isoproterenol, we will make linear lesions.

Chronic:

We ablate Ganglionated Plexi, then CFAEs, cardiovert, then do Antrum Isolation, then move to the right atrium.

Dr. Steven Kalbfleisch, Mid Ohio Cardiology Consultants/Riverside Methodist Hospital, Columbus, OH.

Paroxysmal:

In patients with inducible A-Fib we focus on PV sites with active drivers, and also use fractionated electrograms as targets. With non-inducible A-Fib patients, we do PV isolation with as limited RF applications as possible. We don’t use wide area lesions in order to avoid the complication of left atrial flutter which we ran into when we were doing wide area lesion sets.

Persistent:

We use an electrogram-driven approach staying as anterior as possible in order to stay away from the posterior atria walls and the esophagus. At present we do very few ablations on Chronic A-Fib patients.

Dr. Pierre Jaïs, Central Hospital Un. of Bordeaux, France.

Paroxysmal:

We start with PV ablation. If A-Fib continues, we make linear lesions in the roof of the left atrium which is easier than making Mitral Isthmus ablation lines.

Chronic:

We start with PV ablation.

Then, using an electrogram guided approach, we ablate areas of rapid activity rather than fractionated signals. We feel fractionated activity signals are more the consequence of rapid activity and are found in the direct vicinity of rapid activity signals.  Anatomical areas of the heart which more frequently harbor these sites are: the inferior left atrium, the left appendage, and the Coronary Sinus.

Then we make linear lesions of the roof line and, if necessary, the Mitral Isthmus line. In 85% of Chronic cases it is necessary to make a Mitral Isthmus line.
Our end point is to terminate A-Fib without using drugs or cardioversion. However, it might possibly be better to terminate the procedure after a certain amount of RF energy has been delivered, in order to save the mechanical activity of the atrium. However, atrial activity always recovers, even if in some patients it takes  a year to recover, even after 100 or 110 minutes of delivered RF energy. (see Jaïs.)

Dr. Carlo Pappone, San Raffaele University Hospital, Milan, Italy.

Paroxysmal:

Our approaches to Paroxysmal and Chronic are basically the same. We reconstruct the anatomy of the atrium very well and make impedance maps. We make circumferential lesions just outside the junction of the PVs and the left atrium. We use an irrigated tip catheter. We check for the quality, continuity, and transmurality of the lesion lines. Our end point is the amount of area involved in the lesions—more than 30% of the substrate.

Chronic:

We additionally ablate for right atrium flutter and try to induce atrial tachycardia. In a randomized study with Dr. Morady, our ablation procedure was superior to amiodarone in curing Chronic A-Fib patients.

Dr. Francis Marchlinski, University of Pennsylvania, Philadelphia, PA.

Paroxysmal:

Our goal for all types of A-Fib is proximal PV isolation and the identification of triggers in order to eliminate them. For Paroxysmal younger patients we do less. We only isolate the PVs that demonstrate these triggers.

Persistent/Chronic:

We ablate all PVs and non-PV triggers based on repeated and spontaneous initiation of A-Fib triggers using isoproterenol in incremental doses and/or with induction of A-Fib and then cardioversion with or without low dose isoproterenol.

Our end point is documentation of electrical PV isolation and no provocable triggers. We don’t have to completely circumferentially surround the vein. We specifically try not to target the posterior wall until we have isolated all the other segments and the posterior wall remains connected, so that we can limit the amount and energy required on the posterior wall. We use on-line echocardiogram monitoring to titrate the energy and duration of the ablation. We limit the duration to 20 sec. or less on the posterior wall.

Dr. Andrea Natale, the Cleveland Clinic, Cleveland, OH.

Paroxysmal:

We do what we now call Antrum isolation and include the Superior Vena Cava which covers most of the trigger sites.

Chronic:

For patients with atrial myopathy we do standard ablation more anteriorly and in the Septum. Then we cardiovert and make additional lesions based on fast Fourier analysis of the electrograms.

Dr. Vivek Reddy, Massachusetts General Hospital, Boston, MA.

Paroxysmal:

We isolate the PVs in an extraostial fashion as defined by use of the Lasso catheter. In the past, we have been frustrated by recurrence, which the vast majority of the time is related to resumption of conduction from the PVs. We are much more aggressive at the end of the procedure in order to identify potential breaks in the lines. We use Isoproterenol at 20 micrograms to look for resumption of conduction. We also look for non-PV triggers. We also look at the Superior Vena Cava; but if the Phrenic Nerve is near where we would isolate, we are not aggressive. We rarely do a Cavotricuspid Isthmus Line in the right atrium unless the patient has a history of atrial flutter or has flutter inducible during the procedure.

Chronic:

In addition to the above, we make linear lesions in the roof line in order to avoid having to make a Mitral Isthmus line. Frequently, however, we have to make a Mitral Isthmus line which often requires ablating within the Coronary Sinus which can be harrowing.

Then we ablate Complex Fractionated Electrograms in the areas Dr. Jaïs has shown—Anteriorly, in the Septum, and also near the base of the Left Atrial Appendage.

Then we place lesions in the Coronary Sinus though we are concerned about safety of the esophagus (which is posterior to the mid Coronary Sinus) and the Coronary Artery.

If the patient is still in A-Fib, we cardiovert with Ibutilide. The end point is conversion to sinus rhythm. If we use Ibutilide, we don’t try to re-stimulate A-Fib. We do try to re-stimulate if we don’t use Ibutilide.

Panelists/Audience Comments:

Dr. Jaïs pointed out that for the first time since he started attending these meetings when they began eleven years ago, there is a consensus that we should isolate the Pulmonary Veins, that this is the core of the procedure, the first step that everybody agrees on.

Dr. Ruskin asked the panelists what precautions they take to prevent Atrial-Esophageal Fistula. Some suggestions mentioned were:

  • Minimize power—10-15W.
  • Use irrigated tip catheters.
  • Short duration ablation times—10-15 sec. and/or move the catheter as soon as an area is electrically isolated.
  • Use of a temperature probe (see d’Avila). But no temperature rise doesn’t mean it is impossible to have esophageal damage. However, a temperature rise makes us move the ablation catheter.

Use Intercardiac Echo (ICE) to identify the location of the esophagus. Some panelists said it was hard to identify the location of the esophagus using ICE.
One panelist who used Circumferential Antrum ablation of the PVs said the lesions do overlay the esophagus at some point.

It was asked if Cryo Catheter ablation might be safer to use near the esophagus. In animal studies both Cryo and RF created lesions on the esophagus. Both lesions healed within a month, but the Cryo lesions had less fibrosis and seemed less damaging than RF.

In a question about open tip vs. closed tip irrigated catheters, cooling seems greater with open tip and there is less chance of thrombus.

(From this patient’s perspective, it seems like there is an ever increasing number of differently named catheter ablation procedures to cure A-Fib—such as “Focal Ablation,” “Pulmonary Vein Ablation,” “Pulmonary Vein Isolation,” Segmental Ablation,” Circumferential Ablation,” “Empirical Ablation,” Pulmonary Vein Antrum Ablation,” “Anatomically Based Circumferential PV Ablation,” “Left Atrial Catheter Ablation.” But the comments of the above panelists shows there is a consensus on catheter ablation for A-Fib. Nearly everyone starts with the Pulmonary Veins, then moves to similar areas of the heart, though not necessarily in the same sequence. This similarity of approaches across different medical centers is very encouraging for A-Fib patients.

Not so encouraging is the risk of Atrial-Esophageal Fistula, particularly with the more extensive catheter ablation procedures which routinely ablate near the esophagus. Procedures have yet to be identified and/or employed to significantly reduce this risk.

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Update on Mechanisms and Therapy for Atrial Fibrillation from The 11th Annual Boston Atrial Fibrillation Symposium 2006

David Keane, Vivek Reddy, Jeremy Ruskin on behalf of the B.A.F.S. faculty

Key points:

Endocardial sites of complex fractionated atrial electrograms during atrial fibrillation tend to correlate with the sites of ganglionated plexi located in the epicardial fat pads.

Ablation at sites of complex fractionated atrial electrograms results in progressive slowing of atrial fibrillation cycle lengths and has a resulting organizational effect on atrial activation.

Pulmonary vein isolation is insufficient as a stand-alone procedure for most patients with persistent atrial fibrillation – as a result it may be challenging for stand-alone ablation devices which solely isolate pulmonary veins to achieve regulatory approval for a population of patients beyond paroxysmal AF.

The recently-demonstrated multi-component ablation strategy for patients with persistent atrial fibrillation may ultimately replace the role of percutaneous left atrial appendage closure devices in appropriate patients.

Although the risk of significant complications from catheter ablation of atrial fibrillation is recognized, in individual cases such as highly-symptomatic young patients facing decades of drug therapy, catheter ablation may occasionally be appropriate as a first-line therapeutic option at centers with a high volume of experience.

Catheter Ablation as First Line Therapy

“Catheter ablation should be offered as first line therapy for patients with atrial fibrillation” was the subject of a key debate at this year’s 11thAnnual Boston Atrial Fibrillation Symposium. It was accepted that adoption of first line catheter ablation for atrial fibrillation would not reflect most of the clinical series published to date or comply with current guidelines (Prystowsky). It was also acknowledged, however, that the large randomized trials of rhythm (with antiarrhythmic drugs) versus rate control for atrial fibrillation did not include the typical profile of patients currently undergoing catheter ablation (Natale).

Although the risk of sudden death from proarrhythmic effects of anti-arrhythmic drug therapy in patients without structural heart disease or coronary artery disease is accepted to be small, the profile of patients undergoing catheter ablation has evolved over the last seven years from predominantly young patients with lone paroxysmal fibrillation initially to patients with persistent atrial fibrillation with heart failure more recently. In the latter group of patients. the risk of proarrhythmia from antiarrhythmic medications is of significant concern and some patients may thus decline to undergo an initial trial of antiarrhythmic drug therapy before pursuing catheter ablation. This may particularly be the case when amiodarone is the antiarrhythmic drug under consideration. Similarly, young patients with symptomatic recurrent atrial fibrillation potentially facing decades of drug therapy may opt to proceed directly to catheter ablation – particularly at centers with substantial experience (Natale and Prystowsky).

The relative roles of catheter ablation versus antiarrhythmic drug therapy for atrial fibrillation will ultimately be determined by a number of ongoing randomized trials. One recently completed randomized trial at two centers by Oral and Pappone and colleagues recently compared 3 months amiodarone and electrocardioversions versus 3 months amiodarone and electrocardioversions and catheter ablation for patients with chronic atrial fibrillation. Of patients who were managed with 3 months of amiodarone and electrocardioversion only 4% were in sinus rhythm at one year. Of patients who underwent catheter ablation (32% required a repeat procedure), 74% were in sinus rhythm at one year. While the procedure of catheter ablation for atrial fibrillation is currently being tested by ongoing randomized trials including a mortality trial, the continued evolution and improvement in catheter ablation techniques for atrial fibrillation, will require many of these trials to be repeated in due course. In the interim, the majority of patients with atrial fibrillation undergoing catheter ablation will continue to be those who are symptomatic and have failed a trial of antiarrhythmic drug therapy. To date the only completed study indicating improved survival following catheter ablation compared to medical therapy was retrospective and not randomized (Pappone).

Whether the optimal management of patients with atrial fibrillation who are asymptomatic and young will involve catheter ablation will depend on prospective randomized trials of long-term morbidity and mortality. One example of a special consideration for catheter ablation in a patient with asymptomatic atrial fibrillation might be if a patient is unable or unwilling to take coumadin and were alternatively considering implantation of a left atrial appendage occlusion device. The prevalence of silent atrial fibrillation among patients without symptoms as well as those with atrial fibrillation which is intermittently associated with symptoms is underappreciated (Camm). The complications of silent atrial fibrillation (including stroke and tachycardia mediated cardiomyopathy) are similar to patients with symptomatic atrial fibrillation (Camm). It should also be borne in mind when deciding on a management strategy for patients with silent atrial fibrillation that their quality of life is reduced independently from the objective measures of illness severity (Camm).

Antiarrhythmic Drug Therapy

While antiarrhythmic agents with new mechanisms of action are not expected to become available in the short term, the effect of angiotensin converting enzyme inhibitor drugs and angiotensin II receptor blockers on atrial remodeling and atrial fibrillation burden continues to look promising. A number of ongoing trials will define their potential role in patients with atrial fibrillation with underlying left ventricular systolic or diastolic dysfunction. The therapeutic role of these agents, however, is likely to remain in the realm of mildly beneficial auxiliary therapy rather than as direct antiarrhythmics (Kowey). The role, if any, of statins in the prevention of atrial fibrillation recurrence post cardioversion is also under investigation in prospective trials. It should be recognized that the anti-inflammatory impact of statins on atrial fibrillation appears limited with one prospective trial showing no benefit (Kowey).

With regards to early clinical and pre-clinical pharmacologic developments, interest remains in the further evaluation of antiarrhythmic drugs that affect channels predominantly found in the atria but not the ventricles in order to minimize the risk of sudden death. These include selective blockers of Ikur (ultra-rapid delayed rectifier current) which do not prolong the QT interval (Kowey). Atrial repolarizing delaying agents have a combined effect on potassium and fast sodium currents and have a low torsades potential in the ventricle. Attention is also being paid to the development of gap junction modulators where it is hypothesized that restoration of intercellular conduction in pathological states might be antiarrhythmic (Kowey).

Anticoagulation

Anticoagulation with coumadin continues to be of concern with a 1 % risk per annum of significant hemorrhage inclusive of a 0.3% risk per annum of intracranial hemorrhage which carries a high mortality rate. For patients facing long-term medical management of atrial fibrillation, these risks accumulate to significant concern in the long-term and continue to be one of the driving forces behind the development of non-pharmacological therapy. The efficiency of home monitoring of anticoagulation in recent studies indicate that the risks of thromboembolism (under treatment) and hemorrhage (over treatment) on coumadin may be reduced by self monitoring at home rather than attendance at a hospital based anticoagulation clinic. In the US, the FDA has not approved the oral direct thrombin inhibitor ximelagatran on account of concerns of hepatotoxicity (Waldo). Whether this drug will undergo further evaluation outside of the US remains to be determined. Alternative oral direct thrombin inhibitors remain under clinical trial.

The AFFIRM trial demonstrated that in patients with an indication for anticoagulant therapy, (presumed) resumption of sinus rhythm by rhythm control with antiarrhythmic drug therapy does not obviate the requirement for ongoing anticoagulant therapy (Waldo). However, many patient who currently undergo catheter ablation of atrial fibrillation are under 65 years of age (younger patients are usually more symptomatic than older patients), and do not have congestive heart failure, hypertension, diabetes, or history of a cerebrovascular event. i.e. many candidates for catheter ablation of atrial fibrillation do not meet current American College of Chest Physician guideline criteria for long-term anticoagulation. Many of these patients in practice are prescribed anticoagulant therapy while they have atrial fibrillation prior to undergoing catheter ablation. However, if their atrial fibrillation was eliminated by catheter ablation, then discontinuation of anticoagulant therapy would seem appropriate and particularly so if the absence of asymptomatic atrial fibrillation recurrences is confirmed. It should be recognized that Kottkamp and Hindricks have shown the prevalence of asymptomatic atrial fibrillation alter catheter ablation to be significant particularly if seven day ambulatory recordings are made at 3 or 6 monthly intervals post ablation (Kottkamp). In a study of serial 5 day wireless monitoring after pulmonary vein isolation at Johns Hopkins University, 60% of patient activated recordings during symptoms were found to be non-atrial fibrillation events (Calkins). At 6 month follow-up, 13% of patients had exclusively asymptomatic recurrences of atrial fibrillation compared to 37% with symptomatic recurrences (Calkins). Thus a decision to discontinue anticoagulation post catheter ablation of atrial fibrillation is complex and reliance on the presence of symptoms alone may be limited and may be prone to either underestimation or overestimation of atrial fibrillation recurrences.

Although one of the left atrial appendage occlusion devices remains under clinical evaluation, clinical trials of the longest standing device has been halted in view of FDA requirements for comparative data with oral anticoagulants – a standard deemed to be too expensive to be met by the manufacturer. A number of adverse events have occurred in the clinical follow-up of these devices and it is unclear whether that they will offer a safer option than oral coumadin. Given the recently reported efficacy of catheter ablation for persistent atrial fibrillation, the principle alternative to a lelt atrial appendage occlusion device may be the option of undergoing catheter ablation of atrial fibrillation itself rather than implantation of a permanent device. This may particularly hold true if the complication rate of catheter ablation can be reduced, given that a number of device dislodgements have occurred after left atrial appendage occlusion devices implantation and a number of deaths have occurred post implantation. The details of these adverse outcomes are awaited.

Ganglionic plexi and their influence on pulmonary vein myocardial physiology

While the role of automatic, triggered and stretch induced firing as well as local reentry of the pulmonary vein myocytes in paroxysmal atrial fibrillation is widely accepted, the contribution of the pulmonary veins in long-standing persistent atrial fibrillation is less clear.

Ganglionic plexi and their influence on pulmonary vein myocardial physiology

While the role of automatic, triggered and stretch induced firing as well as local reentry of the pulmonary vein myocytes in paroxysmal atrial fibrillation is widely accepted, the contribution of the pulmonary veins in long-standing persistent atrial fibrillation is less clear.

The physiology of pulmonary vein myocytes was reviewed at this year’s symposium (Jackman). The action potential of pulmonary vein myocytes appears to progressively shorten from the proximal pulmonary vein antrum towards the distal pulmonary vein. As a result the action potential of distal pulmonary vein myocytes may be only 50% as long in duration as those of myocytes in the pulmonary vein antra. The progressively shortened refractory period may facilitate both spontaneous firing as well as local reentry within the pulmonary vein myocardial sleeve. The action potential of the pulmonary vein myocytes may be so short that intracellular calcium may not have fully returned to baseline before the action potential is completed. This may further facilitate early alter depolarizations through sodium – calcium exchange whereby three sodium ions are exchanged for each calcium ion (resulting in a net inward current). Ganglionic stimulation or application of norepinephrine appears to result in calcium transient triggered firing of pulmonary vein myocytes. Parasympathetic stimulation of pulmonary vein myocytes or application of acetylcholine results in shortening of the pulmonary vein myocyte action potential (Jackman).

The dependency of the pulmonary vein myocardial physiology on ganglionic plexi tone appears significant. Although there is a close physiologic link, anatomically the ganglionic plexi controlling pulmonary vein myocardial activity is more remote and the link is mediated by a complex network of neurons. Electrical stimulation or pharmacologically blockade at sites of ganglionic plexi in epicardial fat pads appears to exert regional electrophysiological changes outside the immediate vicinity (Patterson, Jackman). These regional and remote effects are felt to relate to the rich innervation of the area and extensive neuronal networking. Studies at the University of Oklahoma would indicate that in the left atrium, the sites of ganglionated plexi (as detected by subthreshold high frequency stimulation) are located (i) superior to the left superior pulmonary vein, (ii) infero-posterior to the left inferior pulmonary vein extending towards the distal coronary sinus, (iii) anterior to the right pulmonary veins and (iv) infero-posterior to the right inferior pulmonary vein extending towards the proximal coronary sinus (Jackman).

Complex Fractionated Atrial Electrograms

The anatomical location of ganglionic plexi described above by Jackman bear an anatomical relationship to the distribution of complex fractionated atrial electrograms described by Nademanee. Complex fractionated atrial electrograms described by Nademanee usually are low voltage multiple potential signals between 0.05 – 0.25mV. In some patients complex fractionated atrial electrograms have very short cycle length «100ms) without multiple prolonged potentials (Nademanee). It is proposed that sites demonstrating such high frequency activity with a shorter cycle length than anywhere else in the atria drive the rest of the atria (Nademanee). A number of software programs have been developed to automatically detect complex fractionated atrial electrograms in order to generate a 3-dimensional map to group the distribution pattern of these sites. These programs, however, continue to require oversight and manual editing. The sites of complex fractionated atrial electrograms vary from consistent to intermittent or transient. Overall, however, over an adequate sampling period, marked temporal and spatial stability is observed (Nademanee). The distribution of sites of complex fractionated atrial electrograms is more widespread in patients with persistent rather than paroxysmal atrial fibrillation.

Studies of finite element analysis of rotors and fractionated fibrillatory conduction (Jalife) as well as clinical studies of frequency gradients during multielectrode mapping (Jais and Haissaguerre), indicate that continuous fractionated atrial electrograms may represent the immediately adjacent zone of fibrillatory conduction rather than the precise sites of primary microreentrant rotors. Thus one shift in interest may be more towards the identification and ablation of sites of very high frequency regular activity immediately adjacent to or sites surrounded centrifugally by continuous fractionated electrograms (Jalife). The interelectrode distance on conventional ablating catheters may make such precision mapping challenging and customized multielectrode 2-dimensional array catheters may facilitate the localization of such sites.
Thus, complex fractionated atrial electrograms may represent not only sites of autonomic ganglia but also sites immediately adjacent to microreentrant rotors. It has been claimed that endocardial ablation at sites of ganglionic plexi (in particular the right inferior fat pad superior to the proximal coronary sinus and medial to the ligament of Marshall) may acutely terminate atrial fibrillation (Pappone). Such termination may relate to elicitation of acute transient regional autonomic modulation rather than abolition of the chronic substrate of atrial fibrillation. In contrast, termination of atrial fibrillation seen after progressive prolongation of atrial cycle length and stepwise organization of atrial activity by a series of completed ablation lesion sets appears to be more likely to render atrial fibrillation non-inducible and translate into long-term freedom of atrial fibrillation recurrence.

One current inconsistency is the extent to which the location of complex fractionated atrial electrograms corresponds to epicardial sites of fat pads containing ganglionated plexi. While at some centers the sites at which complex fractionated atrial electrograms are ablated correspond closely, at other centers (Bordeaux, Munich) including our own, such recordings are also encountered at sites not known to be rich in epicardial ganglionic plexi such as the base of the left atrial appendage and the fossa ovalis (anterior to the location of right anterior epicardial fat pad). The mechanism of generation of complex fractionated electrograms at such sites may relate to the merging of bundles of myocardium with different longitudinal orientation. Such bundles may act as a functional bottle neck of activity from the 3-diminsional reentry of the pectinate muscles of the left atrial appendage and from the left atrium and from the right atrium.

Non-pulmonary vein triggers

While most labs are now spending considerable time post pulmonary vein isolation on localization and ablation of complex fractionated atrial electrograms during atrial fibrillation, time spent on the localization of atrial ectopic activity during sinus rhythm after completion of pulmonary vein isolation varies considerably from lab to lab. Depending on the frequency, number of foci and mapping tools, this latter process can be prohibitively time consuming as a routine clinical approach outside of a research protocol. It was questioned (Marchlinski) whether Asian patients may have a higher proportion of right sided foci (including the superior vena cava) compared to other patients based on the higher proportion of right sided foci reported by Lee and Chen. In the University of Pennsylvania, the relative contribution of non-pulmonary vein triggers has been systematically studied (Marchlinski). In this North American population, 15% of patients with paroxysmal atrial fibrillation have been found to have non-pulmonary vein triggers. The proportion of triggers arising from the posterior left atrial wall has declined as the area of myocardium incorporated in more proximal pulmonary vein antrum ablation has increased. AV nodal reentrant tachycardia or AV reentrant tachycardia has been found in 3% of their patients undergoing pulmonary vein isolation for atrial fibrillation. This proportion is up to 5% of their patients with a paroxysmal pattern of atrial fibrillation and as high as 7.5% of women with paroxysmal atrial fibrillation (Marchlinski). In patients with permanent atrial fibrillation, the right atrium and septum are found to be more commonly involved in non-pulmonary vein triggers (Marchlinski). Most non-pulmonary vein triggers predominate in the mitral annulus and coronary sinus, tricuspid annulus (near the coronary sinus ostium), the crista terminalis and Eustachian ridge, the limbus of the fossa ovalis and the superior vena cava (Marchlinski). Other less frequent sites include the ligament of Marshall, the right and left atrial appendage, inferior vena cava, and patients with persistent left superior vena cava. Right atrial ectopic activity may be more frequently encountered in patients with recurrence of atrial fibrillation occurring more than one year after pulmonary vein isolation (Hsieh, Kuck).

Catheter ablation of persistent atrial fibrillation

The patient population amenable to catheter ablation of atrial fibrillation continues to expand. Recently this has included patients with persistent atrial fibrillation and patients with heart failure. At this year’s meeting, Jais presented the results of the current multi-step approach to catheter ablation in patients with persistent atrial fibrillation in Bordeaux. In their current approach, pulmonary vein isolation represents only the first of four steps of their procedure. Their approach involves the systematic incorporation of multiple ablation strategies in patients with persistent atrial fibrillation. Application of their methodical step-wise approach to catheter ablation of persistent atrial fibrillation was demonstrated by Haissaguerre and Jais in a live case demonstration transmitted from the Bordeaux lab.

The background of this development has been disappointing clinical results from conventional pulmonary vein isolation in patients with persistent atrial fibrillation. The recurrence of symptomatic atrial fibrillation and requirement for a repeat catheter ablation procedure is 50% in patients with persistent atrial fibrillation who have undergone conventional pulmonary vein isolation as a stand alone procedure, even when performed at centers with extensive experience such as the Bordeaux lab (Jais). This relatively high rate of a repeat procedure appears to be particularly the case when pulmonary vein isolation is conventionally performed close to the ostium (ostial – antral transition zone) guided by a multielectrode circumferential mapping catheter. In such a conventional approach close to the ostium, isolation of the pulmonary veins can be achieved with significantly less radiofrequency applications than required by wide area encirclements in the left atrium encompassing the ipselateral pulmonary vein antra as well as adjacent left atrium. It is likely that conventional periostial ablation results in less impact on the substrate maintaining atrial fibrillation and less impact on the epicardial neural networks which (particularly the right and left inferior ganglionic plexi) lie at a significant distance from the pulmonary vein ostia.

The relatively poor success rate of conventional pulmonary vein isolation for patients with persistent atrial fibrillation has over recent years given rise to the pursuit of alternative or auxiliary approaches to pulmonary vein isolation. These have included 1) wide area circumferential left atrial ablation, 2) linear ablation connecting anatomical barriers of left atrial conduction (for the impact of such lesions on organization of atrial fibrillation as well as the prevention of atypical left atrial flutters), 3) endocardial ablation at sites rich in epicardial ganglionic plexi (fat pads) as established by the elicitation of a vagal response by high frequency subthreshold stimulation (identified as an abrupt reduction in the rate of AV nodal conduction), and 4) ablation at sites of continuous fractionated electrograms during atrial fibrillation.

While in the initial phase of pulmonary vein isolation, catheter ablation was typically performed after electrical cardioversion, catheter ablation is now routinely performed during atrial fibrillation. This has the advantage of being able to observe any organizational impact of ablation lesions on the level of organization of atrial fibrillation and emergence of atrial flutters, as well as identify sites of complex fractionated atrial electrograms (Nademanee).

In the live case demonstration from Bordeaux, in a patient with persistent atrial fibrillation of one year duration, catheter ablation was first performed to achieve pulmonary vein isolation. Subsequent lesion subsets included linear ablation across the left atrial dome, ablation along the right and left inferior ganglionic plexi above the mitral annulus and including in the coronary sinus, ablation at the orifice of the left atrial appendage, and posterolateral mitral isthmus ablation. Following each step the mean cycle length duration is measured of the electrograms in the right and left atrium and coronary sinus. With each step, prolongation of 8 to 16ms in atrial cycle length was observed. In addition to slowing of atrial cycle length, a progressive regularization of atrial activity could be seen.  Linear ablation of the posterolateral mitral isthmus presents a significant challenge as it is prone to creation of a persistent gap which may on occasion be proarrhythmic with emergence of an incessant mitral isthmus flutter (Wharton). And during the ablation itself, it may also be vulnerable to perforation or other complication as it is known to be as thin as 1.5mm in depth; while not definitively known, it is true that these complications may be more likely to occur when an irrigated RF catheter is used.

One significant limiting factor to the widespread adoption of this multi-step approach to catheter ablation in a single setting for patients with persistent atrial fibrillation is the time involved. While conventional pulmonary isolation can be achieved in most high volume centers in less than three hours of laboratory time, the addition of this stepwise approach for patients with persistent atrial fibrillation in the experienced hands at the Bordeaux lab, brought the procedure time to over 260 minutes and a fluoroscopy time of over 80 minutes. Such procedural durations may be more easily adopted in countries with direct government funded healthcare without pressure generated by volume (direct case) based reimbursement (Kalbfleisch). The introduction of advanced but expensive 3-dimensional imaging and navigation systems with either remote or direct manually guided ablation may reduce radiation exposure to patients and operators. However, the total procedure duration may still significantly reduce the income for an active laboratory and have to be run as a loss leader unless reimbursement rates are adjusted for complex ablation procedures.

An alternative strategy to adoption of a systematic methodical approach to catheter ablation is one of a tailored approach to each patient (as presented by Morady for a group of mostly, but not exclusively, paroxysmal AF patients). In such an approach, ablation in each patient is based on electrogram patterns and findings at the time of the procedure. It is proposed that such an approach minimizes the requirement for ablation on the posterior left atrial wall to minimize the risk of atrio-esophageal fistula (Morady). The relative merits of a systematic versus individualized approach will hopefully be compared in a randomized study in due course.

Atrial remodeling post catheter ablation

In contrast to early ablation strategies of catheter maze procedures, pulmonary vein isolation appears to have a consistently favorable impact on atrial remodeling with marked reduction in atrial dimensions (Wilbur). The mechanisms for such a reduction include (i) reverse remodeling associated with resumption of sinus rhythm, and (ii) direct effects on the atrium as well as a possible indirect impact on ventricular function. Some studies have shown an early reduction in left atrial dimensions irrespective of outcome and thus make additional contributory mechanisms beyond remodeling likely. Such potential mechanisms may include the acute procedural impact of ablation of a significant portion of atrial myocardium, and post ablation contraction fibrosis. Reduction in left atrial volumes are observed acutely on 3-dimensional mapping post ablation (Pappone) and longer term benefits on left atrial dimensions (and in some studies ventricular dimensions) have been documented on serial echocardiographic and MRI studies (Calkins and Marchlinski). In the recently completed randomized trial by Oral and Pap pone of catheter ablation described above, maintenance of sinus rhythm was associated with a reduction in left atrial dimension and improvement in left ventricular ejection fraction. The findings of such studies suggest that patients with significant left atrial dilatation should not be excluded from undergoing pulmonary vein isolation. It should be recognized that some studies have indicated that despite improvement in left atrial dimensions, left atrial contractile and reservoir functions do not normalize. It is felt that the extent of recovery of left atrial function relates to the duration of persistent atrial fibrillation pre-ablation.

Atrial Fibrosis

In addition to the finding of large left atrial dimension (>6 – 7cm), an intraprocedural finding of extensive left atrial fibrosis (in particular a large area of low voltage in the posterior wall) appears to be associated with a higher recurrence of atrial fibrillation or emergence of left atrial flutters post ablation (Natale). Thus far, neither 1.5 Tesla MRI nor 64-slice CT scanning appear reliable in detecting atrial fibrosis pre-procedure, and there appears to be few clinical predictors of the finding other than a history of mitral stenosis, rheumatic fever, and a long-standing history of atrial fibrillation.

Recovery of pulmonary vein conduction in patients with recurrence of atrial fibrillation after pulmonary vein isolation

In the experience at Hamburg, in a high proportion of patients who are brought back to the electrophysiology laboratory for recurrence of atrial fibrillation after pulmonary vein isolation, recovery of conduction from the PV’s is recorded. This is interpreted by many that such a finding indicates that the mechanism of recurrent atrial fibrillation is directly linked to the recovery of conduction from the pulmonary veins (Kuck). In a study at the Cleveland Clinic of patients with and of patients without recurrence of atrial fibrillation post ablation, a correlation was found between the extent of conduction delay from the pulmonary veins and freedom of atrial fibrillation recurrence (Natale). On the other hand, other published studies have shown that the success of catheter ablation is not dependent on the endpoint of isolation. In particular, publications from centers known to perform wide area circumferential ablation in the manner described by Pappone have found no correlation between the achievement of isolation at the time of procedure and subsequent freedom of atrial fibrillation recurrence. The reasons for this apparent contradiction of findings may relate to the extent of impact on ganglionic plexi at different centers and possibly extent of applications made within the antra and direct elimination of important activity within the encircled area.

The timing (many months) of late recurrences of atrial fibrillation in some patients after pulmonary vein isolation and the finding of recovery of conduction from pulmonary veins in such patients suggest that a significant interval of time should be allowed to pass before patients are returned to the electrophysiology laboratory for a repeat procedure (Jais). It should be acknowledged, however, that it is unknown if the mechanism of late recurrence of atrial fibrillation post pulmonary vein isolation relates to the recovery of conduction from the pulmonary veins (which could occur early post ablation) or to the regeneration of neuronal connections in the epicardium (which may take longer than myocardium to regenerate).

The endpoint of non-inducibility of sustained atrial fibrillation is adopted at some centers for patients with paroxysmal atrial fibrillation, particularly at centers who proceed to ablation at sites of complex fractionated atrial electrograms after achieving pulmonary vein isolation. This endpoint becomes more difficult to achieve in patients with persistent rather than paroxysmal atrial fibrillation, and appears most difficult to achieve in patients with long-standing permanent atrial fibrillation (a term which is rapidly becoming obsolete as catheter ablation techniques are applied more widely).

Balloon based catheter technologies

One measure to reduce procedure duration may be the introduction of circumferential ablation tools including balloon and coil based ablation platforms. Three balloon based ablation techniques are now in clinical trials in North America and Europe. These include cryothermy, ultrasound, and laser ablation. The efficacy of cryoablation in effectively achieving isolation of the pulmonary vein antra was demonstrated in a live case demonstration from the Massachusetts General Hospital (Reddy) in a patient with paroxysmal atrial fibrillation. After confirming electrical PV isolation using a Lasso catheter, electroanatomical voltage mapping was performed atop a registered 3D MRI image to assess the location of the electrical isolation in relation to the PV ostia and antra. These pre- and post- cryoballoon ablation voltage amplitude maps from the live case can be seen in Figure 2. One advantage of the cryoballoon is that even if there is recovery of conduction at some points, the ablation of most of the area within the antrum in addition to a ring of myocardium should lessen the likelihood of atrial fibrillation recurrence.

Phrenic nerve injury and esophageal injury are still a concern with the balloon based systems. None of the currently available balloon based systems have the facility to pace from the point of ablation on the balloon surface and thus continuous phrenic nerve pacing at a high level within the superior vena cava may represent a more reliable approach to reduce the risk of phrenic nerve injury (Packer). The intensity of pain felt by patients undergoing ultrasound balloon ablation would suggest that significant pericardial heating may occur with these techniques. While cryothermal balloon ablation may not be associated with pain, it remains to be seen if recovery of conduction from the pulmonary veins will be as low as that associated with the thermal techniques.

While these various balloon strategies may reduce procedure time, the currently available prototypes require transseptal punctures with an outer sheath size of 14 to 20 French. Adoption of a balloon based platform does not eliminate the risk of phrenic nerve or esophageal injury. And for systems which require full circumferential ablation at each application, touch-up applications with such balloons become less attractive. The requirement for the pulmonary vein antrum to conform to the circular balloon shape rather than compliance of the balloon to the elliptical configuration of pulmonary vein orifices (with an aspect ratio of 1.5) remains a limitation.

While these various balloon strategies may reduce procedure time, the currently available prototypes require transseptal punctures with an outer sheath size of 14 to 20 French. Adoption of a balloon based platform does not eliminate the risk of phrenic nerve or esophageal injury. And for systems which require full circumferential ablation at each application, touch-up applications with such balloons become less attractive. The requirement for the pulmonary vein antrum to conform to the circular balloon shape rather than compliance of the balloon to the elliptical configuration of pulmonary vein orifices (with an aspect ratio of 1.5) remains a limitation.

MRI integration and robotic navigation

The value of pre-procedural MR imaging to provide a roadmap for catheter ablation of atrial fibrillation is well recognized (Mansour). More recently colorized 3-dimensional impedance mapping has been found to provide reliable definition of the pulmonary vein antrum (Pappone). As a catheter is advanced towards the pulmonary vein the impedance rises and this feature may add to an anatomical based map (Pappone). The integration of a previously acquired MRI or CT 3-dimensional data set into catheter navigational/guidance systems provides supplemental information to the operator (Reddy). Limits with this approach include, that if the process of registration is flawed or an off-set is introduced, then misinformation rather than more information is provided.

While multislice CT may currently provide higher resolution imaging of atrial anatomy than MRI, radiation exposure is of concern.

Currently the acquisition of a pre-procedural 54-slice CT scan of the cardiac and pulmonary vein anatomy exposes the patient to a significant amount of radiation equivalent of 250 chest x-ray examinations and thus MRI studies (particularly if they need to be repeated) offers significant less concern for the long-term safety of the patient. Furthermore, while real-time MRI guidance is a realistic option within a ten year period and has already been validated in pre-clinical studies at Johns Hopkins University (Calkins), real time CT scanning (at least with currently-available technology) would likely involve a prohibitive degree of radiation exposure to the patient.

The most widely available system of robotic navigation for catheter ablation uses an adjustable external magnetic field to control the position and angulation of an intracardiac electrode at the end of a flexible and floppy catheter shaft. The force applied to the electrode tip is small and thus it is anticipated that the risk of cardiac perforation will be reduced compared to manually guided steerable catheters. At one center, over 150 patients have undergone catheter ablation of atrial fibrillation by robotic navigation without any reported complications (Pappone).

Another robotic navigation approach utilizes a steerable two-piece sheath with direct mechanical external controls of this system. Any standard ablation catheter may be fixed just protruding from the tip of this sheath system, so that when the operator manipulates a 3D joystick and the software interface, he or she is in effect manipulating the tip of the ablation catheter itself. In addition to catheter ablation for atrial fibrillation, this robotic navigation system has also been used to perform transseptal puncture and coronary sinus­ based epicardial catheter ablation (Reddy).

Remote magnetic or robotic navigation for catheter ablation offers the potential to: 1) have a predetermined lesion set applied to a patient’s atrium which may be less dependent on the experience of the local operator, and 2) reduce operator radiation exposure (Pappone). Performance of robotically navigated ablation from a remote international site is likely to be met with reluctance from third party payers and the insurance industry. In addition, if these system are able to live up to their promise of rendering these procedures safe, effective and quick for even minimally-experienced operators, the need for utilizing a remote international site is unclear.

Surgical developments

The key emphasis of surgical developments remains concentrated on video-assisted thoracoscopic epicardial pulmonary vein isolation with customized circumferential microwave, ultrasound, and bipolar radiofrequency ablation techniques (Kress). This allows the patient to avoid a sternotomy and instead leaves the patient with a number of port access incisions (Kress). An advantage of a thoracoscopic approach is that it allows direct study ± ablation of ganglionic plexi in the epicardial fat pads (Jackman). A disadvantage is that it does not lend itself well to the recording or ablation of many endocardial sites including the septum.

Regulatory Requirements

One challenge recognized at the meeting from a regulatory approval perspective was that if a tool is developed to effectively isolate the pulmonary veins, it may not necessarily translate into clinically meaningful elimination of atrial fibrillation. Thus, obtaining FDA approval for a custom stand alone pulmonary vein isolation device may be more challenging as demonstration of pulmonary vein isolation as a stand alone procedural endpoint is not unacceptable to the FDA. This stance may make it challenging for industry developing a stand alone pulmonary vein isolation device to obtain an indication for patients with persistent atrial fibrillation unless packaged with a secondary ablation system in IDE trials.

Complications

Phrenic nerve palsy continues to be a concern particularly for balloon based pulmonary vein isolation techniques. In physically active patients this complication can give rise to significant symptoms of dyspnea on exertion. Fortunately, there is a high rate of spontaneous recovery of nerve conduction within a three to six month period post ablation injury.

Left atrial appendage isolation is a recently recognized but very rare complication (Jais). This can occur as a complication of systematic ablation at the orifice of the appendage in patients with persistent atrial fibrillation and the risk of this complication should be minimized by leaving an adequate arc anteriorly at the orifice without ablation (Jais). The thromboembolic stroke potential of such a complication is as yet unknown.

While the complication of clinically significant pulmonary vein stenosis has decreased significantly in frequency with the progressive proximal withdrawal of the ablation zone from the pulmonary vein ostium back into the left atrium, the complication of atrio-esophageal fistula continued to be a theme of major interest at this year’s meeting. Esophageal fistula formation continues to occur and along with thromboembolic stroke, are the complications of greatest concern. It is now estimated that atrio-esophageal fistula may have occurred in over fifty patients world-wide. The precise incidence of this complication will remain difficult to determine in the absence of a systematic international registry. Because of the relatively low incidence of this clinically significant complication, much debate exists over intraprocedural factors involved in its genesis.

Steps hypothesized at this year’s meeting to minimize the risk of this complication include minimizing perpendicular electrode orientation in the posterior left atrial wall, additional caution if an 8mm electrode is utilized, maintaining a peak power setting of < 31 Watts in the posterior left atrial wall when an irrigated electrode is used, and keeping the duration of radiofrequency applications to less than 20 seconds in the posterior left atrial wall. In Milan, where almost 10,000 cases have now been performed with a technique of moving the ablating electrode at least every 15 seconds, only 1 case of atrio-esophageal perforation has occurred (Pappone). It has been shown in a thigh muscle canine preparation in vivo that at a fixed power of 30 Watts with fixed contact pressure and perpendicular electrode orientation, that the lesion size produced by a non-irrigated electrode is just as large as that of an irrigated electrode (Nakagawa). However, by virtue of reliable temperature control with a non-irrigated 4mm electrode, it is likely that a power controlled irrigated 3.5mm electrode will produce a deeper lesion in vivo. In addition, the thromboembolic potential of irrigated electrodes is now universally accepted to be significantly lower.

The use of esophageal radiographic paste was also brought into question, where it may have contributed to the development of adult respiratory distress syndrome in one patient who aspirated during the procedure (Calkins). Furthermore, it has been suggested that esophageal motility during the catheter ablation procedure may potentially be increased by esophageal radiographic paste.

At some centers, an esophageal temperature probe is used routinely during PVI procedures. While the probe may have the added advantage of providing a radiographic marker for one point in the esophageal lumen, caution has been raised about any potential mechanical impact of the probe on the esophageal wall. Cases of atrio-esophageal fistula have occurred despite the use of an esophageal thermometer probe and it would seem that while the detection of an intraluminal esophageal temperature rise may offer a useful positive feedback for interruption of power delivery at that site in the posterior left atrium, the absence of a such a temperature rise does not provide a high-enough negative predictive value (d’Avila).

Upon the clinical suspicion of atrio-esophageal fistula within a week or two of catheter ablation, urgent action may be required to avoid a fatal outcome. This may involve an urgent imaging study to confirm the diagnosis and emergent surgical repair when clinically appropriate. Caution has been raised over the use of esophagoscopy in this setting if inflation of air into the esophagus is utilized as this may potentially precipitate fatal air embolization (Marchlinski).

While the natural history of atrio-esophageal fistula conveys a high fatality risk and emergent surgical repair may offer one of the most effective management strategies it should be borne in mind that our knowledge of this complication is still in its infancy and much remains to be learnt from registries as well as individual case reports. In one case, esophageal perforation in the absence of atrio-esophageal fistula was managed successfully in a conservative non-surgical manner (Calkins). Thus, each case should be taken on its own clinical considerations and ideally should involve a joint medical and surgical decision.

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Conclusion

Over the last year, the most significant development with implications for a large population of patients was the adoption of a systematic multi-step approach to patients with persistent atrial fibrillation pioneered by the Bordeaux group. This methodical approach currently involves prolonged procedure and fluoroscopy time and patients need to be prepared to undergo a repeat procedure when required. Ultimately with perhaps the further adoption and evolution of non-fluoroscopic guidance techniques, the procedure may become less time consuming, more automated, safer, less dependent on operator experience, and have a lower requirement for repeat procedures.
Despite the known limited efficacy and potential risks of currently available antiarrhythmic drugs, drug therapy remains the first line therapeutic option for patients with symptomatic recurrent atrial fibrillation. The role of catheter ablation continues to evolve, however, and may occasionally be considered as a first line option in special instances. It is likely that the debate on catheter ablation as first line therapy for atrial fibrillation will appear periodically at the Annual Boston Atrial Fibrillation Symposium (see www.afsymposium.com).

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Return to AF Symposiums by Year

Return to Index of Articles: AF Symposium: Steve’s Summary Reports

Last updated: Friday, August 28, 2015

References    (↵ returns to text)
  1. Atrio-esophageal fistula, thus far reported only after circumferential pulmonary vein ablations, may be related to the more extensive ablation lesions applied to the posterior left atrium.” Prystowsky, “AF Ablation as First-Line Therapy.” Circulation 2005;112:1214-1231, p. 1227.
  2. Atrio-esophageal fistula, thus far reported only after circumferential pulmonary vein ablations, may be related to the more extensive ablation lesions applied to the posterior left atrium.” Prystowsky, “AF Ablation as First-Line Therapy.” Circulation 2005;112:1214-1231, p. 1227.
  3. Ritchie, James “UC doctor rebuked for not divulging financial tie to ArtiCure.” Cincinnati Business Courier, December 28, 2005, http://cincinnati.bizjournals.com/cincinnati/stories/2005/12/26/daily12.html.  And Armstrong, David “Surgery Journal Threatens Ban For Authors’ Hidden Conflicts.” The Wall Street Journal, December 28, 2005.
  4. James L. Cox, “The Role of Surgical Intervention in the Management of Atrial Fibrillation,” Texas Heart Institute Journal, 2004; 31 (3): 257-265.
  5. Garcia-Fernandez, Journal of American College of Cardiology 42:1253-8, 2003
  6. Keane, David. “Emerging Concepts on Catheter Ablation of Atrial Fibrillation from the Tenth Annual Boston Atrial Fibrillation Symposium.” J Cardiovasc Electrophysiol. Vol. 16.pp.1025-1028, September 2005.
  7. Fuster, “ACC/AHA/ESC guidelines for the management of patients with atrial fibrillation.” J Am Coll Cardiol 1002;38:1231-1266.
    van Walraven, “Oral anticoagulants vs aspirin in nonvalvular atrial fibrillation.” JAMA 2002;288:2441-2448″
  8. Hylek, “Risk factors for intracranial hemorrhage in outpatients taking warfarin.” Ann Intern Med 1994 120:897-902.

Boston AF Symposium – 2003

Boston AF Symposium, JANUARY 17-18, 2003

The annual international Boston A-Fib Symposium is one of the -most important conferences on A-Fib in the world. It brings together researchers and doctors who share the latest information. Unlike other heart related conferences, it concentrates only on A-Fib. But if you haven’t read and understood most of A-Fib.com, it may be difficult reading.

Each presentation is listed by both the last name and by the topic of the presenter. If a doctor made more than one presentation, they are listed as (1) and (2). You can access a presentation either by the doctor’s name or by the topic. (All presentations are not summarized.)

TOPIC DOCTOR
New medications for A-Fib Allissie
Current minimally invasive and robotic surgical techniques for A-Fib Argenziano
The development of MRI 3-D imaging for PVIs Calkins
Right Atrial Linear Ablation in right atrium dominant A-Fib Chen
RACE study (Rate Control vs. Electrical Cardioversion for Persistent A-Fib) Crijns (1)
Rate Control vs. Rhythm (Antiarrhythmic Drug) Control for Persistent A-Fib Crijns (2)
Genetic predictors of A-Fib Ellinor
Stroke prevention in A-Fib Ezekowitz
The Bordeaux group’s current Pulmonary Vein Isolation techniques Jaïs (1)
Comparing antiarrhythmic drug therapy to Pulmonary Vein Isolation Jaïs (2)
Optical mapping of A-Fib Jalife
Bi-atrial non-contact mapping reveals three types of A-Fib activation Lemery
Examination of the cellular activity of the Pulmonary Veins compared to other areas of the left atrium Nattel (1)
Using drugs to counteract atrial remodeling in A-Fib Nattel (2)
Optical mapping of A-Fib reveals inflamed cells due to fibrosis and inflammation Olgin
The PVI procedure currently in use in Milan called “anatomically based circumferential PV ablation” Pappone
Guidelines for Drug Use in A-Fib. New Antiarrhythmic Drugs in Development—Azimilide. Prystowsky
Rate & Rhythm Control (Antiarrhythmic Drugs). The AFFIRM Study. Wyse

 

DR. HARRY J. CRIJNS, UNIVERSITY HOSPITALS OF GRONINGEN AND MAASTRICHT, THE NETHERLANDS

Dr. Crijns discussed the results from the RACE study (Rate Control Versus Electrical Cardioversion for Persistent Atrial Fibrillation).

In this study of patients with Persistent A-Fib, one randomized group received oral anticoagulants and rate control drugs; the other received oral anticoagulants, Electrical Cardioversion and antiarrhythmic drugs ( first attempt, sotalol; second attempt, flecainide or propafenone; third attempt, amiodarone.) Electrical Cardioversion, rather than antiarrhythmic drugs, was used to restore patients to sinus rhythm; while the antiarrhythmic drugs were used to maintain patients in sinus rhythm. Serious problems (“primary end points”) such as heart failure, stroke, etc. were approximately the same with the exception of severe antiarrhythmic side effects (0.8% vs. 4.5%). 39% of the antiarrhythmic group was in sinus rhythm versus 11% of the rate control group. (This was not a randomized study to compare rate control and/or antiarrhythmic drugs to placebos.)

A subgroup analysis of patients with hypertension revealed more serious problems (primary end points) in the antiarrhythmic group, while those with normal blood pressure had fewer problems. “Hypertension may be associated with increased risk of the primary endpoint” in patients taking antiarrhythmic drugs.

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DR. HUGH CALKINS, JOHNS HOPKINS SCHOOL OF MEDICINE, BALTIMORE, MARYLAND

Dr. Calkins described experimental developments using MRI (Magnetic Resonant Imaging) to produce live 3-D images of the heart during catheter ablation procedures. Current practice uses Fluoroscopy, a form of X-ray, to produce 2-D images of the heart. Fluoroscopy over time can expose both patients and staff to significant radiation.

“Stereotactic Ablation with MRI/CT Guidance” consists of:
a) A miniature passive magnetic field sensor in the ablation catheter
b) An external ultralow magnetic field emitter (location pad)
c) A processing unit containing the three dimensional MR images.

The location pad is placed under the subject. Three electromagnetic coils in the location pad each generate ultralow magnetic fields. Three orthogonal antennae in the tip of the ablation catheter identify its position and orientation in space in relation to these magnetic fields. These antennae also display the catheter’s position on the 3D-MR images in real time. In this experiment Fluoroscopy was used to confirm the catheter’s position.

In the structural and animal models used in this experiment, the MR imaging was very accurate and precise.  This study demonstrated that it is now possible to combine an electromagnetic navigation system with true live 3-D MR images.

(Author’s Note: This could be a very important development for A-Fib. Patients and staff using this system would be exposed to less X-ray radiation. Doctors seeing live, real time 3-D images of the heart could more easily and effectively perform catheter ablations.)

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DR. CARLO PAPPONE, SAN RAFFAELE UNIVERSITY HOSPITAL, MILAN, ITALY

Dr. Pappone described the PVI technique used in Milan called “anatomically based circumferential PV ablation.” Circumferential lesion lines are made around the ostia (opening) of each Pulmonary Vein to isolate these veins from the left atrium while reducing the risk of PV stenosis (swelling). The circumferential lines are made at a distance of more than 5 mm from each PV ostia.

Dr. Pappone’s success rate for patients monitored over a three year period was 87%. He had approximately equal success with both Paroxysmal (occasional) and Chronic (all the time) A-Fib. A typical procedure took only forty minutes.

In what he termed “electroanatomical remodeling” Dr. Pappone found that successful circumferential PV ablation significantly reduced left atrial size and improved its transport function (how well the heart pumps out blood) over a three year monitoring period.

(Author’s Note: This is one of the first  significant findings about the long term effects of PVIs. For those of us suffering from A-Fib, it’s welcome news that some of the bad remodeling effects of A-Fib can perhaps be reversed by a successful PVI.)

Dr. Jaïs from the Bordeaux group and other doctors said that they have not been able to replicate Dr. Pappone’s  results in their facilities.

(Author’s Note: The fact that other doctors to date have not been able to replicate Dr. Pappone’s work does not call into question his work and results. Dr. Pappone may have developed a unique combination of equipment, facilities, techniques and personal skills that may not translate easily to other environments.)

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DR. SHIH-ANN CHEN, TAIPEI VETERANS’ HOSPITAL, TAIPEI, TAIWAN

Dr. Chen discussed using right atrial linear ablation to cure Right Atrium dominant A-Fib. (Patients with focal and Pulmonary Vein A-Fib are not candidates for Right Atrium ablation.) Simply making linear lesions to compartmentalize the Right Atrium isn’t very effective.

Using noncontact mapping, Dr. Chen found that A-Fib reentry circuits go through the low right atrium isthmus and through the crista terminalis gap between low voltage zones. Dr. Chen makes short lesion lines (1-4 cm) in these areas to successfully eliminate right atrium A-Fib in 80% of patients.

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DR. MICHAEL ARGENZIANO, COLUMBIA-PRESBYTERIAN MEDICAL CENTER, NEW YOUR, NY

Dr. Argenziano described minimally invasive and robotic surgery for A-Fib.

The standard Maze operation, though successful in a high percentage of cases, is invasive. It involves breaking through the sternum, cardiopulmonary bypass, stopping the heart from beating, cutting the heart into sections, and/or making multiple incisions. This open heart surgery is traumatic for the patient and can have complications.

Dr. Argenziano’s surgical approach starts by cutting into the left atrium near the right pulmonary veins to perform pulmonary vein isolation, usually in patients having other cardiac operations. He makes an encircling lesion around the four pulmonary vein openings, and makes another lesion from the encircling lesion to the mitral annulus. He then either amputates the left atrial appendage or makes a circular burn at the base of the appendage to isolate it. He adds a connecting line from the pulmonary vein isolating line to the appendage isolation line. This ablation rarely adds more than 20 minutes to the main cardiac operation. He uses RF, microwave, ultrasound, or laser energy to make the lesions. His success rates approach 80%.

Though the majority of these operations are performed along with other heart operations, he also uses this procedure for patients who only have A-Fib and no other heart problems. He gains access to the heart through a 6 cm incision in the chest. This procedure can be done while the heart is still beating. He also uses robotics to perform the procedure.

(Author’s Note: A person using robotics looks like someone playing video games, only dressed in white. It’s remarkable how this surgical approach is becoming similar to and converging with the PVI procedure.)

In patients undergoing a right atrial operation and in those with a history of atrial flutter (“in whom right-sided initiating foci are common”), he makes a longitudinal incision in the right atrium and a RF lesion from the bottom of this incision to the tricuspid annulus.

After the operation, 69% of his patients experience at least one episode of A-Fib, probably due to the time it takes for the lesions and scars to heal and achieve complete electrical isolation. To keep patients in sinus rhythm, he administers amiodarone in the operating room, followed by a 24-hour intravenous drip and 6 weeks of low-dose oral therapy. He also administers three months of anticoagulation for all patients, whether they are in sinus rhythm or not.

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DR. PIERRE JAÏS, CENTRAL HOSPITAL UNIVERSITY OF BORDEAUX, FRANCE

Dr. Jaïs described how the Bordeaux group’s current Pulmonary Vein Isolation techniques are achieving success rates of 82% in curing patients with Paroxysmal (occasional) or Persistent A-Fib. (Success is measured if a patient is in sinus rhythm without taking any antiarrhythmic medications six months after a PVI.) An even higher success rate of 91% is achieved when including patients who are in sinus rhythm while still using antiarrhythmic drugs.

In a PVI the four myocardial sleeves extending into the Pulmonary Veins are ablated (“disconnected”). But A-Fib often returns due to “non PV foci” (other areas of the heart besides the Pulmonary Veins that produce A-Fib signals) or due to “recurrence of initial PVI” (areas of the heart that were ablated but for some reason start producing A-Fib signals again). These areas or foci are often difficult to identify, localize and ablate.
To block these non PV foci, the Bordeaux group then makes a linear lesion connecting the lateral mitral annulus to the ostium (opening) of the left inferior Pulmonary Vein. This is called a “mitral isthmus ablation.” This linear lesion blocks these A-Fib signals from spreading to the rest of the heart.

Coronary Sinus mapping and ablation are used to verify the completeness of the linear lesion and to correct any gaps.  “…ablation through the Coronary Sinus is often crucial to achieve mitral isthmus block.”

The Bordeaux group has found that 50% of patients with Chronic (all the time) A-Fib need at least two procedures to be cured of their A-Fib.

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DR. PIERRE JAÏS, CENTRAL HOSPITAL UNIVERSITY OF BORDEAUX, FRANCE

Dr. Jaïs in his second presentation described a study now being conducted to compare antiarrhythmic drug therapy with catheter ablation for A-Fib.

Patients with Paroxysmal (occasional) A-Fib will be randomized into two groups, one treated with antiarrhythmic drugs (flecainide, propafenone, quinidine, dofetilide, amiodarone and/or sotalol), the other with radiofrequency catheter ablation (PVI and left atrial linear lesions). Patients will be treated at multiple centers and monitored for a period of one year. Mapping will be used to identify and ablate specific areas of the heart producing A-Fib signals (Segmental Ablation). Up to three ablation procedures of medical treatments using drugs can be performed. Linear lesions will be performed if needed as judged by the doctor.

The principal objective is to compare how often A-Fib reoccurs in the two groups. The study will also examine the two group’s quality of life, the effectiveness of amiodarone in particular, the secondary effects of both approaches, the rate of withdrawal from oral anticoagulants, and in cases of failed ablations whether previously ineffective drugs work to keep patients in sinus rhythm.

Patients must be in Paroxysmal A-Fib for at least six months and resistant to at least 2 antiarrhythmic drugs of different classes. (Author’s note: these are the criteria used by many centers today before performing a PVI.)

Patients will be treated by antiarrhythmic drugs or by radiofrequency ablation for 90 days.  In cases of ablation treatment failure, doctors can switch to antiarrhythmic drugs after 90 days. In cases of drug treatment failure, doctors can switch to ablation after 90 to 180 days. Patients will be monitored for a year.

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DR. STANLEY NATTEL, INSTITUTE OF CARDIOLOGY OF MONTREAL, CANADA

Dr. Nattel’s second presentation discussed using drugs to counteract atrial remodeling from A-Fib.

One type of remodeling is Atrial Tachycardia (rapid heart rate), the mechanism by which “A-Fib begets A-Fib.” It appears to be initiated by Calcium Channel current overload (Ca²+) and usually involves a lack of regulation or control of L-type Ca²+-current. (“L” stands for Long Lasting or High Voltage Activation which is the main pathway for Calcium Channel current in the heart.) Dr. Nattel indicated that genetic reprogramming may be involved in long-term (days) remodeling.

A second type of remodeling is caused by CHF (Congestive Heart Failure) and involves structural remodeling in the form of atrial fibrosis, and ionic (chemical) remodeling where increased Sodium and Calcium Channel currents (Na+, Ca²+) trigger A-Fib.

There are different types and mechanisms of remodeling which respond differently to treatment. Drugs with T-type Ca²+ channel blocking action, like mibefradil and amiodarone, do seem to prevent Atrial Tachycardia remodeling (“T” stands for Transient or Low Voltage Activation Calcium Channel current), though clinical studies are somewhat contradictory. But with regards to structural remodeling, “atrial fibrosis, once established, may be largely irreversible.”

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DR. GEORGE WYSE, UNIVERSITY OF CALGARY, CANADA

Dr. Wyse discussed the AFFIRM (Atrial Fibrillation Follow-Up Investigation of Rhythm Management) trial which enrolled 4,060 patients in Canada and the US. Patients had to be over 65 or at high risk of stroke. Patients were randomized to rhythm or rate control groups. Doctors could choose from drugs on a list of drugs approved for use in A-Fib. (AFFIRM and other future studies will help identify which particular drugs were effective.) Doctors were encouraged to keep all patients on anticoagulation. The study looked primarily at mortality, how many patients died in each group. Most patients with A-Fib were Persistent (needs cardioversion), but some (around 20%) were Paroxysmal (starts and stops by itself).

There was no significant difference in deaths between the rate and rhythm control groups, though there were more deaths in the rhythm group. There were more hospitalizations and adverse drug effects in the rhythm control group. The authors concluded that “the advantages of rate control in such patients has been under-appreciated.” In fact “rate control may be preferred in some patients.” “Rate control should more frequently be considered as a primary therapy…in patients such as those enrolled in AFFIRM.” “…rate control is at least as good as rhythm control, and has some potential advantages.”

Most of the strokes occurred in patients who either stopped warfarin or had an INR below 2.0. There was no significant difference in strokes between either group. (Patients in the rhythm control group could be taken off of warfarin after 1, but preferably 3, months of continuous sinus rhythm. Only 70% of the rhythm group were on warfarin therapy, compared to 85-95% of the rate control group.) The rate of intercerebral bleeding was 0.3%.

One important conclusion of the AFFIRM trial was that, “anticoagulation should not be stopped when the patient is in sinus rhythm, because…the majority of strokes occurred when the warfarin was stopped or subtherapeutic.

“Quality of life and functional capacity shows no differences between the two treatment (groups).” Only a small number of patients (<5%) received non-drug therapies such as a PVA.

One important figure was the high number of patients in the rate control group who were in sinus rhythm.

(Author’s notes: Newer antiarrhythmic drugs such as dofetilide (Tikosyn) were probably not a part of this study.

Not all antiarrhythmic (rhythm control) drugs are created equal. They work differently and have different success rates. Also, individuals often react differently to medications. A drug that may be ineffective and even toxic to one person may be beneficial to another.

From a patient’s perspective, most people in A-Fib want to be in sinus rhythm. A rate control therapy that keeps the heart from racing too fast but that doesn’t stop the A-Fib, probably isn’t an option that most people in A-Fib would be happy with unless there were no other options.

Since the A-Fib patients in this study were older (over 65) or at high risk of stroke, the lack of significant difference in death between the rate and rhythm control groups could be attributed to the patients’ age and  overall state of health rather than to the use of rate or rhythm control drugs. In other words, older patients in poor health might have died irrespective of whether they were using rate or rhythm control drugs. However, the increase in hospitalizations and adverse drug effects in the rhythm group do indicate that antiarrhythmic drugs are associated with more adverse side effects than rate control drugs.)

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DR. HARRY J. G. M. CRIJNS, ACADEMISH ZIEKENHUIS MAASTRICHT, NETHERLANDS

Dr. Crijns and his associates compared rate control to rhythm control drug therapy in patients with Persistent (lasting 24 hours or longer) A-Fib. In the rate control group patients received digitalis, and/or a calcium-channel blocker and/or a beta-blocker. In the rhythm control group patients received sotalol. If sotalol didn’t work, then flecainide or propafenone was tried, then amiodarone. Electrocardioversion was used in the rhythm control group to restore sinus rhythm. All patients received anticoagulant (blood thinning) drugs.

Looking only at whether rhythm or rate control prevented death or serious heart problems, “Rate control is not inferior to rhythm control…and may be appropriate therapy in patients with a recurrence of persistent A-Fib after electrical cardioversion.” The study also examined quality of life issues such as which group felt better, led a more satisfying life, etc. and did not find major differences between the groups.

In patients with persistent A-Fib undergoing repeated electrical cardioversions and taking antiarrhythmic medications, the A-Fib tends to reoccur and the drugs tend to have bad side effects. Despite the electrical cardioversion and rhythm control drug therapy, at the end of the study only 39% of the rhythm control group were in sinus rhythm (as compared to 10% in the rate control group). “Obviously, safer and more effective methods of maintaining sinus rhythm are needed, and such methods may help reduce morbidity in the future.” Since in this study antiarrhythmic drugs and electrical cardioversion didn’t succeed in keeping patients in sinus rhythm, future rhythm control drugs that work better may get better results than rate control drugs.

One very important finding of the Crijns study is that it didn’t seem to matter whether a patient was in sinus rhythm or in A-Fib in terms of the risk of death and serious heart problems. “This finding suggests that the cardiovascular risk is not reduced with rhythm control even when sinus rhythm is maintained.” This may be because effective rate control may also prevent heart failure.

Another important finding of the Crijns study is that patients with risk factors for stroke may have a stroke when anticoagulation therapy is stopped. In this study anticoagulants were stopped after a patient was in sinus rhythm for one month. But six people in this group had strokes, and all but one were in sinus rhythm. This study found that almost all patients with persistent A-Fib had one or more risk factors for stroke. “Therefore, anticoagulant therapy can be stopped only rarely.”

A large number of strokes occurred in both groups, perhaps because so many patients had risk factors for stroke. There was also a smaller amount of bleeding episodes. “Most strokes occurred at an INR below 2.0. Likewise most bleeding episodes occurred at an INR that exceeded. 3.0.” This study stressed how important it is to carefully monitor the anticoagulant levels in patients with A-Fib.

In this study, “the use of antiarrhythmic drugs contributed significantly to the incidence of major cardiac end points in the rhythm-control group but not in the rate control group.” Patients in the rhythm-control had more major heart problems. In this particular study patients on rhythm control who had hypertension or who were female, had a much higher number of “primary end-point events.” But since this research wasn’t designed to study these subgroups, the report only suggested that these subgroups be further studied.

The authors of this study stressed that it only applied to patients with persistent A-Fib, and didn’t necessarily apply to patients with new A-Fib. “Rather than rate control, cardioversion in combination with prophylactic (rhythm control) drugs is one of the first options in such patients.”

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DR. JOSE JALIFE OF SUNY UPSTATE MEDICAL UN., SYRACUSE, NY

The first presentation at the Boston A-Fib Symposium introduced what could be breakthrough concepts for the understanding of A-Fib.

In what Dr. Jalife called “Optical Mapping,” we could actually see how A-Fib signals work in a heart. In a fascinating, very insightful media presentation, you could see the various frequencies swirling around in a sheep’s heart in A-Fib. (I will try to obtain a copy of this video and include it in A-Fib.com as soon as I find the time to learn flash animation.) Each A-Fib frequency was assigned a different color, what Dr. Jalife called dominant frequency maps. In the right atrium the frequencies were all mixed up and colliding with each other (random reentry), but in the left atrium the frequencies moved in a rotor pattern as though they were rotating around a point in the left atrium. Dr. Jalife introduced the term “mother rotor” as his hypothesis for the mechanism of A-Fib. The higher frequencies of A-Fib were in the left atrium, whereas the right atrium had slower frequencies.

Dr. Jalife hypothesized that, at least in some cases, A-Fib in the left atrium comes from high frequency sources (rotors), whereas the right atrium fibrillates because of signals received from the left atrium and at lower frequencies than the left atrium.

The sheep’s heart was pushed into A-Fib by burst pacing and by administering Acetylcholine (ACh), a chemical involved in the transmission of nerve impulses in the body. Dr. Jalife and his colleagues showed how in this sheep’s heart acute A-Fib came from high frequency rotors in the left atrium, while the right atrium fibrillated because of conduction from the left atrium. This is because the left atrium is more affected by ACh than the right atrium. Dr. Jalife hypothesized that the mechanism of chronic A-Fib may be similar to what we saw in this sheep’s heart even in the absence of ACh, because so-called “electrical remodeling” affects the left atrium more than the right.

(Dr. Alexey Zaitsev collaborated with Dr. Jalife. He did the above experiment and generated the data.)

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DR. JEFFREY OLGIN, KRANNERT INSTITUTE OF CARDIOLOGY, INDIANAPOLIS, IN

Dr. Olgin also discussed optical mapping of A-Fib. His emphasis was on the cellular and intercellular level. He showed examples from a dog with chronic Mitral regurgitation (A-Fib is often seen with congestive heart failure, mitral valve disease and hypertension). In the close-ups of A-Fib cell tissue, one could clearly see significant differences in the cells (tissue or myocyte discontinuities or “non-uniform anisotrophy”) and inflamed cells due to fibrosis and inflammation.

In contrast to the classical theory of A-Fib as due to multiple wavelet reentry, Dr. Olgin hypothesized that this chronic A-Fib was due to these cell or tissue differences which slow and disrupt normal conduction patterns in the heart.

(Note: Dr. Olgin is moving to the Un. of California San Francisco June 1, 2003. He will be the Chief of Cardiac Electrophysiology. UCSF will have an A-Fib Center. He has been performing PVA(I)s since 1997 and has done several hundred. Among other initiatives he will study the genetics of A-Fib. He is moving his NIH-funded lab on researching the mechanisms of A-Fib to UCSF and will start an A-Fib research group.)

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DR. MAURITZ ALLESSIE OF THE NETHERLANDS

Dr. Allessie, known for clinically identifying that “A-Fib begets A-Fib,” talked about new medications for A-Fib.

His first visuals showed how easily and quickly a goat’s heart can be remodeled to persistent (Chronic) A-Fib after only one or two weeks of burst pacing (similar to a pacemaker except that signals are generated to produce A-Fib). He showed how certain current class IC drugs like Flecainide actually widen the “excitable gap,” the time period during an ECG heart beat signal when the heart is easily stimulated into A-Fib.

Some class III drugs like Sotalol shorten the “refractory period,” the time period during an ECG heart beat when the heart is not easily stimulated into A-Fib. He also said that Class III drugs lose their efficacy because of electrical remodeling, and don’t work at high A-Fib rates.

He showed his results of an promising experimental “Early Class III” drug produced by Aventis now called AVC 118. It prolongs the refractory period, doesn’t lose its efficacy after remodeling or at high A-Fib rates, and is safe. It can be used to chemically cardiovert someone in A-Fib. (It may be quite some time before this drug is approved for use in the US.)

Despite his reservations about current drugs, Dr. Allessie did say that “(new) Drugs are the only hope we have because of the high number of people in the general population who have A-Fib.”

Answering a question from the audience, Dr. Allessie said Verapamil (a calcium-channel blocker rate control drug) may work to help someone with Paroxysmal (occasional) A-Fib from getting an attack. But, if one is in A-Fib, Verapamil makes it worse, it speeds up the A-Fib rate.

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DR. STANLEY NATTEL, INSTITUTE OF CARDIOLOGY OF MONTREAL, CANADA

Dr, Nattel examined the cellular activity of the Pulmonary Veins as compared to other areas of the left atrium. He looked at the “cardio myocyte sleeve(s)”—an area of heart tissue extending into the Pulmonary Veins. He found that these areas of the Pulmonary Veins differed significantly from other areas of the left atrium in some of their cellular currents and potentials.54 His findings indicate there is a cellular predisposition in the Pulmonary Veins to trigger and perpetuate A-Fib, but “further work is needed to determine the underlying mechanisms of such activity.”

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DR. MICHAEL D. EZEKOWITZ, DREXEL SCHOOL OF MEDICINE, PHILADELPHIA, PA

Discussing stroke prevention for patients with A-Fib, Dr. Ezekowitz said warfarin therapy (INR between 2.0-3.0) reduces the risk of stroke by 68%.

Patients with lone A-Fib under 65 years old “generally do not require any form of (stroke) protection.”

(Author’s Note: There is some disagreement about this age cutoff. Some experts are now advocating 60 as the age cutoff.)

Many patients in this group use aspirin, but there is no evidence that it works. Aspirin at 325mg is sufficient for patients with A-Fib under age 75 without risk factors. However, aspirin was found to be only 2% more effective than a placebo. Patients over age 75 need warfarin therapy.
But the reality in practice is that the elderly are the least likely to be anticoagulated. “…between 15 and 45% of patients are actually anticoagulated.”

Reasons cited for not anticoagulating patients are a fear of bleeding and the difficulty of monitoring patients to keep their INR at the proper levels. But according to Dr. Ezekowitz the actual risk of hemorrhagic stroke is 0.39%. A new generation of anticoagulants in development doesn’t require monitoring and could solve many of the difficulties associated with warfarin therapy. Melegatran is an oral thrombin inhibitor in Phase III trials.

Mechanical alternatives to stroke prevention are in development such as a device to shut off the left atrial appendage so that blood will not pool or clot there (the left atrial Occluder).

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DR. ROBERT LEMERY, OTTAWA HEART INSTITUTE, OTTAWA, CANADA

Dr. Lemery discussed his preliminary studies of “Bi-Atrial Non-Contact Mapping” (mapping both atria by using basket-shaped catheters with 64 electrodes in each atrium to determine how the atria are activated by A-Fib signals). He found three main types of atrial activation.

  1. left atrial drivers cause the right atrium to fibrillate following conduction over interatrial connections,
  2. the right atrium independently sustains A-Fib, even after pulmonary vein isolation (ablation),
  3. both atria fibrillate independently without activation over interatrial connections.

He is currently analyzing how often the different activation patterns occur.

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DR ERIC PRYSTOWSKY, THE CARE GROUP, INDIANAPOLIS, IN

Dr. Prystowsky discussed the ACC/AHA/ESC Guidelines in the Management of Atrial Fibrillation selecting medications for patients primarily on the basis of safety.

1. For patients with minimal or no heart disease, the object is to “minimize organ toxicity,” to select drugs that will not harm the rest of the body such as flecainide, propafenone and sotalol. They can cause “proarrhythmia” (an increase in heart rhythm problems), “but in patients without heart disease this risk is extremely small.”

If these drugs don’t work, then amiodarone and dofetilide can be considered. And “in experienced hands one might choose (Pulmonary Vein) Ablation (Isolation) for a primary cure.”

2. For patients with congestive heart failure, only dofetilide and amiodarone have been demonstrated to be safe in randomized trials.
a. For patients with congestive heart failure and significant lung disease, “I would likely consider dofetilide as my first choice,”
b. For patients who have congestive heart failure and who are “hypokalemic” (have low levels of potassium), he would choose amiodarone.

3. For patients who have coronary artery disease, sotalol is recommended because of its beta blocking and antiarrhythmic effect. Amiodarone and dofetilide combined with a beta blocker can also be used. Propafenone and flecainide aren’t recommended.

4. For patients with hypertension, he recommended propafenone or flecainide.
a. For patients with hypertension and substantial left ventricular “hypertrophy” (increase in size), amiodarone is preferred because it has the least proarrhythmic effect.

Dr. Prystowsky discussed some new antiarrhythmic drugs that might be available soon in the US.

Azimilide is a Potassium Channel Blocker not chemically related to sotalol, amiodarone, or dofetilide, though it is a Class III drug. It prolongs the QT interval and refractoriness (the time during a heart beat when the heart is not easily stimulated into A-Fib). (In an EKG signal the QT interval represents the time the ventricles are pumping and at rest.) Azimilide is absorbed well by the body and can be given as a once-a-day dose. It is effective with A-Fib patients, and is safe for patients who have had a heart attack and whose left ventricles don’t function well.

He also mentioned that digitalis in his opinion is grossly over prescribed, that only 1-2% of A-Fib patients have Vagal A-Fib, that he personally hasn’t prescribed Class 1A drugs as first line therapy in nearly ten years.

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DR. PATRICK ELLINOR, MASSACHUSETTS GENERAL HOSPITAL, BOSTON, MA

Dr. Ellinor has been studying individuals with Lone A-Fib to identify “phenotypic” or genetic predictors for A-Fib. Recently, he and his colleagues have found that many patients with Lone A-Fib appear to have a family history of A-Fib. Using families with inherited A-Fib, they have identified a new genetic locus (or region) for A-Fib, distinct from the Chromosome 10 or KCNQ1 regions.

Dr. Ellinor welcomes individuals with a family history of A-Fib (generally 3 or more members of a family) to participate in the study to identify genes for A-Fib. You can contact him directly to learn more about the study.

Patrick T. Ellinor, MD, PhD
Cardiac Arrhythmia Service
Massachusetts General Hospital
55 Fruit St., GRB 109
Boston, MA 02114
617-726-5067
Fax: 617-726-2155
E-mail: pellinor at partners dot org (Dr. Ellinor’s E-mail address is spelled out to prevent automatic search engines from flooding him with advertisements.)

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Last updated: Sunday, February 15, 2015

Boston AF Symposium – 2004

Boston AF Symposium, January 16-17, 2004

The annual international Boston A-Fib Symposium is one of the most important conferences on A-Fib in the world. It brings together researchers and doctors who share the latest information. Unlike other heart related conferences, it concentrates only on A-Fib. But if you haven’t read and understood most of A-Fib.com, it may be difficult reading.

OVERVIEW

I was most impressed at how much the theory and practice of treating A-Fib is evolving. Last year I reported on the work of Dr. Pappone in Italy. Now three of the leading medical centers in the US seem to be using variations on his methods—the Un. of Michigan, the Mayo Clinic, and John Hopkins Un. But there are problems. Twenty percent of patients after ablation have Atrial flutter. I’ll go into this in detail when I summarize the presentation of the UN. of Michigan’s Dr. Morady.

From a public health and patient’s perspective, perhaps the most important talk was given by Dr. John Camm from England. He called attention to “silent” or asymptomatic A-Fib. A great number of people have A-Fib and  aren’t aware they have it. Not only are they at great risk of stroke, but A-Fib leads to many other heart problems. The question was posed, “Should we start screening people for A-Fib when they reach a certain age?”

Ximelagaron, the new blood thinner to prevent stroke in A-Fib, looks like it might be approved in the US in late 2004 or 2005. It will certainly be a welcome and much needed improvement over warfarin (Coumadin). Besides the benefits you’ve already heard about, it also reduces the risk of hemorrhagic stroke compared to warfarin.

Cryoablation (freezing heart tissue during an ablation) is being used, but it’s too early to tell how effective it is. One major center doing experimental Cryoablation reported a case of stenosis from a procedure. That’s definitely a red flag. Cryo was supposed to avoid stenosis. But again it’s too early to draw any definite conclusions.

Dr. Pappone reported a variation on his ablation procedure that achieved a 99% success rate, but it seemed to apply only to a very small and select group of patients.

The Boston A-Fib Symposium was very well attended. (I got stuck in an overflow room and had a hard time getting to ask doctors questions. I was one floor down. By the time I got to the next floor after a presentation, it was hard to find the speaker.It was really c-c-c-cold in Boston—5 degrees, windy, and snow! For us California types snow is that white, wet stuff you go to when you want to ski, not something that covers the courtesy bus logo while you’re freezing at the airport curb waiting for that ____ bus!

(Author’s Note: These summaries are dedicated to the memory of Dr. Brian McGovern of Massachusetts General and the Atrial Fibrillation Foundation who was killed April, 2003. Though I met Dr. McGovern only once, his death was like losing a best friend. I was most fortunate to have Dr. McGovern share with me over a box lunch some of the history of the Boston A-Fib Symposium and the Atrial Fibrillation Foundation. He was a charming, smart, experienced, knowledgeable, down-to-earth doctor dedicated to helping people with A-Fib. We will never forget him.
In his introductory remarks Dr. Jeremy Ruskin of Massachusetts General dedicated the Boston A-Fib Symposium 2004 in memory of Dr. McGovern. Many speakers began their talks by expressing how Dr. McGovern affected their lives and how he is missed.)

Dr. John Camm, St. George’s Hospital Medical School, London, England

Author’s Note: From a public health aspect, perhaps the most important presentation was by Dr. John Camm on silent (asymptomatic) A-Fib.

Patients with A-fib often experience symptoms such as palpitations, difficulty breathing, chest discomfort and anxiety, sweating, fatigue, and dizziness. But many people with A-Fib (33%) experience no obvious symptoms and no noticeably impaired quality of life. These people are at risk not only of stroke which occurs four to five times more often, but also of heart failure due to irregular and fast heart beat. There is a threefold risk of heart failure in A-Fib. Due to silent ischemic attacks (a clot that blocks an artery) and silent cerebral infarcts (strokes), patients may develop mental problems ranging from forgetfulness to dementia. Forty percent of A-Fib patients have one or more silent cerebral infarcts. Patients with A-Fib report a substantial deterioration in attention and memory.

From a patient’s perspective, we need to be concerned not only about the obvious symptoms of A-Fib, but also about the long term risks of A-Fib—stroke, heart failure, reduced mental capacity. These long term risks are especially important if you have silent A-Fib.

Dr. Camm cited several studies such as:

  • AIDA (Automatic Interpretation for Diagnosis Assistance) where half the patients with A-Fib experienced silent A-Fib,
  • the CARAF study where silent A-Fib patients were most likely to be male and older,
  • the PAFAC German study in which 89% had silent A-Fib, and
  • the ALFA study where many patients with permanent A-Fib (16.2%) reported no obvious symptoms.

According to Dr. Camm, “The persistent and permanent forms of A-Fib are less symptomatic…” In one study 80% of people who had a stroke didn’t know they had A-Fib.

Even patients with symptomatic A-Fib have silent A-Fib episodes. In monitoring Paroxysmal A-Fib, silent episodes occur ten to twelve times more frequently than symptomatic episodes. Under drug therapy symptomatic A-Fib episodes may turn silent, because the heart rate does not accelerate or become irregular. This is of particular concern to those of us on antiarrhythmic drugs. Even though we are A-Fib symptom free, we may still have silent A-Fib. 

Dr. Camm pointed out that quality of life may deteriorate in patients with silent A-Fib. In the CTAF study (Canadian Trial of Atrial Fibrillation) patients with paroxysmal or persistent A-Fib reported better quality of life and had significantly higher scores in most estimates while they were in sinus rhythm. In Dr. Camm’s own study patients with silent A-Fib reported significantly lower perception of general health compared to age-matched healthy subjects.

Dr. Camm concluded, “…the risk of morbidity and mortality due to A-Fib is probably the same as in patients with A-Fib symptoms.” But patients with silent A-Fib had a higher mortality rate (7%) than those with A-Fib symptoms (3%), perhaps because they weren’t being treated appropriately. Patients with silent A-Fib are more likely to develop heart failure, stroke, and mental problems because their A-Fib remains unrecognized and untreated for longer. Early treatment is of particular importance. Appropriate anticoagulation and adequate rate or rhythm control can prevent most of the serious outcomes of silent A-Fib.

As Dr. Ruskin pointed out at the conclusion of Dr. Camm’s presentation, these finding have huge public health implications. Someone in the audience asked, “should we screen everyone age 60 and above for A-Fib?”

Dr. Camm mentioned that successful AV Node ablation and the insertion of a pacemaker produced a remarkable improvement in cardiac performance and better reported quality of life.

Dr. Stanley Nattel, Institute of Cardiology of Montreal, Montreal, Canada

Dr. Nattel discussed whether the field of genetic research can help treat and cure A-Fib, whether we can currently identify a genetic basis or determinant for A-Fib or for how A-Fib works. Unfortunately today there are, “…very few genetic models of pure AF.” There are however, many genetic models or syndromes in which A-Fib is present and even prominent.

Some of these potential basic mechanisms leading to A-Fib are:
Gene mutations that shorten the wavelength of electrical signals in the heart by either reducing the refractory period (the length of the wavelength) or the conduction velocity (the speed of the wavelength). These genes that affect the Potassium currents (K+) in the heart are: KCNQ1/KvLQT1; KCNH2/HERG.

Gene mutations associated with ventricular arrhythmogenesis (abnormal heart beat) and possible relationships to the atria.

Gene mutations affecting multiple areas:
1. Ankyrin-B
2. Lamin

Gene mutations linked to familial A-Fib. Only the chromosomes are known. The particular genes on these chromosomes have not yet been identified.
1. Chromosome 6
2. Chromosome 10
Dr. Nattel discussed genetic models of A-Fib in mice and how this research might be applied to humans. Too much Rho A may lead to cardiomyopathy (chronic heart disease) and conduction problems. Too much TGFbetta may lead to atrial fibrosis.

Answering questions from the audience Dr. Nattel pointed out that the atria are more prone to fibrosis, because the atria walls are thinner and tend to balloon out in volume overload conditions like some kinds of acute heart failure.

Reducing the conduction ability of Connexin 40, a protein that connects cells, may be involved in the remodeling effect of A-Fib.

Dr. Stanley Nattel, Institute of Cardiology of Montreal, Montreal, Canada

Dr. Nattel’s second presentation discussed ionic vs. structural remodeling in A-Fib.

In an experimental study, dogs were put into Congestive Heart Failure through ventricular fast pacing for two weeks, which also caused A-Fib in the dogs. In the ionic remodeling of the dogs’ hearts some ionic heart currents were decreased1, while others were increased2.  In the structural remodeling of the dogs’ hearts a 5-fold increase in atrial fibrosis occurred (in fibrosis there is an increase of connecting fibrous tissue in the heart).

The dogs were then allowed to recover for four weeks. The dogs’ hearts recovered their normal functions and dimensions. All changes in ionic currents resolved.  But the dogs were still in A-Fib, and their hearts’ fibrous tissue content remained at five times normal.

Dr. Nattel concluded, “…these results suggest that structural remodeling (atrial fibrosis) and not ionic remodeling is the principal A-Fib-promoting component to this experimental Congestive Heart Failure…” Atrial fibrosis may be an important cause of A-Fib and may be irreversible.

Answering questions from the audience Dr. Nattel pointed out that not all cases of Congestive Heart Failure develop A-Fib.
1(atrial transient-outward [Ito ], slow delayed-rectifier [Iks], L-type Ca2+ [Ica.L] 2(NaCa++ exchange current [INCX]

Dr. Fred Morady of the University of Michigan, Ann Arbor, MI.

Dr. Morady reported on the outcomes of a Un. of Michigan study comparing Segmental vs. “Left Atrial Catheter Ablation” (Dr. Pappone, who first developed this procedure, calls it “Anatomically Based Circumferential PV Ablation”).

STUDY PROCEDURE: Eighty patients with Paroxysmal (occasional) A-Fib were randomly assigned to either the Segmental or Left Atrial Ablation group. In the Segmental group, areas in the Pulmonary Vein openings producing A-Fib signals were burned off (isolated) using a 4 mm catheter at 35 Watts. Whereas in the Left Atrial Ablation group an 8 mm catheter at 70 Watts was used to make “drag lesions” in a circular pattern around the Pulmonary Vein openings. (A wider catheter at a higher Wattage was safely used, because the drag lesions created were well outside the Pulmonary Vein openings with little risk of Stenosis [swelling of the Pulmonary Vein openings]). The time it took to perform the ablation procedures for both groups was approximately 2 ½ hours. One-third of the patients in the Left Atrial Ablation group also received spot lesions within the drag lesion circles to eliminate spiking A-Fib signals.

(AUTHOR’S NOTE: The great innovation of Dr. Morady and Dr. Pappone is the use of what I would call the “drop and drag” technique of making linear circular lesions. Instead of trying to make continuous, perfect linear lesions which can be difficult and time consuming, they simply drop and drag the catheter to make the linear circular lesions, even though there may be gaps left in the lesions. Though A-Fib signals may still get through these gaps and cause Atrial Flutter, over time scar tissue and fibrosis usually close these gaps. This procedure represents a major change in treating A-Fib. Instead of concentrating on the Pulmonary Veins and Pulmonary Vein Potentials, the emphasis is on creating blocking lesions in the left atrium. After this procedure Pulmonary Vein Potentials may still remain. As Dr. Morady said, “It doesn’t matter if the triggers are still there……Our focus has swung from triggers to substrate modification [changing the left atrium].”
This “drop and drag” technique may soon become the standard way of doing Pulmonary Vein Ablations. It is easier, faster, requires less operator skill, and seems to get somewhat better results than other PVA procedures.)
(In 2007 it appears that Dr. Pappone’s lesions are now very similar to linear lesions and have few or no gaps. He makes many short, overlapping passes with the catheter rather than the “drop and drag” technique.)

RESULTS: After nine months 88% of the Left Atrial Ablation group were A-Fib symptom free versus 67% of the Segmental group. (The Segmental group did not receive any linear lesions as are used in some centers.) 20% of the Left Atrial Ablation group had Atrial Flutter after the procedure, but most of these Atrial Flutter patients lost this flutter and were in sinus rhythm after four and one-half months. Only 2% had to have another procedure to eliminate the flutter.

(Author’s Note: From a patient’s perspective, this risk of Atrial Flutter may not be acceptable if one can get close to the same success rate from the more advanced Segmental procedures. Also, leaving A-Fib triggers in the heart may have long term consequences, though the studies of Dr. Pappone do not show any long term consequences.)

Dr. Morady also talked about how to get closer to 100% success rate for curing A-Fib. He discussed ablating the Mitral Annulus, the roof of the heart, the great cardiac vein, the Coronary Sinus, Bachman’s Bundle, the Left Atrial Appendage and sites adjacent to the Pulmonary Veins.
(Last updated 2/12/08)

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Last updated: Sunday, February 15, 2015

Boston AF Symposium – 2007

Boston AF Symposium, January 11-13, 2007

The annual international Boston A-Fib Symposium is one of the most important conferences on A-Fib in the world. It brings together researchers and doctors who share the latest information.  But if you haven’t read and understood most of A-Fib.com, it may be difficult reading.

OVERVIEW

The overall tone or mood of the 2007 Boston A-Fib Symposium seemed to be one of confidence in a maturing field—that this Symposium was more about fine tuning rather than major changes.

Atrio-Esophageal Fistula

Was a definitive method found to avoid the rare complication atrio-esophageal fistula (where the ablation catheter unintentionally burns a hole through the back of the heart and into the esophagus)? No. But every major center seemed aware of this possible complication and was taking steps to prevent it, such as:

1. Limiting ablation time at the back of the heart to 15 seconds.
2. Using an esophageal temperature probe and stopping the particular ablation whenever there is a rise in esophageal temperature.
3. Using an Echocardiogram to locate the exact position of the esophagus relative to the heart, and then not ablating in areas near the esophagus.
4. Using an irrigated tip catheter at low wattage in the back of the heart.
5. Using a Cryo catheter in the back of the heart (Cryo [freezing] catheters seems to cause less tissue damage).

But because atrio-esophageal fistula is such a rare complication (approximately one case out of 1000 ablations), it may be some time before a particular method of avoiding atrio-esophageal fistula is proven better and more effective than others.
(See below/Marchlinski: Preventing Atrial Esophageal Fistula)

Silent A-Fib

Though “silent” A-Fib especially in “cured” A-Fib patients was still a  concern, being A-Fib symptom free was recognized as a major improvement in quality of life and overall health from both a patient’s and doctor’s perspective. (In this author’s opinion, doctors should be proud of the great number of their patients who are now A-Fib symptom free. Successful catheter ablation for A-Fib is one of the great medical breakthroughs of our time. One doctor commented on how fewer patients he sees who are in Persistent A-Fib, because so many have been “cured” before they get to that point.)

Silent A-Fib episodes after successful catheter ablation seem to be more often of short duration. Are these silent A-Fib episodes as dangerous in terms of causing a stroke as in symptomatic A-Fib? Intuitively patients feel more healthy and less prone to stroke when they are A-Fib symptom free, though this has yet to be proven scientifically.

New Research and Medical Developments in A-Fib

Autonomic Ganglionated Plexi sites on the outside of the heart may be very important in generating A-Fib signals, according to Dr. Jackman. It may be possible by ablating only these seven Ganglionated Plexi areas to eliminate A-Fib signals and symptoms. However, this hypothesis is years away from being clinically tested and proven. (See Jackman Autonomic Ganglionated Plexi.)

Randomized clinical trials of the CryoAblation balloon catheter have begun in the US. (The 2006 Boston A-Fib Symposium featured a live demo of a Cryo balloon catheter ablation at Massachusetts General.) (To this author, Cryo [freezing] ablation seems to be significantly safer for patients than standard RF ablation. [See 2006 Boston AF: Ablation Catheters that Use Cryo.] However, Cryo ablations currently take more time to perform than RF ablations. The Cryo balloon catheter will likely allow a doctor to perform a Cryo ablation and isolation of the Pulmonary Vein openings more easily and much faster than current methods. The Cryo balloon catheter may become a major improvement in the treatment of A-Fib. It has already been approved in Europe, with close to 100% success rate in isolating the PVs, and 75-80% success in keeping patients free of A-Fib without anti-arrhythmic drugs.)

The A-Fib medical community seemed somewhat in awe of the French Bordeaux group’s recently reported 95% success rate in curing Persistent A-Fib. (The French seem to have definitely raised the bar for curing A-Fib. Their methods and success rates will probably soon become standard operating procedure for many centers in the US.) Dr. Jaïs reported on recent A-Fib developments in Bordeaux to be summarized later.

Current catheter ablation procedures, particularly the more complicated ones, are not being adequately covered by insurance and government programs.  This is a concern for patients who may eventually be excluded from ablation treatment because insurance companies won’t reimburse adequately for complicated catheter ablation procedures. More lobbying needs to be done to improve current reimbursement rates.

The medication ranolazine (brand name Renexa), recently approved by the FDA for chronic angina (chest pain associated with lack of blood to the heart), may help suppress A-Fib by blocking sodium channels in the atrium. (Ranolazine may become an effective antiarrhythmic medication because it is atrial-selective—it affects only the atria and not the ventricles. However, the data on Ranolazine is ALL experimental and there are NO DATA in humans at this time. So, the potential benefit of ranolazine in A-Fib is intriguing but speculative at this point.)

Author’s note: This author was impressed by the willingness of A-Fib doctors to confront, discuss and learn from their most difficult and/or least successful cases. For example, in the live case demo a patient was chosen who had had two previous ablations to isolate the Pulmonary Vein openings, and in whom all four pulmonary vein openings were again generating A-Fib signals into the heart. Another doctor presented a talk on his center’s patients who needed a third and fourth ablation procedure to cure their A-Fib. Doctors share both their successes and their failures in order to help Symposium participants improve their A-Fib patient care.

The 2007 Boston A-Fib Symposium was an extra 1/2 day longer in order to devote more time to the Basic Science of A-Fib (such as chemical currents, nerve structure, and physical mechanisms of the heart during A-Fib), and to surgical operations to cure A-Fib.

Two ablation demonstrations live via satellite were presented. The first from Massachusetts General featured a patient who had had two previous catheter ablations but whose Pulmonary Vein openings were reconducting again. The second case was from Germany and featured a demo of the Stereotaxis remote catheter ablation system(The excitement generated when a patient’s A-Fib is stopped is similar to a goal or touchdown in a soccer or football game.)

Participants in the 2007 Boston A-Fib Symposium were given an update/summary of the 2006 Boston A-Fib Symposium by Drs. David Keane, Vivek Reddy and Jeremy Ruskin.

Update on Mechanisms and Therapy for A-Fib from the 11th Annual Boston A-Fib Symposium 2006. 

(This update was written by doctors for doctors and may be somewhat difficult for patients to read. However, it is an excellent summary not only of the main points of the 2006 Symposium but of all the issues of concern to A-Fib patients today.)

 

TOPICS DOCTOR TITLE OF PRESENTATION
Limitations of the Maze Operation. Body Surface Mapping of the Heart Damiano Future Directions in A-Fib Surgery: Can We Make the Atria Fibrillation-Proof?
5-Step Ablation Treatment for Chronic A-Fib Haïssaguerre 5-Step Ablation Treatment for Chronic A-Fib
The Role of Autonomic Ganglionated Plexi in A-Fib Jackman The Facilitation of A-Fib by Communication Between Autonomic Ganglionated Plexi
Doctors’ Overview of the 2006 Boston A-Fib Symposium Keane, Reddy, Ruskin Update on Mechanisms and Therapy for A-Fib from the 11th Annual Boston A-Fib Symposium 2006
Using Different Surgical and Ablation Treatments for A-Fib Kress Surgical Therapy for A-Fib: Selected Cases and Techniques
Regrowth/Reconnection of Ablated Areas Requiring Additional Ablations Marchlinski Third and Fourth PV Isolation/Ablation Procedures: Outcomes and Insights
EKGs Can Reveal Where A-Fib Originates in the Heart Morady The Interpretation of the ECG Morphology During PACs, Atrial Tachycardia & Atrial Flutter

Dr. Francis Marchlinski of the University of Pennsylvania, Philadelphia, PA gave a presentation on “Third and Fourth PV Isolation/Ablation Procedures: Outcomes and Insights.”

One of the major concerns of both A-Fib doctors and patients is the occasional reoccurrence of A-Fib after an apparently successful Pulmonary Vein Ablation (Isolation) procedure. Dr. Marchlinski studied patients who needed not only a second but sometimes a third and even a fourth ablation procedure to cure their A-Fib.

At the Un. of Pennsylvania, 887 A-Fib patients received basically the same ablation treatment: Proximal or Antral PV Isolation along with Ablation of Non-PV (Pulmonary Vein) Triggers. Some patients were Paroxysmal, others were Persistent/Permanent (35%). Some patients needed a second ablation procedure which achieved a 87% success rate; 34 patients (4%) needed a third ablation procedure, and 4 (1%) needed a fourth. Two patients were never cured. (One had Mitral Valve Replacement and Maze surgery and still had recurrent A-Fib; another had two more ablation procedures at another institution and still had recurrent A-Fib.)

FINDINGS:

Dr. Marchlinski identified the following characteristics of A-Fib patients most likely to need a 3rd or 4th ablation.

  • Male
  • Larger left atrium
  • More non-PV triggers
  • Heart disease or significant hypertension

(By identifying these characteristics, patients more at risk of needing additional procedures can be identified. Further research may produce additional treatments to prevent them from needing repeat ablations.)

Dr. Marchlinski found that most patients needed repeat procedures because of regrowth or reconnection in the Pulmonary Veins. Of the patients undergoing 3rd and 4th ablation procedures, 65% had all four PVs partially or completely reconnected.

Answering a question from the audience Dr. Marchlinski explained that during ablation both Entrance and Exit block were verified in 100% of patients, that the reoccurrence of A-Fib probably wasn’t due to missed ablation spots.

Someone asked if there was a greater risk of complications during a second ablation procedure than during the first. According to Dr. Marchlinski, the complication rate for a second ablation is the same as for a first one.

Author’s Note: This study is very encouraging for A-Fib patients. The success rate for Pulmonary Vein Ablation procedures is often listed as 70-85%. But, when including those who had a 3rd and 4th procedure, the Un .of Pennsylvania achieved a near perfect cure rate.

Also, Dr. Marchlinski has identified the main reason why patients need repeat ablation procedures—reconduction or regrowth of ablated areas in the Pulmonary Veins. Further research may now be focused on eliminating this reconduction/regrowth.

Dr. Marchlinski’s study indicates that, if you choose to have a PVA(I) procedure, you may need a second procedure to be cured (approximately 26% chance). And there is a 5% chance you may need a 3rd or 4th procedure. This need for multiple procedures is most likely not due to a failed initial procedure, but because of spontaneous regrowth/reconnection of the ablated area.)

PREVENTING ATRIAL ESOPHAGEAL FISTULA

Dr. Marchlinski also described his procedure for trying to prevent atrial esophageal fistula (unintentionally burning a hole through the heart into the esophagus). He uses Echo (Electrocardiograph) and CT/MR (Computed Tomography and Magnetic Resonant Imaging) in an online monitoring system to identify the location of the esophagus in relation to the back of the atrium. If the ablation catheter is near the esophagus, he uses shorter bursts of energy during ablation. “We don’t avoid (ablating near the esophagus) completely if it is required for isolation.”

Dr. David Kress of the Midwest Heart Surgery Institute in Milwaukee, Wisconsin discussed “Surgical Therapy for A-Fib: Selected Cases and Techniques.”

Many cardiac surgeons specialize in one kind of surgery. Dr. Kress described how he uses not just one type but rather an array of different surgical techniques (Radial Maze, Wolf Bipolar RF,Saltman Microwave, Box Lesion Ultrasound), as well as mapping and ablation techniques (ablation of Autonomic Ganglionated Plexi and CryoCath Catheters), depending on the different needs of his A-Fib patients.

For example, one patient with A-Fib also needed surgery to replace an Aortic Valve. Dr. Kress replaced the Aortic Valve, and in the same surgery he used both the Saltman Microwave box lesions and the Wolf Bipolar RF Clamp to isolate the Pulmonary Veins. He also mapped and ablated the Autonomic Ganglionated Plexi (a newer ablation technique that can be performed from outside the heart). According to Dr. Kress, mapping and ablation of Autonomic Ganglionated Plexi increases A-Fib surgery success by 10%.

During surgery on a 73-year-old man with Aortic Stenosis (swelling), he performed a Box Lesion Ultrasound operation, but A-Fib electrical activity continued. He then cut into the left atrium and ablated the remaining A-Fib signal sources with a CryoCath catheter.

In another example, a 49-year-old woman with A-Fib and Hypertrophic Cardiomyopathy also needed a new Mitral Valve. During her surgery Dr. Kress replaced her Mitral Valve, performed a Radial Maze operation and used a CryoCath catheter to make the Radial Maze connecting lesions (as an adjunct to the typical extensive cutting and sowing of the Radial Maze operation).

Author’s Note: Dr. Kress’ approach may represent the future of A-Fib surgery. Cardiac surgeons, instead of specializing in one type of surgery, may develop expertise in many different surgical and ablation techniques. In some centers surgeons and Electrophysiologists already work together to treat A-Fib patients.

REMOVING THE LEFT ATRIAL APPENDAGE

Almost all current surgical techniques include cutting out and/or stapling shut the Left Atrial Appendage. According to Dr. Kress, “Left Atrial Appendage removal is often the most important part of the (operation)…(because) the patient can stop taking Coumadin.” Coumadin can be stopped even if the patient is still in A-Fib. Sometimes after the Left Atrial Appendage operation, small Appendage pouches or sacs remain which could produce clots and stroke. But according to Dr. Kress’ experience, after 3-4 months these pouches or sacs generally fill in with fiber and become relatively smooth walled, thereby reducing the risk of stroke.
Someone from the audience asked, “Is removal of the Left Atrial Appendage a suitable substitute for Coumadin?” Dr. Kress thought so, but acknowledged there were no clinical studies demonstrating this.

Author’s comment: The author believes that Dr. Kress is correct, and that future studies will demonstrate that removal of the Left Atrial Appendage is indeed a substitute for Coumadin.
ADDITIONAL COMMENTS

According to Dr. Kress, Microwave energy using the Flex-10 catheter is currently the most accepted method and has the best delivery system to position the catheter.

He warned that the Microwave catheter, if oriented improperly, can burn unintended areas.

According to Dr. Kress, all current Mini-Maze operations have the drawback of “unreliable transmurality” (the lesions or burns on the outside of the heart aren’t effective unless they penetrate through to the inside of the heart, but this doesn’t always happen).

Dr. Kress also warned that, “surgery on older and out-of-shape patients can have minor and major complications because they are under General Anesthesia.”

Dr. Ralph Damiano, Jr., of Barnes Jewish Hospital in St. Louis, MO talked about “Future Directions in A-Fib Surgery: Can We Make the Atria Fibrillation-Proof?”

Dr. Damiano described how and why the Maze operation for A-Fib is not as effective for certain groups of patients, and what he is doing to improve this. (The Maze operation was the first and one of the most effective treatments for A-Fib, though it involves open heart surgery and is a very invasive and physically traumatic experience.)

BACKGROUND

For many years Dr. Damiano used the Maze III (cut and sew) operation on patients with A-Fib who also had other heart problems which required surgery. In addition, he performed the Maze operation on A-Fib patients with no other heart problems (the Lone Maze). After years of follow-up, over 90% were free of A-Fib and off of Coumadin, though some still needed to take antiarrhythmic drugs. Five years ago he switched to using the Bi-Polar RF Clamp (to replace the cut and sew incisions with RF ablation lines), which he calls the Cox Maze IV operation. The RF clamp produces transmural conduction block, but is less apt to harm or damage the heart’s circulation system (the original Maze incisions sometimes did harm the heart’s circulatory system). He also uses a Uni-polar device to ablate areas of the heart which the Bi-Polar clamp can’t reach.

Dr. Damiano described the original Maze as a “salvage” operation at a time when it wasn’t possible to map the mechanisms of A-Fib. The placement of the cut and sew incisions was “empirically derived” (the incisions worked without knowing exactly what A-Fib mechanisms were affected). Even today the importance or effectiveness of each incision is unknown. The underlying theory of the Maze operation “Multiple Wavelet Macro-Reentrant Circuits” may be incorrect or inappropriate for many patients. (There can be multiple mechanisms responsible for A-Fib including focal drivers, single and multiple rotors, as well as reentrant circuits.) According to Dr. Damiano, “It is naive to think that one operation would fit all patients.”

PATIENTS WITH POOR MAZE OPERATION SUCCESS RATES

Even though his success rates for the Maze operation are high, there are some groups of A-Fib patients who don’t do well.

1. People who have been in A-Fib for over ten years. (This suggests that A-Fib over time may result in permanent remodeling which may not be reversible.)

2. People with very large left atriums (over 9 cm) have a poor success rate. (He cited studies relating to the “Critical Mass Theory” which found that as the size of the Left Atrium increases, the success rate for curing A-Fib decreases.1

3. People with shorter Effective Refractory Periods (ERP) and shorter A-Fib wavelength have poorer success rates.

Dr. Damiano indicated that the full Maze operation my be overkill for some A-Fib patients. For others (such as those mentioned above) it may not have the desired success rates. He suggested that surgeons in the future may not rely on a single operation approach, but may use mapping techniques to tailor operations to the needs of individual A-Fib patients.

BODY SURFACE MAPPING

Dr. Damiano described a pre-operative mapping technique called Body Surface Mapping that is completely non-invasive (the Prime ECG Electrocardiographic Body Surface Imaging by Heartscape Technologies, Inc.). Eleven easily-applied self-adhesive plastic strips containing 80 data collection points, or leads, cover the front and back of the body. This “jacket” of electrodes using CT and MRI techniques maps the structure of the heart and pinpoints where A-Fib signals originate. It’s similar to an ECG but with 80 leads instead of 12. It provides a 360 degree view of the heart’s electrical activity. The surgeon can use this mapping system to most effectively place the Maze ablation lines. (In simpler cases of A-Fib where A-Fib signals come from only one or two spots in the heart, less invasive procedures can be tailored to particular patients, thus avoiding the “overkill” and trauma of a Maze operation.)

(Author’s Note: The Body Surface Mapping system is currently not in clinical use but is in clinical trials for the detection of heart attacks. The clinical trial began Nov. 6, 2006 and is entitled “The Optimum Cardiovascular Diagnostic Evaluation Enabling Faster Treatment of Myocardial Infarction” [OCCULT-MI trial]
Dr. Damiano’s application of Body Surface Mapping to A-Fib may be a major innovation in the treatment of A-Fib. Body Surface Mapping may one day provide as much information as standard catheter mapping techniques without the need of inserting a mapping catheter into the heart.)

Dr. Fred Morady of the University of Michigan, Ann Arbor discussed “The Interpretation of the ECG Morphology During PACs, Atrial Tachycardia & Atrial Flutter.”

Dr. Morady showed how an ECG can not only reveal whether or not a patient has A-Fib, but also where an arrhythmia signal originates in the heart.

PULMONARY VEIN ARRHYTHMIA SITES

A negative or isoelectric (neither positive nor negative) P wave in lead I and a positive P wave in Lead V1 predicts almost 100% of the time that the arrhythmia comes from the Pulmonary Veins.2(The P wave is formed when the atria contract to pump blood into the Ventricles—see The EKG Signal).

A positive P wave in leads II and III indicates that the arrhythmia comes from the Superior Pulmonary Veins.

A negative or biphasic (both positive and negative) P wave in lead aVL suggests that the arrhythmia comes from the left rather than the right PVs.

A-FLUTTER SITES

Sometimes after surgery or ablation, a patient develops Atrial Flutter (Dr. Morady described instances where a full six years after surgery a patient developed Atrial Flutter). This Flutter often comes from either the Left Atrium or from the Cavotricuspid Isthmus in the Right Atrium. Negative or biphasic P waves in leads V1 through V6 suggests the Flutter may come from the Cavotricuspid Isthmus in the Right Atrium, whereas positive P waves in leads V1 through V6 indicate the Flutter may originate in the Left Atrium. (The usual suspect areas in the Left Atrium are the Coronary Sinus, Atrium Roof, and Mitral Isthmus, though the ECG currently does not help identify these signal areas.)

Report on the French Bordeaux Group’s Treatment for Chronic A-Fib

(Though related to Dr. Jaïs presentation, this summary is based on the Heart Rhythm Society’s DVD “Latest Atrial Fibrillation Techniques,” 2007.)

The French Bordeaux group now uses a five-step process to treat Chronic A-Fib.

1. They start by isolating the Pulmonary Vein openings. They also eliminate potentials at the base of the Left Atrial Appendage, but do not isolate or electrically disconnect the whole of the LAA which could possibly lead to clots forming in the LAA and A-Fib stroke. (“RSPV” stands for Right Superior Pulmonary Vein, “LSPV” Left Superior PV, “RIPV” Right Inferior PV, “LIPV” Left Inferior PV, “LAA” Left Atrial Appendage.)

(Ablating at the base of the LAA as part of the first step in treating A-Fib is a new approach and may become a very important first step in the ablation treatment of A-Fib.)

2. Next they make a roof line linear ablation linking the Right Superior Pulmonary Vein with the Left Superior Pulmonary vein opening to create complete electrical block.

3. They then work in the Inferior Left Atrium and the Coronary Sinus. They make an incomplete blocking line between the Right Inferior and Left Inferior PVs in order to slow down the rapid atrial electrical activity.

They treat the Coronary Sinus as though it were another heart structure or Left Atrium, rather than just another vein opening. They disconnect the CS from the Left Atrium and ablate potentials along the Mitral Annulus. They also slow down Coronary Sinus electrical activity by ablating both inside and outside the CS with a lower wattage power, usually 25 Watts. (Treating the Coronary Sinus as another Left Atrium is a new approach. Most current A-Fib ablation procedures tend to stay away from the Coronary Sinus because of the risk of Stenosis (swelling). The French Bordeaux group, by using a low wattage, irrigated tip catheter, ablates within the Coronary Sinus without damaging it.)

4. The fourth step is eliminating organized atrial activity in areas such as:

  • Anterior Left Atrium & Left Atrial Appendage
  • Septum
  • Posterior Left Atrium
  • Superior Vena Cava
  • Right Atrial Septum

5. The fifth step is to create a Mitral Isthmus blocking linear ablation line from the Mitral Annulus to the Left Inferior PV. The goal is to eliminate all potentials along this line.

In practice, even after these five steps, rapid atrial activity often remains. It has to be mapped, traced to its source and ablated. Often the top of the Left Atrial Appendage has to be ablated.

This whole procedure requires a great deal more time, effort, persistence, skill and experience than normal left ablation procedures. (Author’s note: The Bordeaux group also uses a Cavotricuspid Isthmus [CTI] line in the right atrium for A-Flutter.

(Please be advised that this five-step process for treating Chronic A-Fib is relatively new and isn’t available today at most A-Fib medical centers.)

Dr. Warren Jackman of the Un. of Oklahoma discussed “The Facilitation of A-Fib by Communication Between Autonomic Ganglionated Plexi.”

Dr. Jackman’s research identified a method of possibly eliminating A-Fib that is very different from any in use today.
According to Dr. Jackman there are seven areas of Autonomic Ganglionated Plexi (GP) on the outside surface of the heart that may trigger or maintain A-Fib. Most are located within epicardial fat pads (“epicardial” refers to the outside surface of the heart in contact with the Pericardium. This photo was taken from outside the heart during a Minimally Invasive Surgical Ablation of A-Fib.)

When stimulated, these GP areas can produce or trigger A-Fib at the Pulmonary Veins. In addition, the GP areas are interconnected, with the result that stimulating one GP can trigger A-Fib signals from a PV in a different area of the heart. The Autonomic Ganglionated Plexi areas consist of 10% Sympathetic Neurons, 10% Parasympathetic Neurons, and 80% Interconnected Neurons. (A Neuron is an electrically excitable cell in the nervous system that processes and transmits information.) There may be as many as 1000 neurons in a GP area.

Preliminary research on animals indicates that ablating the seven GP areas may stop the Pulmonary Veins from producing A-Fib signals.

Author’s Note: Surgeons performing the Maze and Mini-Maze operations report that ablating the Autonomic Ganglionated Plexi areas improves the success rate of their operations by 10%. [See Ablating Autonomic Ganglionated Plexi during surgery.] Surgeons doing these operations are able to ablate the GP areas since they normally access the heart from the outside; whereas Pulmonary Vein Ablation (Isolation) procedures usually stay inside the heart.

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Last updated: Wednesday, July 6, 2016

References    (↵ returns to text)
  1. Importance of Geometry and Refractory Period in Sustaining Atrial fibrillation: Testing the Critical Mass Hypotheses.” Byrd et al. Circulation 2005; DOI: 10.1161/CirculationAHA.104.526210
  2. Tse et al. Journal of Interventional Cardiac Electrophysiology, 2001;5:167-172.

Boston AF Symposium – 2009

Boston AF Symposium, January 15-17, 2009 “Atrial Fibrillation: Mechanisms and New Directions in Therapy”

The annual international Boston A-Fib Symposium is one of the most important conferences on A-Fib in the world. It brings together researchers and doctors who share the latest information.  However, if you haven’t read and understood most of A-Fib.com, it may be difficult reading.

OVERVIEW-HIGHLIGHTS

The overall mood of the 14th annual Boston A-Fib Symposium seemed to be one of confident expectation, reflecting perhaps the mood of our country anticipating the presidential inauguration. One might also describe this Symposium’s signature or most prominent concern as the “CFAE (Complex Fractionated Atrial Electrograms) vs. Dominant Frequency Controversy.”

List of Presentations

Merits of GP (Ganglionated Plexi) Ablation 

 

CFAEs vs. Dominant Frequency

Several doctors made presentations on Electograms in A-Fib, reflecting the importance and ongoing controversies in the field. According to Dr. Jose Jalife of the Un. of Michigan in Ann Arbor, the areas of Dominant (highest) Frequency found in the atria indicate sites of A-Fib generation. These Dominant Frequency areas do not coincide with areas of CFAEs (Complex Fractionated Atrial Electrograms). Dr Jalife disagrees with Dr. Nademanee (who discovered CFAEs) about the importance of CFAEs in ablation. Dr. Shin-Ann Chen of Veteran’s General Hospital in Taipei, Taiwan found that areas of CFAEs change their location after the Pulmonary Veins are successfully ablated. His current protocol is to first ablate the PVs, then make linear lines, and only then ablate CFAEs. This differs from Dr. Nademanee who first ablates areas of CFAEs. Dr. Moussa Mansour of Massachusetts General in Boston recommended using areas of Dominant Frequency as a target for ablation. Though areas of DF and CFAEs are related, their regions overlap only in about 50% of cases. Dr. Vivek Reddy of the Un. of Miami added yet another term to the current Electrogram lexicon “EGMCL” (Electrogram Mean Cycle Length). He recommended that high density mapping be done after PV ablation in order to identify “pockets” of CFAE sites which he termed “EGMCL.” From a clinical perspective, in order to organize the chaotic electrograms often found in Chronic A-Fib, the Bordeaux group ablates areas of Dominant Frequency first.

Future Alternatives to Warfarin

“Warfarin’s days are numbered!” according to Dr. Michael Ezekowitz of Lankenau Institute for Medical Research in Wynnewood, PA. One could almost hear a collective sigh of relief from the doctors in attendance who cope every day with the dosage and side effects problems of warfarin. Dr. Ezekowitz confidently asserted that there will soon be available more user-friendly anticoagulants. He described seven drugs in advanced clinical trials to replace warfarin, and said that some, if not all of them, may be approved by the FDA within a minimum of five years. (Author’s Note: At the present time, 2 or 3 are close to approval, while the rest are much further out because they are in early trials. Dabigatran may be approved in the next 12-24 months, because its phase 3 trials are far along and look impressive. The next closest is rivaroxiban, but it’s just recruiting for Phase 3. [Thanks to Mallanie True Hills for these insights.])

Robotic vs. Magnetic Navigation/Ablation

Robotic navigation and ablation seemed the clear winner in a debate between Dr. Andrea Natale of the Texas Cardiac Arrhythmia Institute in Austin, TX (Hanson robotic) and Dr. Carlo Pappone of San Raffaele University Hospital in Milan, Italy (Stereotaxis magnetic). From the data presented, the Hanson Robotic system appeared more ergonomically user-friendly and more directly responsive to the operator. While Stereotaxis uses a mouse and click system with what Dr. Natale described as a 5-7 second delay, Hanson uses a motion controller with a flexible guide catheter directly responsive to an operator’s touch that replicates an operator’s natural hand movements. According to data presented by Dr. Natale, the Stereotaxis system is prone to charring which can cause clotting and stroke, while the Hanson system uses a flexible irrigated tip catheter less prone to charring. The Hanson robotic system is pressure sensitive, while Dr. Pappone acknowledged that the Stereotaxis system to date sometimes doesn’t provide enough pressure when making ablations. The Hanson system is portable and easily attaches to a procedure table.

Comments added June 20, 2009: A correspondent who wishes to remain anonymous pointed out that the Hansen robotic system does require extensive manual skill, whereas the Stereotaxis magnetic system is automated. (To this author, this is a major difference between the two systems. Even with skilled, experienced operators it is still possible with a robotic system to have misplaced ablation burns or accidents such as perforations. Whereas the magnetic system using a mouse to make the ablations seems safer, ultimately more efficient, and more capable of being used by new operators.
The Stereotaxis system now uses an irrigated-tip catheter which is less prone to charring.)
(Before each presentation, doctors disclose any potential conflict of interest. Dr. Natale disclosed he is a partner with Dr. Burckhardt, the CMO of Stereotaxis.)
Merits of GP (Ganglionated Plexi) Ablation

In another dramatic debate Dr. Eric Prystowsky of the Care Group in Indianapolis, IN (Con) and Dr. Warren Jackman of the Un. of Oklahoma in Oklahoma City, OK (Pro) argued the merits of GP (Ganglionated Plexi) ablation. Dr. Prystowsky agreed with Dr. Jackman that GPs contain nerve systems that affect the Pulmonary Veins, and that Pulmonary Vein Ablation works perhaps because it cuts across and disrupts these nerve pathways to the PVs. However, Dr. Prystowsky seemed to carry the day by pointing out that GPs not only affect the Pulmonary Veins but also contain nerves that extend to the ventricles of the heart and also affect the GI (Gastro Intestinal) system. Surgeons who have ablated the GPs while doing a Mini Maze operation have found that the GI has been compromised. Dr. Prystowsky cautioned that ablating the GPs with nerves leading to the ventricles may possibly produce ventricular electrical instability with possible sudden cardiac death. (This is a cautionary hypothesis. Further research is necessary to establish how ablating the GPs affects the ventricles.) The previous presenter, Dr. Dainius Pauza, described in detail how nerves in the GPs extend to the ventricles in his talk on the “Neural Anatomy of the Heart and Pulmonary Veins. (Author’s Note: Dr. Prystowsky raised a serious question for A-Fib patients. Does ablating the GPs risk damaging the nerve electrical system which affects the ventricles, and which may even lead to future sudden cardiac death? Until more research establishes how these GP nerves actually affect the ventricles, we should be cautious about having our GPs operated on or ablated.)

Moving from Conscious Sedation to General Anesthesia

In the U.S. a trend may be developing to use General Anesthesia during ablation (in Conscious Sedation the patient is lightly sedated rather than completely unconscious during General Anesthesia). Dr. Andrea Natale of the Texas Cardiac Arrhythmia Institute and Dr. David Packer of the Mayo Clinic in Rochester, MN said that they have moved to General Anesthesia because:

  • there is less patient movement which helps decrease re-conduction problems,
  • the esophagus doesn’t move,
  • patients like it better because they don’t experience any discomfort or pain.

In a later presentation Dr. Pierre Jaïs said that the Bordeaux group uses Conscious Sedation. One reason is that with General Anesthesia doctors can’t tell if a patient develops a thrombus or clotting which might cause a stroke. Of the attendees 42% indicated they use General Anesthesia, while 58% use Conscious Sedation. (Symposium attendees used a touchpad audience feedback system to answer questions from the presenters, making the Symposium more of an interactive process. Though not a scientific survey, this interaction system gave a sense of the general attitudes and practices of the attendees.)

The Dronedarone Symposium

The 14th Boston A-Fib Symposium was unusual in that it featured a debate on dronedarone, a drug not currently in use and not yet approved by the FDA. Dr. Albert Waldo of University Hospital of Cleveland (Pro) and Dr. Douglas Packer of the Mayo Clinic in Rochester, MN (Con) debated whether all A-Fib patients should be treated with dronedarone. The debate moderator, Dr. Peter Kowey of Lankenau Hospital in Wynnewood, PA, said the ATHENA study of dronedarone is a model for antiarrhythmic drug trials. (Dronedarone is intended to replace amiodarone.) The ATHENA clinical trial found that dronedarone wasn’t quite as effective as amiodarone, but was much safer. Dr. Packer acknowledged the positive results of the ATHENA study, but argued that catheter ablation may be better for an A-Fib patient than an antiarrhythmic drug like dronedarone. He also pointed out that the ATHENA trial didn’t specify what dosage of dronedarone to use. A very high dosage may produce GI (Gastro Intestional) problems. Dr. Waldo presented a sobering statistic that in 2050 16 million people in the US will have A-Fib vs. about 3 million today. It is predominately older people who get A-Fib. For people over 80, for whom catheter ablation may not be possible, dronedarone may become their only option.

FDA a Big Hit

One of the most interesting and anticipated sessions featured Dr. Randell Brockman of the FDA who moderated a panel and audience discussion of A-Fib ablation. The panel featured some of the most well known doctors in A-Fib. Dr. Brockman had many questions for the panel and audience, and used the audience feedback system to tabulate responses. This session provided an opportunity for regulators and A-Fib doctors to share their concerns and to understand each other’s different perspectives. One concern raised at this session was the problem of relapse after a successful ablation. Is one year of monitoring enough? Dr. Pierre Jaïs said there was a 25% relapse rate after five years, while Dr. Prystowsky said most patients remain clear of A-Fib after one year. Dr. Wyn Davies of St. Mary’s Hospital in England said that successfully ablated A-Fib patients should be followed and monitored throughout their lifetime. Dr. Carlo Pappone said catheter ablation should not be a first line therapy for A-Fib patients, that drug therapy should be tried first before moving to catheter ablation. While the complication rate for catheter ablation is low and the complications are anticipated and normally well handled, still complications do occur and are a somewhat harrowing experience that doctors would rather avoid. Dr. Pierre Jaïs in a later panel echoed Dr. Pappone.

Dublin, Ireland and Mass. General Live Satellite Ablations

In a live satellite transmission form Dublin, Ireland (a ‘first” for the Boston A-Fib Symposium), Dr. David Keane of St. Vincent’s University Hospital in Dublin performed an ablation on a patient with Paroxysmal (occasional) A-Fib using the new Bard Mesh catheter (not yet approved in the US). The Mesh catheter is both a mapping and an ablation catheter. Thirty-six strands of variable braded wire meshwith an electrode array can be expanded into a balloon-like shape to map and ablate the Pulmonary Vein openings. These wire strands also contain 36 bipoles to record electrogram (electronic A-Fib signals) info in the heart. The Mesh catheter can ablate in a complete circle or in any one of four color coded quadrants for a partial burn. The Mesh catheter burns at 100 Watts for 180-300 seconds. Dr. Douglas Packer commented that multi-array catheters can get very hot. In point of fact, in the ablation from Dublin, Dr. Keane had to make 11 burns to completely isolate one vein. The second live satellite transmission was the ablation of a Persistent A-Fib patient at Massachusetts General by Dr. Moussa Mansour. He was able to successfully ablate the patient’s A-Fib, but an Atrial Tachycardia remained. Speakers throughout the Symposium commented on how difficult it is to find and ablate these Atrial Tachycardia which often remain after A-Fib is ablated. Dr. Mansour later reported that he was never able to find and ablate his patient’s Atrial Tachycardia. He instead had to perform an Electrical Cardioversion to restore her to Sinus Rhythm.

Major Medical Breakthrough in imaging—3D Rotational Angiography

At a luncheon sponsored by Phillips several presenters described 3-D Rotational Angiography which appears like a 3-D fluoroscopic (X-ray) image of the heart made while the camera rotates around the body. Electrogram (electronic information such as the location of A-Fib sources) can be superimposed over these live 3-D images. Real time image integration will be available shortly.

To this author 3-D Rotational Angiography is a major medical breakthrough in imaging and mapping the heart.

Non-Invasive Ablation

The last presenter of the Symposium, Dr. Wyn Davies of St. Mary’s Hospital in London, described what may become another medical breakthrough—a non-invasive method of performing ablations using focused-beam X-Ray. The CyberKnife system can focus X-Ray beams on precise spots in the heart without damaging adjacent areas. Similar systems have already been used in many patients to ablate cancer tumors without damaging other tissues. A robotically controlled linear accelerator can track and compensate for respiratory and heart beat motion. However, unlike RF or Cryo ablation, the results of these X-Ray ablations will not be known till 30 to 60 days after the ablation. A system with this much delay may never become suitable for complicated cases of A-Fib (Persistent or Chronic A-Fib) where there are often many different sources of A-Fib pulses not easily mapped and ablated.

The Atrial Selective Drug Ranolazine

The medicine ranolazine, recently approved by the FDA, is of great interest to A-Fib doctors, because it is atrial selective (it only affects the atrium and not the ventricles). Though it has not been approved by the FDA to treat A-Fib, panelists said that it is being used off-label* combined with amiodarone (also atrial selective. This combination seems to reduce the excitability of A-Fib areas of the heart. *”Off-label” means outside of licensed indication—the clinical application of prescribed drugs for indications other than those approved by the FDA. Off-label uses are legal and may be in the best interests of patients. But they have not received the same degree of independent scrutiny through randomized clinical trials as have approved indications. One can not advertise or market a drug for something other than what has been approved by the FDA.

Update on the Watchman Device

Dr. Zoltan Turi of Cooper University Hospital in Camden, NJ, in discussing mechanical devices to prevent stroke, indicated that the Watchman Deviceshowed the most promise, had completed its clinical trials, and was close to getting FDA approval.

Catheter Ablation Survey

Up to this time the last comprehensive survey of the methods, safety and efficacy of catheter ablation for A-Fib was completed in 2002. Dr. Riccardo Cappato of the Istituto Policlinico San Donator in Milan, Italy reported on an updated survey of 2003-2006. This survey showed there was a larger success rate of ablated patients free of antiarrhythmic drugs in 2006 than in 2002, the overall success rate of ablations was similar in 2002 and 2006, but the complications rate for 2006 was lower.

Surgery for A-Fib

Dr. Ni Ad of the Inova Heart and Vascular Institute in Washington, DC described his Full Maze minimally invasive operation using Cryotherm energy with a 93% success rate. He recommends that patients with Paroxysmal A-Fib have a Catheter Ablation procedure. Dr. James Edgerton of the Heart Hospital in Plano, TX uses the Wolf Mini Maze bipolar clamp combined with an extended lesion line set, and staples shut the Left Atrial Appendage. Dr. Ralph Damiano, Jr. of Barnes Jewish Hospital in St. Louis uses Body Surface Mapping and Dominant Frequency Mapping while ablating with the bipolar clamp.He stresses tailoring the operation to the needs and structural geometry of each patient. A typical Cox Maze lesion set may be too much for some patients and not enough for others. He mentioned that the Mini Maze operation is less successful in patients with large atriums. Also, a Mini Maze can not be re-done or touched up, because of the scarring from the operation. He said that the bipolar clamp lesions do not disrupt or impede circulation or nerve paths in the heart.

A-Fib Induces Fibrosis

Dr. Stanley Nattel of the Un. of Montreal, Canada reported that lone A-Fib may induce fibrosis and collagen formation in the heart.

(Author’s Note: Dr. Nattel’s research may help resolve the chicken and the egg controversy of whether A-Fib induces fibrosis or vice versa.
This is an important finding for A-Fib patients who face the choice of staying in controlled A-Fib by taking medications or having a Pulmonary Vein Ablation. It seems the more one stays in A-Fib, the more fibrosis and collagen are formed in the atrium [the remodeling effect]. Fibrosis is most likely permanent, whereas other effects of A-Fib can often be reversed. For patients considering a PVA(I), it’s probably better to get an ablation and cure one’s A-Fib sooner rather than later.)
However, Dr. Nicholas Peters of St. Mary’s Hospital and Imperial College in London, England stated that, even though A-Fib is a progressive disease which tends to get worse over time, some patients never progress from Paroxysmal (occasional) A-Fib to Persistent or Chronic (permanent) A-Fib.

Visually Measuring the Success of a PVA(I)

Dr. Andre d’Avila of the Un. of Miami proposed a novel way of assessing the success of a Pulmonary Vein Ablation. He showed that, before a successful PV ablation, the Pulmonary Vein sheaths expand and contract as the heart beats. But after a successful PVA(I), these PV sheaths no longer change in volume. Imaging or visualizing PV contraction would be a non-invasive and relatively easy method of  confirming PV isolation.

Genetics may play a significant role in the development of A-Fib

Dr. Dan Roden of Vanderbilt University described how genetic research may become important to A-Fib patients. He predicted that within five years research may identify what genes predispose a patient to A-Fib. Then personalized therapy can be developed based on the patient’s genes. “Lone A-Fib” (A-Fib without a known cause) may actually be caused by genetics. Technology Update For those of you interested in new A-Fib therapy products showcased at the Symposium, see http://www.jafib.com/published/webFormat/Khaykin/khaykin.pdf (Thanks to Dick Inglis for this reference.)

PRESENTATIONS

Dr. Dan Roden of the Vanderbilt University School of Medicine discussed how genetics may play a important role in a patient’s development of A-Fib. The title of his presentation was “AF as part of the spectrum of monogenic cardiac diseases (HCM, LQTS, Brugada, sodium channel mutations & SA function, HCN Mutations and SN Dysfunction).” (These medical terms and abbreviations are described in the footnote at the end of this report.)

The Role of Genetics in the Development of A-Fib

Dr. Roden pointed out that most discussion of A-Fib is concerned with the downstream aspects of A-Fib such as treatment options. But we should be as concerned with the upstream triggers of A-Fib such as genetics.

Genetic Research

Genetic research is important to A-Fib patients, because genetic variants may predispose people to A-Fib. Dr. Rogan suggested that within five years current genetic research may identify what properties in a patient predispose them to A-Fib. Once this has been determined, a personalized therapy can be developed for each patient based on their underlying genetic predisposition.

Genetic Types of A-Fib

Genetic studies indicate there are different types of A-Fib diseases or A-Fib provokers, such as those mentioned in the above title. According to Dr. Roden, telling someone, “You have A-Fib,” is like saying, “You have cancer,” without indicating what type of cancer.A-Fib is part of the spectrum of “channel-opothy diseases,” particularly of Sodium Channel diseases. (“Channel-opothy” refers to the various chemical and electrical currents that are irregular in a diseased heart.) For example, Dr. Roden pointed out that a Sodium Channel deficiency or genetic mutation on gene SCN5A can lead to “Sodium Channel Deficiency A-Fib” and may be responsible for familial A-Fib. In another example Dr. Roden described how people with Hypertrophic Cardiomyopathy tend to also develop “HCM A-Fib” (22%). The bigger their left atrium and the more severe their heart functions, the more they tend to get HCM A-Fib. Also, people with both Hypertrophic Cardiomyopathy and HCM A-Fib are more likely to develop heart failure.

Lone A-Fib

Lone A-Fib” is usually described as a type of A-Fib without any known causes. But Dr. Roden theorizes that Lone A-Fib is really a genetic disease. He recommended that young people with Lone A-Fib be referred to Dr. Patrick Ellinor at Massachusetts General or to Dr. Dawood Darbar at Vanderbilt for genetic testing, in order to sort out what their genes are and what makes them susceptible to A-Fib.

(Editor’s Note: It may be of great help to both patients and doctors to know what kind of A-Fib one has. Genetic research may make this possible.)

Footnote: “monogenic” controlled by a single gene “HCM” Hypertrophic Cardiomyopathy “LQTS” Long QT Syndrome “SA” Sinoatrial “HCN” Hyperpolarization-activated Cyclic Nucleotide Gated Ion Channel “SN” Sinus Node

Dr. Pierre Jaïs described how the French Bordeaux group ablates atrial tachycardias that often occur after A-Fib has been eliminated. “Advances in the Management of Atrial Tachycardia after AF Ablation.” One of the major problems for doctors performing Pulmonary Vein Ablation procedures is Atrial Tachycardia which remain after A-Fib has been ablated. These Atrial Tachycardia signals are often elusive and difficult to map and ablate. The Bordeaux group currently terminates A-Fib in 84% of cases. But only 13% of these patients return to Sinus Rhythm. While 71% still have Atrial Tachycardias. Instead of using 3-D mapping which can be time consuming and impractical (3-D systems often generate system noise which can mask Atrial Tachycardia signals), the Bordeaux group uses a conventional mapping system using only a multi polar mapping catheter in the Coronary Sinus and an ablation catheter. If the Atrial Tachycardia are regular, they move to Step 3 in the flow chart below and do a focal ablation. If the Atrial Tachycardia are irregular, they move to Step 2 below and check for Macroreentrant circuits (Perimitral, Roof, and Peritricuspid) and perform linear ablations. If the circuits are not Macroreentrant, they move to Step 3. (In the slides below “CL” is the abbreviation for Cycle Length, “PPI” refers to Post Pacing Interval, a method of pacing the atria to find arrhythmias.)

(Editor’s Note: Atrial Tachycardias that remain after an ablation can be a significant problem for A-Fib patients. Often their sources are not found, and a patient is cardioverted hoping the healing process will eventually eliminate these Atrial Tachycardias. But they may come back and lead to more A-Fib or A-Flutter. The Bordeaux Group, by developing a simple, step-wise approach to eliminating Atrial Tachycardias, may significantly improve Catheter Ablation procedures. Another important finding of this study is that so many ablations (71% of “successful” ablations) develop Atrial Tachycardias which can persist after an ablation.)

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Last updated: Wednesday, July 6, 2016

Boston AF Symposium – 2010

15th BOSTON AF SYMPOSIUM, January 14-16, 2010
“Atrial Fibrillation: Mechanisms and New Directions in Therapy”

The annual international Boston A-Fib Symposium is one of the most important conferences on A-Fib in the world. It brings together researchers and doctors who share the latest information. However, if you haven’t read and understood most of A-Fib.com, it may be difficult reading.

Overview and Highlights

The overall mood of the 15th annual Boston A-Fib Symposium seemed to be a sense or feeling of certainty in making progress and moving forward.
One might describe this Symposium’s signature or most prominent topic of interest as “New Achievements in A-Fib Imaging/Mapping.”

4D & 5D Imaging/Mapping in A-Fib

In a thought provoking and somewhat controversial presentation, Dr. Douglas Packer described new developments in A-Fib Imaging/Mapping as “4D and 5D Imaging.”

Over the last few years, A-Fib doctors and medical companies have developed very sophisticated Imaging/Mapping systems for doing A-Fib ablations. For example, in the Satellite Case Transmission presented by Massachusetts General, Dr. Moussa Mansour watched on a monitor a 3D rotating, detailed color cartoon image of the patient’s heart. He then pushed a button to open up the end of the heart and look inside.

Rotational Angiography produces even more astounding images. Instead of cartoon recreations, it shows the patient’s actual heart in a 3D, real time rotation. One can see the heart in every detail and can watch where the ablation catheter is in the heart. (Seeing this for the first time takes one’s breath away.)

Time is the 4th A-Fib Dimension, according to Dr. Packer. An example is the CardioFocus Endoscopic laser balloon Ablation System. The doctor operating the CardioFocus catheter can directly see in color 3D real time where the CardioFocus laser balloon is positioned in the heart. The operator also sees tissue change imaging (A-Fib 4D), how the heart tissue is affected over time as the Near Red Laser Light ablates in overlapping arcs around the Pulmonary Vein opening. (This system is not yet approved by the FDA for use in the US.)

The 5th A-Fib dimension would include other parameters such as integrated temperature sensing imaging probes (and contact force imaging—how much pressure an ablation catheter applies when ablating heart tissue).

Athletes and A-Fib

Athletes and endurance training was the subject of two sessions and a great deal of discussion. Dr. Stanley Nattel presented studies indicating that high level physical training doubled the risk of developing A-Fib. In Dr. Nattel’s animal lab experiments, high level exercise training (30+ miles/week) developed A-Fib by two mechanisms:

  1. increasing Vagal tone,
  2. producing structural remodeling of the heart—atrial overload leads to atrial enlargement, increases atrial fibrosis and ventricular hypertrophy.

Dr. Riccardo Cappato described how A-Fib hurts athletes’ performance and their ability to exercise. It also makes them ineligible for competitions because they fail pre-qualifying tests (other professions and avocations such as pilots have this same problem).

Because athletes often cannot tolerate antiarrhythmic drugs and/or refuse to take them, Dr. Cappato and other doctors in a panel discussion say they recommend Pulmonary Vein Ablation as first line treatment for athletes. A successful PV ablation restores athletes to full competition intensity and makes them re-eligible to compete.

Current guidelines state “catheter ablation of A-Fib in general should not be considered as first line therapy.” At least one antiarrhythmic med should be tried first.

But the guidelines also state, “in rare clinical situations, it may be appropriate to perform catheter ablation of AF as first line therapy.” Dr. Eric Prystowsky, who was instrumental in writing the current A-Fib guidelines, stated that he uses PV Ablation as first line therapy for athletes because of the above reasons.

Ablation Not a Permanent “Cure” For A-Fib

When counseling patients with A-Fib, a successful A-Fib ablation is considered the only current hope of a permanent “cure” for A-Fib (as compared to, for example, Rhythm or Rate control drugs which tend to lose their effectiveness over time). But a study by Dr. Francis Marchlinski cast doubt on this hypothesis.

He persuaded patients who had experienced successful PV ablations and who were A-Fib symptom free, to be re-examined in the EP lab. He found that some had Regrowth/Reconnection in their ablated vein openings even though they were A-Fib symptom free. He also examined patients who had Regrowth/Reconnection and reoccurrence of A-Fib after a successful PV ablation.

He estimated that there is a 5-6% chance of Regrowth/Reconnection each year, out to five years. He doesn’t have data for beyond five years.

Contact Force Sensing

A Mini-Symposium was devoted to the subject of Contact Force Sensing.
When performing an ablation, doctors monitor power, duration, and temperature; but not how hard the ablation catheter presses on heart tissue. Insufficient ablation catheter contact can produce lesions that don’t work or that do not penetrate heart tissue, while too much contact or pressure can cause perforation or damage to adjacent structures like the esophagus.

Dr. Karl-Heinz Kuck described a study using the TactiCath contact force sensing system which found a high variability of force applied both between different operators (which one would expect), and during an ablation by one operator. 12% of ablation burns had a low force contact of under five grams. (Perhaps this is one of the causes of re-occurrence of A-Fib after ablation.) 82% of patients had a force of over 100 grams applied at least once during their ablation. This could potentially cause steam pop, puncture, and clotting.

Dr. Hiroshi Nakagawa explained how Contact Force Sensing catheters would eliminate the above problems.

Dr. Dipen Shah presented studies which showed that Contact Force Sensing:

  1. Improves lesion effectiveness
  2. Reduces ineffective applications (by indicating insufficient contact force)
  3. Reduces collateral damage
  4. Improves safety
  5. Predicts sites of conduction recovery

Stroke Prevention

A Mini−Symposium was held on Stroke Prevention in A-Fib.

Dr. David Singer described why A-Fib is a major risk factor for stroke. Because in A-Fib the left atrium doesn’t contract to push blood into the ventricle, clots can easily form especially in the Left Atrial Appendage.

Warfarin (Coumadin) reduces the risk of stroke by 68% and is safe at the proper levels. Warfarin’s risk of producing an hemorrhagic stroke is only 0.3%/year compared to a normal risk of 0.1%/year. But warfarin is underused. 40% of people who should be on warfarin don’t take it, perhaps because of its side effects, bleeding risk, and the difficulty in maintaining proper INR levels.

Aspirin is much less effective, only reducing the risk of stroke by approximately 21%. Clopidogrel, when taken with aspirin, reduces the risk of stroke by approximately 28%. But it significantly increases the risk of major hemorrhage, mostly gastrointestinal.

The good news, both for patients and doctors, is stroke rates in A-Fib are declining.

Dabigatron to Replace Warfarin?

The RE-LY study found that dabigatron reduces the risk of stroke by 30% while also reducing the risk of intracranial bleeding by 30% (dabigatron dose 150 mg). It also reduces vascular death. Unlike warfarin which needs four days loading to be effective, dabigatron works right away. It doesn’t have to be monitored for INR levels. (Both doctors and patients are impatiently waiting for FDA approval for dabigatron, which hopefully will come soon.)

The Watchman Device to Prevent Stroke

The Watchman Device works by closing off the Left Atrial Appendage where 90% of clots/strokes come from. (See The Watchman Device.)

Dr. Zoltan Turi showed a slide of a man who had a Watchman Device installed, but died nine months later from other causes. His family graciously allowed doctors to do an autopsy to examine how the Watchman device had worked. The Watchman Device was covered over by smooth heart muscle tissue which looked like any other part of the heart.

Data from the Watchman Device study showed that it is safe, effective and easily installed (one doctor said he installed them in 20 minutes). A surgeon speaking at the Symposium said he had to remove Watchman Devices (implying that this is a major problem with the Watchman Device). Acknowledging there was a short learning curve when first installing the Watchman Device, Dr. Turi said that to date only four have had to be removed.

An FDA preliminary panel has approved the Watchman Device. But the vote was close, 7 to 5. All agreed that the Watchman Device worked, but some wanted to see more than 800 cases. Clinical trials of the Watchman Device have been extended.

FDA at the Boston A-Fib Symposium

Dr. Randall Brockman and Dr. Jun Dong from the FDA both expressed the FDA’s willingness to help and encourage the development of effective therapies for A-Fib. Dr. Brockman pointed out that A-Fib is a major public health issue (some have called it an epidemic). He also expressed the FDA’s interest in developing an A-Fib Registry (SAFARI). (He was asked why new devices or drugs seem to be always started in Europe.)

Dr. Dong explained the FDA’s Investigational Device Exemption (IDE) and how it could be used by both industry and physicians. He welcomed physician-initiated trials and gave the audience his email address and office phone number.

Measuring Quality of Life in A-Fib

Having A-Fib can be devastating. A-Fib can affect General and Mental Health, as well as Physical and Social Function.

Some A-Fib symptoms can be described and objectively quantified by degree and severity: Palpitations, Dyspnea (difficulty breathing), Chest Pressure and Pain, Dizziness, Presyncope, Syncope (fainting), Exercise Intolerance and Fatigue.Other symptomsare more subjective: such as Anxiety and Depression.

‘Quality of Life’ is a subjective phenomenon based on each person’s perception, experience, beliefs, and expectations. What may be intolerable for one person may not be all that bad for another. Dr. Jeremy Ruskin is proposing an A-Fib Symptom Classification System that also includes Quality of Life. Such a system or universally accepted shorthand would facilitate communication between doctors and patients, and between health care providers.

 

CLASS  SYMPTOM SEVERITY
 I. Asymptomatic  
II. Mild Having a mild effect on a patient’s qualify of life, mild awareness
of symptoms in Persistent/Permanent A-Fib, rare episodes (less than a
few a year) in Paroxysmal A-Fib
III. Moderate Having a moderate affected quality of life, moderate awareness of symptoms on most days in Persistent/Permanent A-Fib,
more common episodes (more than every few months) and/or more
severe symptoms in Paroxysmal A-Fib.
IV. Severe Having a severe effect on quality of life, very unpleasant
symptoms in Persistent/Permanent A-Fib, frequent and highly
symptomatic episodes in Paroxysmal A-Fib; Syncope (fainting);
Congestive Heart Failure because of A-Fib

    

Dr. Jeremy Ruskin Honored

Dr. Jeremy Ruskin from Massachusetts General Hospital was honored for his 15 years of organizing the Boston A-Fib Symposium. He was given a Chelsea clock from Boston and was enthusiastically applauded for his years of service to the A-Fib community.

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Last updated: Wednesday, September 2, 2015

Boston AF Symposium – 2011

16th Annual Boston AF Symposium, January 13-15, 2011 “Atrial Fibrillation: Mechanisms and New Directions in Therapy.”

Overview/Highlights

The overall mood of the 16th Boston A-Fib Symposium was certainly influenced by the winter blizzards which cancelled many flights into Boston (including the author’s). “Let’s make it work” seemed to be the mantra as the organizers moved presenters who did arrive to take the place of those who were delayed. Talks scheduled for Friday were moved to Thursday morning, while Friday’s sessions started a half hour early so that all speakers could give their talks. To the author, this Symposium’s signature or most prominent topics of interest were Recurrence/Reconduction/Durability of catheter ablations, and the identification and use of CFAEs in catheter ablations. Another important topic was dabigatran (recently approved by the FDA) and other blood thinners as alternatives to warfarin.

Recurrence/Reconduction/Durability of Catheter Ablations

Though Pulmonary Vein Ablation (Isolation) (and the Maze-type operations) are currently the only hope of a long lasting fix to make patients A-Fib free, there is increasing evidence that a successful PVA(I) isn’t always permanent. Dr. Karl-Heinz Kuck from St. George Hospital in Hamburg, Germany described early studies which showed recurrence/reconnection within the first years after an ablation, but no or little recurrence after that. However, at his facility he followed for five years 161 patients who were ablated in 2003-4 and found that there was a steady progressive recurrence rate over time which he hypothesized will continue after five years. He concluded that, “we may not (permanently) cure patients with A-Fib.” Of his patients fixed after a single ablation, 60% remained A-Fib free after five years. Dr. Kuck also cited a recent Bordeaux study of patients ablated in 2001-2. Of patients who had a single ablation, only 30% were A-Fib free after five years. Of those who had two ablations, 63% were A-Fib free after five years. But most patients had two ablations. There was an annual 8.9% recurrence rate over time.) [It should be noted that ablation techniques have changed and improved significantly since those early days of catheter ablation].)

Recurrence Due to Reconnected Pulmonary Veins

Dr. Francis Marchlinski of the Un. of Pennsylvania described how in his experience A-Fib recurrence after a PVI is often due to reconnected Pulmonary Veins. “Since PV reconnection is the rule, and not all patients even attempt repeat procedures, then we may be underestimating true efficacy.”

Editor’s Note: In private conversations and in the question and answer sessions, doctors were very concerned about the durability of RF catheter ablations. In a successful ablation doctors isolate the pulmonary veins and check for entrance and exit block—that no A-Fib signals are getting through the lesion lines that isolate the veins. But current ablation techniques all too often create lesions that don’t last.

Other Causes of Recurrence

Dr. David Wilber of Loyola, Chicago cited several studies which also found approximately a 7% yearly rate of late recurrence. But he suggested the causes may not be only PV reconnection, but also heart health factors such as hypertension, diabetes, large left atrium, obesity, smoking, etc. He pointed out that atrial deterioration and heart disease may progress even if a patient is in sinus rhythm due to factors such as atrial remodeling and fibrosis.

Editor’s comment: People in sinus rhythm certainly have improved heart health and quality of life than when they were in A-Fib. But being in sinus rhythm doesn’t mean one can ignore other health and heart factors.

It was recommended that patients A-Fib free after a catheter ablation be counseled and monitored closely for heart health factors, particularly high blood pressure. They should be warned about the possibility that their A-Fib could return if they don’t take care of their overall heart health.

Watershed Year for A-Fib Patients (and Doctors)—Dabigatran Approved

Dr. Daniel Singer of Massachusetts General and Dr. Jeffrey Weitz of McMaster University, Canada described the major improvements in stroke prevention now available to patients. Not only did the FDA approve the new anticoagulant dabigatran (Pradaxa), but other possible replacements for warfarin made major advances in the approval process—rivaroxaban, apixaban, and edoxaban. They described some of the advantages of dabigatran over warfarin:

  1. Warfarin requires crucial monitoring and requires on average 17 INR tests/year, while dabigatran only needs to be taken twice a day to be effective.
  2. Warfarin often interacts with and is affected by other meds and diet, while dabigatran doesn’t seem to have a great deal of interaction problems.
  3. It takes four days for warfarin to be effective or to be eliminated from the body, but dabigatran can be effective in 30 minutes to two hours.
  4. Warfarin can cause bleeding problems, but dabigatran in clinical trials produced a 60% reduction in intracranial bleeds compared to warfarin.
  5. Warfarin is affected by genetics. People starting warfarin need to be tested for variations in the CYP2C9 and VKORC1 genes, while this isn’t necessary when starting dabigatran.)

Aspirin Therapy

According to Dr. Singer, warfarin reverses the risk of stroke in A-Fib, but aspirin doesn’t. In three clinical trials using dosages of 75 mg (baby aspirin) and 325 mg, aspirin produced a Relative Risk Factor of 21% (0-38%), but had no significant impact on severe/fatal stroke.

Editor’s Note: People at low risk of an A-Fib stroke (CHADS2 score of 0-1) are often put on aspirin antiplatelet therapy. But we know that aspirin is not very effective in preventing an A-Fib stroke. Dabigatran, however, would give real protection from an A-Fib stroke. In the clinical trials dabigatran provided a 34% reduction in stroke compared to warfarin.1. The author predicts that dabigatran will replace aspirin for patients at low risk of an A-Fib stroke.

Satellite Case Transmission

One of the highlights of the Boston A-Fib Symposium is always the Live Case Transmission of A-Fib procedures from around the world. This year six different cases were presented, four of them pre-taped. (Previous Symposiums only had two.) The first was from Milan, Italy. Dr. Claudio Tondo from Milan and Dr. Moussa Mansour from Massachusetts General demonstrated the Laser Balloon Catheter (not yet FDA approved in the US) in an ablation on a patient (CardioFocus, Inc., Marlborough, MA). By using a balloon laser delivery system, the variable size balloon can be positioned in a vein opening to encircle the vein. Two overlapping laser energy ablations can usually completely isolate the vein without any gaps. The catheter features direct visualization (endoscopic). The doctor sees directly through the catheter the area he/she is ablating. This is an example of what the doctor sees. “LSPV” is the Left Superior Pulmonary Vein, “LIPV” is the Left Inferior Pulmonary Vein. http://www.cardiofocus.com/pdf/Schmidt_CircEP_Laser.pdf Some doctors expressed reservations that the Laser (and the recently FDA approved Cryo) Balloon catheters might be penetrating the interior of the Pulmonary Veins possibly causing future stenosis (swelling). In the Laser Balloon Catheter trials there were cases of phrenic nerve paralysis. In a taped presentation Dr. Pierre Jaïs from the French Bordeaux group showed an ablation using 3D Rotational Angiography which produces a 3D real time X-Ray image of the heart (Philips Medical Systems). A 3-D reconstruction of a left atrium obtained by rotational angiography

  • LOA indicates left anterior oblique
  • RAO fight anterior oblique
  • CRAN cranial
  • CAUD caudal

Dr. Jaïs said the Bordeaux group routinely does Caviotricuspid Isthmus lesions (Flutter Ablation) in the right atrium during a Pulmonary Vein Ablation (Isolation) procedure. It only takes an extra ten minutes. They do it while waiting to check back on other lesions. They never completely isolate the Left Atrial Appendage which could possibly lead to clots forming in the LAA and A-Fib stroke. If they have to ablate deep inside the LAA, they are careful not to hit the Phrenic Nerve. Dr. Gerhard Hindricks from the Un. of Leipzig, Germany showed a pre-taped ablation featuring 3-D mapping and an electro-magnetic system which compensated for heart movement. Dr. Andrea Natale showed a pre-taped “Convergent” ablation featuring both a Surgeon and an EP working on the same patient. The surgeon used an Endoscopic Catheter which has a light delivery system so that the doctor has direct vision of where they are ablating, similar to the Laser Balloon Catheter above. The surgeon gained access to the outside of the heart through the diaphragm (unlike standard Mini-Maze operations which make traumatic holes between the chest ribs). He did not have to deflate the lungs to ablate the heart (which can be damaging, especially to older patients). After the Surgeon was finished, the EP went inside the heart to ablate areas not touched by the surgery. As explained by Dr. Natale, this Convergent Procedure is used primarily in difficult cases such as long standing Chronic A-Fib.  The Surgeon makes basic ablation lines thereby allowing the EP more time to hunt for and ablate more elusive A-Fib sources within the heart.

Editor’s comment: Surgeons working with EPs to improve the results of Mini-Maze operations has the potential of improving the results of Mini-Maze surgeries for A-Fib patients. However, the convergent procedure had 2 deaths out of a very small number of patients…one atrioesophageal fistula and one death from a large stroke. 
For most A-Fib patients, this “Convergent” operation seems overly invasive and risky, and so far has had poor results.

Dr. Natale mentioned that he never uses amiodarone during an ablation, because it can suppress A-Fib triggers and source areas in the heart. Dr. Moussa Mansour, live from Milan Italy, demonstrated another potentially important development in the catheter ablation field—the Contact Force Sensor Catheter (TactiCath, Endosense, SA). It uses three optical fibers to measure “microdeformation”—how much the catheter tip bends when pressed against heart tissue. The force applied changes the wavelength of light in the optical fibers. The force applied during an ablation shows up on a imaging/mapping system as either yellow, green or red. Doctors can see when they make an ablation how much force they applied to a particular spot. Dr. Vivek Reddy of Mount Sinai Medical Center, New York showed a pre-taped demonstration of a novel noose device that closes off the left Atrial Appendage (Lariat II, SentreHeart, Inc., Palo Alto, CA) in cases where the patient can not tolerate anticoagulants like Coumadin. (The Watchman device which closes off the Left Atrial Appendage requires a patient be on anticoagulants for a couple of months.) From the inside of the heart a balloon is placed inside the Left Atrial Appendage to expand it and make it accessible to the noose device which is inserted from the outside of the heart. The positioning balloon is withdrawn before the Lariat noose is closed around the base of the Left Atrial Appendage. The noose completely closes off the Left Atrial Appendage which dies and is no longer electrically active. The Lariat II snare device has already been approved by the FDA.

USING CFAEs IN ABLATING PERSISTENT A-FIB

CFAEs are Complex Fractionated Atrial Electrograms (an electrogram is a picture of the electrical activity of the heart as sensed by a pacemnaker or catheter in the heart). They are low voltage electrical signals with very short cycle lengths used to identify areas in the heart that need to be ablated. Dr. Jose Jalife of the Un. of Michigan showed how CFAEs can have different forms of waveform propagation, such as Collision, Block, Pivot Point and Slow Conduction. Dr. Mauritz Allessie of Maastricht Un. in the Netherlands described his “double layer hypothesis”—that in cases of persistent A-Fib two layers of dissociated fibrillation waves mutually feed each other eternally. Editor’s Note: Dr. Allessie’s description of a new mechanism to explain how A-Fib works in persistent A-Fib patients is a potential game changer. Dr. Allessie had the following warning about using CFAEs, “If you see an area of continuous electrical activity, do not immediately jump to the conclusion that you have found an area of A-Fib nest or driver.” Dr. Sanjiv M. Narayan of the Un. of California, San Diego, working with the French Bordeaux group, described five different types of CFAEs. He hypothesized that Type I CFAEs (rapid localized activity with low amplitude, rapid rate, and narrow spectral organizational index) might indicate localized rapid reentry and be clear cases of “Focal” A-Fib that should be ablated. (MAP stands for Monophasic Action Potential catheter mapping.) Dr. Shin-Ann Chen of Taipei Veteran’s General Hospital, Taiwan, described how in cases of long standing Persistent A-Fib there are so many CFAEs that it is difficult to ablate them all (his facility has a guideline to limit CFAE ablations to only three sites). He proposes a “Similarity Index” or “New Regularity Index” to identify CFAE sites to ablate. Using non-linear analysis he identifies CFAE sites similar in consistency of interval, electrogram morphology, and voltage amplitude in a particular patient. Ablating these sites results in more successful termination of A-Fib than using other factors such as dominant frequency analysis, fractionated interval analysis, or harmonic index. Dr. David Wilber of Loyola Un., Chicago, explained how current observational systems of identifying CFAEs to ablate are subjective and non-reproducible. However, “automated electrogram analysis provides a rapid, objective, and systematic method of identifying sites with CAFEs” to be ablated. He discussed three different algorithms being tested:

1. Counting peak to peak intervals

2. Counting short coupling intervals between discrete & complex fractionated electrograms

3. Looking at continuous CAFEs

“But we are still searching for the optimal criteria to identify the most useful characteristics for successful ablation.” He also described how pharmaceutical intervention—using the antiarrhythmic drug ibutilide (Corvert) shrinks the number of CFAE sites by prolonging cycle length and decreasing some of the short cycle lengths. Dr. Moussa Mansour of Massachusetts General Hospital in Boston cited several studies indicating that ablating CAFEs is an effective strategy for treating persistent A-Fib. CFAEs may identify A-Fib drivers, may indicate a nearby autonomic ganglionated plexus, or may identify areas of slow conduction for a local reentrant circuit. But current definitions of CFAEs and procedural end points are not uniform. And CFAE areas may be extensive in persistent A-Fib, covering as much as 86% of left atrium sites and requiring extensive ablation. Dr. Mansour discussed several strategies to differentiate “Active” CFAEs from “Passive” (areas that don’t drive or trigger A-Fib).

  1. Pharmacologic intervention reduces the number of CFAE sites. But we don’t know if this affects only the “passive” CFAEs or the “active” CFAEs as well.
  2. Monophasic Action Potential catheters can identify “Far-field” signals which don’t affect A-Fib.
  3. Limiting ablation to Continuous Electrical Activity CFAEs. The Bordeaux group identifies areas with 90% fractionation which may indicate an A-Fib driver
  4. Using a multi-spine catheter for mapping, the Bordeaux group identifies passive activation where a wave simply passes through a field of mapping, whereas Centrifugal activation can represent a driver for A-Fib.
  5. Massachusetts General uses electrical anatomical mapping to identify activation patterns. They found three basic patterns: Colliding Waves (22%), Passive Activation (48%), and Pivot Points (30%). Pivot Points may indicate drivers for A-Fib.
Editor’s comment: The above studies may represent advances in both the understanding and use of CFAEs in ablating persistent A-Fib. Doctors are much closer to finding a definitive strategy for using CFAEs effectively.

MRI (MAGNETIC RESONANT IMAGING) APPLIED TO A-FIB

Dr. Nassir Marrouche of the Un. of Utah described the data enhancement (also called “delayed-enhancement”) MRI process which uses a metallic Gadolinium contrast dye to see in 3D and identify collagen fibrotic areas in the heart. The Gadolinium contrast dye penetrates and stays longer in dead, hardened fibrotic tissue, then washes out later. MRI imaging  does not expose patients to ionizing radiation. Dr. Marrouche uses MRI to “personalize A-Fib treatment.” He separates A-Fib patients by their degree of fibrosis into what he calls four “stages:”

  1. A “Utah 1” patient has little scarring or fibrosis.
  2. A “Utah 2” patient has 5% to 20% of scarring or fibrosis.
  3. A “Utah 3” patient has 20% to 35% scarring or fibrosis.
  4. A “Utah 4” patient has a lot of scarring or fibrosis, over 35%

When considering other factors such as the duration of A-Fib, size of the left atrium, how symptomatic a patient is, whether they are paroxysmal, persistent, long-standing persistent or permanent, what counts—what’s key for success, according to Dr. Marrouche, is the amount of fibrosis in the left atrium. The degree of fibrosis correlates with the danger of stroke. For example a 20%+ degree of fibrosis (stages Utah 3 and 4) indicates a threefold increased risk of stroke. These patients should be kept on Coumadin, Pradaxa, or protected by devices such as the Watchman. Utah Stages 1 and 2 usually only need a PVI to terminate A-Fib. While Utah Stage 3 requires more extensive ablation. Stage 4 is what Dr. Marrouche calls ‘the point of no return. Success rates for catheter ablation are only 3%-4% after one year at Dr. Marrouche’s facility.2 20-30 minutes after an ablation, Dr. Marrouche also uses MRI to check lesion accuracy and safety. If there are problems, the patient can be wheeled back into the EP lab to continue the ablation. Dr. Marrouche is starting the DECAAF trail (Determinant of Catheter Ablation of Atrial Fibrillation using Delayed-Enhancement MRI) at 24 centers around the world. Each patient will have an MRI and be separated into stages before an ablation, then 3 months later will get another MRI to look at the amount of lesions. It’s possible that someone in A-Fib for 6 months could have more scarring/fibrosis than someone in A-Fib for 6 years. In the question and answer session following Dr. Marrouche’s presentation, Dr. Vivek Reddy from Mount Sinai, NY made the following observation, “We should be cautious about equating scarring (fibrosis) with abnormal tissue that should be ablated. There is a discordance between voltage that correlates with scar tissue and CFAEs.” Dr. Pierre Jaïs from the French Bordeaux group, in a study that was developed in collaboration with Dr. Marrouche, addressed this same topic—how do MRI delayed-enhancements (fibrosis) correlate with electrogram characteristics of A-Fib? “We expected to see more fractionation in fibrotic areas, but found just the opposite.” He showed a slide of a patient in persistent A-Fib for 18 months. The patient’s posterior left atrium wall had large delayed-enhancement areas (fibrosis), but no complex fractionated potentials at all. He found this in the vast majority of patients. It was more frequent to find CFAEs in areas of no delayed-enhancement. There was only a 6% overlap of areas of delayed-enhancement and CFAEs, which was an inverse correlation.

Editor’s comments: It must be devastating to sit in Dr. Marrouche’s office and be told you are “past the point of no return,” you are doomed to life in A-Fib because you have too much fibrosis in your heart. What about all the Chronic A-Fib patients who have been made A-Fib free?  Dr. Jaïs’ long-term persistent A-Fib patients, particularly those with underlying heart disease, have a lot of fibrosis but often are made A-Fib free. However, we don’t know if those Chronic patients had more than 35% fibrosis. But one would expect that many did.
A 3%-4% success rate in cases of over 35% fibrosis (Utah Stage 4) is dismal. Could it be that they are targeting for ablation fibrosis areas which research shows do not generate A-Fib signals? One wouldn’t normally expect to see a lot of electrical activity in fibrous tissue. Why not use established protocols for ablating Chronic A-Fib in Utah Stage 4 patients?
What then are the real benefits for patients in using MRI to determine levels of fibrosis? It certainly would be a help for doctors to learn before an ablation how difficult a case might be. But doctors currently get this information from such factors as the duration of A-Fib, size of the left atrium, how symptomatic a patient is, and whether they are paroxysmal, persistent, long-standing persistent or permanent.
Identifying and locating fibrosis areas in the heart doesn’t seem to be much of a help in the ablation procedure.
Level of fibrosis does correlate with the danger of stroke and could be a good tool to identify and treat patients with more risk of stroke.
An MRI might be useful in checking the quality of ablations, but it seems somewhat cumbersome to move a patient back and forth from the EP lab to the MRI room.

Added 4/24/11: In a further study, Stage IV patients were four times more likely to have a stroke than patients with a low level of atrial fibrosis. And the level of fibrosis didn’t always correlate with standard CHADS2 risk scores of stroke. 16.5% of patients with a CHADS2 score of 0 (low risk) and 18.5% with a score of 1 (intermediate risk) had Stage IV atrial fibrosis. Whether you were in paroxysmal or persistent A-Fib didn’t seem to have an impact on the likelihood of stroke rate. Women were three times more likely to have a stroke than men. The researchers hypothesized that, because men tend to get treatment for A-Fib sooner, women had more extensive remodeling and fibrosis than men, which led to a higher stroke risk.3 Editor’s comments: MRIs to measure fibrosis in the heart should become a routine diagnostic tool for anyone in A-Fib. According to this study, the CHADS2 method of evaluating risk of stroke doesn’t work in many cases. Should we retire the CHADS2 and replace it with a more empirical, scientific method such as fibrosis measurement? Some people have argued that there is less risk of stroke if one is in continuous A-Fib rather than paroxysmal (occasional), because one might be more at risk of a clot when the heart stops and starts beating normally. But this study indicates that whether one is paroxysmal or persistent doesn’t seem to influence the risk of stroke. The finding that women are three times more likely to have a stroke than men should be a wake-up call for doctors (and of course for women)! If women hear from their doctor “It’s all in your mind,” or Take a valium,” it’s time to get a second opinion ASAP. An A-Fib stroke is a fate worse than death, if you live through it. Doctors should become more aware of the increased danger A-Fib presents to women. 

HYBRID ABLATION (COMBINING SURGERY WITH CATHETER ABLATION) FOR PERSISTENT A-FIB

Surgeons and EPs Compliment Each Other’s Skills Dr. James Edgerton of Cardiovascular Specialty Associates of North Texas made some interesting comments about Surgeons and EPs (Electrophysiologists). Surgeons excel at making lesion lines. The smooth outside surface of the heart lends itself to this, and the surgeon’s tools are designed for linear ablation. They can see the lines they make and breaks in the lines. While EPs excel at “spot welding.” Catheter tips are punctate by design and can slip off of the uneven surfaces inside the heart. If epicardial (inside the heart) ablation fails, it is because it doesn’t penetrate the endocardium. If endocardial (outside the heart) ablation fails, it is because it doesn’t penetrate to the epicardium. Together these techniques complement each other. If surgeons put a line on the heart, they ought to have a mechanism to prove it is transmural or at least has acute conduction block. Surgeons have difficulty mapping epicardial lesions for several reasons:

  • Pericardial attachments inhibit free movement of a mapping probe.
  • Surgical mapping tools are homemade or (at best) first generation.
  • Surgeons aren’t formally trained in mapping techniques.
  • While EPs can move freely around the inside of the heart, have mature mapping technology, and are formally trained in these techniques.

The “Hybrid” Combined Surgery/Catheter Ablation

Dr. Edgerton described the “Hybrid” combined surgery/catheter ablation procedure which is similar to the “Convergent” Ablation Procedure demonstrated by Dr. Natale in the Satellite Case studies in that a surgeon and an EP work on the same patient. The surgeon, using a bipolar catheter, isolates the Pulmonary veins with encircling lesions, boxes off the posterior atrium wall, makes a connecting lesion to the base of the Left Atrial Appendage, then starts a lesion line down towards the Mitral Annulus which the EP will then finish from the inside of the heart. (Surgeons risk damaging the Circumflex Coronary if they were to continue the lesion line down towards the Mitral Annulus). The surgeon will also encircle and isolate the Superior Vena Cava with less risk of damaging the Phrenic Nerve than with catheter ablation. They simply lift the Phrenic Nerve out of the way before ablating. Surgeons can fully divide the Ligament of Marshall, if necessary. If Ganglionated Plexi are part of the operation, they are targeted and ablated. The EP from inside the heart then completes the line started by the surgeon, does a Caviotricuspid Isthmus line in the right atrium (which current surgery can’t currently access), ablates within the Coronary Sinus (which isn’t possible for surgery without significant risk of bleeding), uses mapping to find and ablate Flutter and CAFEs, and checks for entrance and exit block on all lesions. If part of the operation, they will also check the Ganglionated Plexi lesions.

Traditional Cox Maze Incisions

Convergent Procedure Ablation Lines as done by Dr. Andy Kiser of ACATI. The blue lines are done by the surgeon, the green lines by the EP. Unlike a regular Mini-Maze operation, the patient must be on warfarin for 90 days after the operation. Dr. Edgerton’s center has only done 5 patients so far. Five other centers are doing this “Hybrid” Ablation, but there is very little data available right now. Dr. Edgerton does not normally do Paroxysmal (Occasional) A-Fib cases. “I think they are very well treated with catheter ablation.”

Competition or Collaboration between Surgeons and EPs

Dr. Edgerton described an associate who by using direct patient marketing, evening seminars, etc. “does up to 400 inadequate (A-Fib operations) a year fully sidestepping cardiology and electrophysiology. Although you can get a lot of patients like that, I condemn it. It fully damages the collaborative approach.” Dr. Edgerton, in contrast, believes in working with a fully trained EP. EPs are his best supporters. He depends on EPs for cases. Every patient he has ever operated on had been turned down for a catheter ablation. But he acknowledges that in other parts of the country EPs may see Surgeons as competitors for the same patient base and may be concerned about a loss of revenue. Or there may be ego involved, “I can fix anything.” Or EPs may be concerned about a loss of quality control by sending patients to someone not formally trained in the field. But the Hybrid Ablation answers all these concerns and is the ultimate in collaboration. The EP is right there during the procedure, he has not lost control of the quality or direction of the care of his patient. Dr. Edgerton gave the example of the Medical College of Virginia where Dr. Ellenbogen was the driving force in starting the surgical program working with catheter ablation (but not a Hybrid approach—patients are directed to either catheter ablation or surgery depending on their individual needs). Volumes of both the catheter ablation and surgical programs increased. Patients flocked to a center that has multi-modal therapy available. Practical Problems Dr. Edgerton discussed some of the practical problems associated with the Hybrid Ablation: • Work Flow/Down Time Issues. How do you avoid down time when either the Surgeon or EP is waiting for the other to finish, or the problem of an EP lab or operating room not being used while the EP and Surgeon are working together? One solution is predictable operating times or starting the surgery early in the morning. But minimizing Surgeon down time is more difficult in a Hybrid Ablation. (Dr. Edgerton described how the original Hybrid Ablation procedure was to leave all Surgical wounds open while the EP performed the catheter ablation. The Left Atrial Appendage would be amputated only after all catheters were removed. Now the Surgeon finishes all his work before the EP starts.) • Stages or Simultaneous? It’s possible to do Hybrid Ablation Surgery on a patient, then months later do a catheter ablation. Advantages are that the Surgeon and the EP get to work in their home environment, there are no work flow issues, and maybe some patients won’t need an catheter ablation. Disadvantages are that patients are likely to refuse the second stage, because they feel better and because of the added expense. And two anesthesias increases the complication rate for patients. (One would expect the actual degree of collaboration between Surgeon and EP would be considerably less if they did their work three months apart.) (Northwest Memorial Hospital performs the “Hybrid Maze” in two stages. The Surgeon does a Mini-Maze operation through the chest, then after one month an EP does a catheter ablation. “Stage 1 can be up to 90% effective” and won’t require a Stage 2.)4 Dr. Edgerton prefers the approach where both the Surgeon and the EP take their best shot working together on a patient, the patient has a single anesthetic, and presumably a shorter hospital stay. (Dr. Edgerton’s approach is sequential in that first the surgeon works on a patient, then the EP takes over. In a different “Hybrid” approach, as used for example by Dr. Wilber Su of Heart Rhythm Specialists of Arizona, both the surgeon and the EP work on a patient at the same time. The EP can, for example, tell the surgeon immediately if a particular lesion is effective.)  • Reimbursement Problems In the US system, if you take a patient to the OR and to the EP lab in the same hospital stay, only one will be paid for.

Editor’s comments: From this patient’s perspective, the “Hybrid” and “Convergent” ablations seem very similar. The “Hybrid” Ablation seems more Surgeon driven, while the “Convergent” Ablation seems more EP driven.
Surgeons working with EPs to improve the results of Mini-Maze operations seem to have the potential to improve the results of Mini-Maze surgeries for A-Fib patients.
But patients should consider that the surgery, though called “minimally invasive,” is still major heart surgery. It is invasive, traumatic, complicated, requires considerable surgical skills and experience, and is potentially risky. And added to this are the low but real risks of a catheter ablation. Combining these two levels of risk is probably more dangerous than the sum of the parts.
Which patients should consider a Hybrid Ablation? Possibly someone who has failed one or two catheter ablations, or someone who is morbidly obese (which causes problems for current catheter imaging systems). But it will take more time and data to determine if the “Hybrid” Ablation is better and more effective than current advanced catheter ablation strategies.

Dr. Kowey’s Statement about Ablation

(Due to bad weather the author’s original flight was cancelled. One presentation missed was a debate by Dr. Peter Kowey of Lankenau Hospital, Wynnewood, PA and Dr. Eric Prystowsky of The Care Group, Indianapolis, IN about the merits and proposed features of the SAFARI registry [the Safety of Atrial Fibrillation Registry Initiative]. [SAFARI is a program currently in the planning stages to establish a national registry for A-Fib ablation.]
Dr. Kowey issued a remarkable Disclosure statement which is quoted here. Please be advised it is written as humor and “tongue-in-cheek.”
  • Dr. Kowey doesn’t perform AF ablations, but does refer patients occasionally, and usually under duress.
  • Dr. Kowey would have an AF ablation is he were half dead but awake enough to choose the ablationist.
  • Dr. Kowey would enthusiastically recommend AF ablation for plaintiff malpractice attorneys—especially those who advertise for amiodarone patients on billboards.”

Dr. Kowey’s Disclosure statement also said that he is a consultant, speaker and grantee for over 20 pharmaceutical companies.

The author regrets not being able to report on what was probably a very interesting, lively debate.

Pulmonary Vein Isolation Alone for Long Standing Persistent A-Fib—Dr. Marchlinski

In another surprising presentation, Dr. Francis Marchlinski of the Un. of Pennsylvania said that his institution’s protocol for ablating long standing persistent A-Fib does not include CFAE ablation, Mitral Annular and Left Atrium roof lines, and Coronary Sinus Isolation. (These are considered important steps in other center’s protocols for ablating persistent A-Fib. See Boston AF 2008/Stepwise Approaches for Chronic A-Fib.)

Editor’s comment: Patients with chronic A-Fib may want to be aware that at this time (January 2011) Dr. Marchlinski doesn’t use the stepwise approach that others use, because he has not found the results to be significantly better.

A-Fib and Dementia

Dr. T. Jared Bunch of the Intermountain Medical Center in Utah, in the question and answer session after his talk, gave an example that summed up his presentation. He described how in the hospital he was talking with his patient, a University Professor. The patient would begin a sentence, go into A-Fib and not be able to finish the sentence. Then he’d go back into sinus and finish the sentence. A-Fib was causing him to loose cardiac output and volume of blood to the brain.

Common Causes or Mechanisms of Both A-Fib and Dementia

Dr. Bunch pointed out that A-Fib and Dementia are two diseases that seem to parallel each other. Like A-Fib, Dementia seems to increase with age, diabetes, hypertension, heart failure, smoking history, and systemic inflammation. His center has identified other mechanisms of both A-Fib and Dementia: • Vitamin D Deficiency • ApoE/Genetics  

(Dr. Bunch didn’t have time to elaborate on this genetic component of both A-Fib and Dementia. The author is corresponding with him to obtain more information on this potentially very important genetic finding.)

The above factors cause Microperfusion Deficit (less blood to the brain) and Chronic Hypoxia (loss of oxygen). They often develop Thromboemboli (mini clots) and vascular problems. Ablation Decreases Risk of Dementia and Risk of Stroke and Early Death Dr. Bunch cited several studies and the work of Intermountain Healthcare which showed that people with A-Fib who had an ablation had about the same risk of Dementia as normal people, while people with A-Fib who didn’t have an ablation had much more risk of developing Dementia. But he acknowledged that these studies may be selecting a healthier population rather than ablation having an effect on its own.

(In this patient’s opinion, ablation is probably responsible for decreasing the risk of Dementia by improving blood flow to the brain.)

And people with A-Fib who had an ablation had about the same risk of having a stroke and risk of dying within three years as normal people, while people with A-Fib who didn’t have an ablation were likely to get a stroke within 4-5 years and were more likely to die within three years. In particular, A-Fib patients who developed Alzheimer’s died within six months. Supplements and Drugs to Prevent Dementia Dr. Bunch discussed various supplements used to prevent Dementia:

  • Antioxidant vitamins (E, C, Beta carotene, Flavonoids);
  • They may decrease brain lesions associated with free radical exposure, but evidence is mixed.
  • Vitamins B6, B12, Folate, D; Low levels of folate and D are associated with increased risk of Dementia. Dr. Bunch found that Vitamin D deficiency tracks with the development of both Dementia and A-Fib, but said it is unknown if supplementation reduces risk. (Intuitively one would expect that increasing Vitamin D levels would have a preventive effect on Dementia and possibly on A-Fib.)
  • Omega Fatty Acids/Fish Oil Low intake is associated with Dementia. Studies do show benefit of fish consumption on the risk of Dementia, cognitive decline, or MRI white matter abnormalities.
  • Active Lifestyle Dr. Bunch also pointed out that patients with more active lifestyles have lower risks of Dementia and cognitive decline.

Drugs

Dr. Bunch also discussed various Pharmacologic Therapies used to prevent Dementia:

  • Antihypertensive Agents: Unclear role in prevention, particularly with onset of cognitive decline.
  • Cholinesterase Inhibitors: Long-term use with onset of cognitive decline mildly improves cognitive function compared to placebo.
  • Hormone Therapy: No benefit found.
  • NSAIDS: Lower levels of amyloidogenic Abeta42 protein. Mixed results in clinical trials. One terminated early due to higher risk of heart attack.
  • Statins: Retrospective data suggest lower risk of Dementia. Prospective trials are mixed with some suggesting there is a higher risk of Dementia with statin therapy.Conclusions
  • A-Fib was significantly associated with all types of dementia, particularly in the younger group (under 70 years of age). Patients with A-Fib have higher rates of Dementia compared to those without and have worse outcomes.
  • Early intervention, such as A-Fib ablation, may improve long-term cognitive outcomes and reduce the risk of Dementia to that of patients with no history of A-Fib.

See also previous studies from the Intermountain Medical Center: A-Fib Patients at Risk of Dementia; Ablation of A-Fib Reduces Risk of Alzheimer’s and Dementia; A-Fib Patients at Greater Risk of Developing Alzheimer’s .

Mini-Symposium on Techniques in A-Fib Ablation

Measuring Quality in the EP Lab—Public Reporting “Pursuing Quality in the Interventional AF Ablation Laboratory” Dr. Douglas Packer of the Mayo Clinic in Rochester, MN discussed a topic very important to both doctors and patients—how to measure and report on quality in the EP Center. “Measure something, then you will know something.” “You can’t manage what you can’t measure.” The new health care law will require in two years that A-Fib centers publicly report measurements of efficacy, safety, and process (not just outcome). The Heart Rhythm Society has a task force to develop Performance Measures for A-Fib. Forms are available for doctors to use. The task force is trying to develop:

  • Clear and Explicit Definitions
  • Clinical Coherence of the Variables (a common language and terms)
  • Sufficient and High Quality Timely Data
  • Designation of Appropriate Reference Times
  • Use of Appropriate Outcome and Standard Periods of Assessment and Observation

Dr. Packer described the Mayo Clinic’s recent experience with collecting data for the SAFARI Registry. One nurse had to be taken off line for two weeks to do the work. That kind of commitment isn’t sustainable for the average EP lab. The work needs to be distilled down to something doable. But Dr. Packer pointed out that if EP labs don’t do the work, third parties will, including self-appointed watchdogs that have nothing to do with the process.

Jet Ventilation “Maintaining Catheter Stability to Improve Ablation Outcomes: JET Ventilation, Sheaths and Imaging”

Dr. Francis Marchlinski of the Un. of Pennsylvania discussed how to improve catheter stability during ablations by:

  1. Using detailed landmark imaging to identify anatomic features like ridges which might cause stability problems,
  2. Using a steerable sheath catheter (FlexCath) which can bend 90 degrees and is more flexible than a non-steerable sheath catheter,
  3. Using High Frequency Low Volume Jet Ventilation to limit respiration movement.  A low volume high pressure “jet” of oxygen flows into the airway for a brief time but at a high frequency. The patient receives enough oxygen, but with very little respiration movement. Because the catheter is stable and not affected by respiration movement, more effective lesions can be made.

Dr. Marchlinski’s colleagues at the Un. of Pennsylvania were so impressed and enthusiastic about using Jet Ventilation that he couldn’t pry it away from them to do a randomized study. He did observational studies which showed that when using Jet Ventilation (and steerable catheters), outcomes improved. Less veins reconnected after waiting 30 to 60 minutes after an ablation, and also after 6 months. PVI times were shorter. Patients who had to come back for a repeat ablation had less veins reconnected and smaller segments of veins that needed to be ablated. There was minimal downside risk to patients as long as attention was paid to factors such as CO2 retention. He also protects the patient by allowing for intermittent positive pressure ventilation.

Editor’s Comments: Using Jet Ventilation is a potential game changer for EPs (and perhaps for Surgeons also). Jet Ventilation is a medical breakthrough that could significantly improve catheter ablation.

Where and What to Ablate in the Right Atrium

Dr. Young-Hoon Kim from the Korea University Medical Center, Seoul, Korea, showed how in cases of long standing persistent (Chronic) A-Fib it is often necessary to ablate not only in the left atrium, but in the right atrium as well. CFAEs are often found particularly in the Crista Terminalis and High Septum areas. They are less frequently found at the Low Septum, the junction of the Superior Vena Cava and the Right Atrium, the Sinus Venosum, and the Neck of the Right Atrial Appendage. But when ablating in the Right Atrium, special attention must be paid to not damage the Sinus Node, AV Node, and Phrenic Nerve Sites.

The Role of Left Atrial Appendage Isolation in A-Fib Ablation

Dr. Andrea Natale of the Texas Cardiac Arrhythmia Institute in Austin, TX, described how in cases of patients needing re-do ablations or patients with long standing persistent A-Fib with extensive scarring/fibrosis (over 50%), triggers often originate from the Left Atrial Appendage (LAA). By electrically isolating the LAA through segmental ablation or more extensive ablation, 71% of these difficult patients were rendered A-Fib free. (They also found many A-Fib triggers in the Coronary Sinus.) Dr. Natale stressed the need to map and record from the LAA first, that A-Fib signals from the LAA can spread quickly throughout the heart and be mistakenly identified as coming from other areas. Does electrically isolating the LAA harm how the LAA functions (LAA velocity and mitral inflow)? Dr. Natale found that 2/3 of patients’ LAAs functioned completely normally even though they were electrically disconnected. He didn’t know why. He keeps the other 1/3 of patients on Coumadin to prevent clots forming in the LAA. Or he could use an occluder device such as the Watchman to close off the LAA. Dr. Natale’s findings compliment and confirm other research which points out the importance of the LAA in difficult A-Fib cases, such as the work of the French Bordeaux group which ablates the base of the LAA as part of the first step in ablating for Chronic A-Fib. See Boston AF 2007/Bordeaux Treatment for Chronic A-Fib.)

Improving Results with the CryoBalloon Catheter

Dr. Wynn Davies of St. Mary’s Hospital in London, England discussed the four types of catheters producing encircling lesions—balloon catheters (Cryo and Laser) and curvi linear multi-electrode and mesh catheters which use multi-phase RF. (See Research & Innovation/Technology Innovations/Balloon Catheters and MultiElectrode RF Ablation Catheters.) He has been using the Cryo Balloon catheter and had many tips on its use. He prefers to use an extra stiff guide wire for extra support and  because it is more capable of bending into difficult branches of the PVs. Once the balloon is opened, it can be pushed into the PV antrum as hard as one likes. The contrast dye is used to show there is no leakage.  When the Cryo power is applied, it produces an excellent freeze and isolation. A catheter is placed in the Superior Vena Cava to pace the phrenic nerve whenever Cryo energy is applied to the right PVs. The phrenic Nerve runs very close to the Right Superior Vein and can sometimes run close to the Right Inferior Vein. He waits for cryo adherence before starting phrenic nerve pacing. He primarily uses the larger 28mm balloon catheter. He starts in the left upper vein, then moves to the left lower vein, then moves to the right upper and lower veins.  The encircling lesions overlap each other. He applies Cryo energy for five minutes per ablation, but others have used 4-6 minutes. Further studies are ongoing to determine how much time is necessary for a good CryoBalloon ablation. In a European study of 350 patients, an average of 11 Cryo ablations were required to isolate the PVs (under 3 per vein). 97% of the veins were isolated, the vast majority with the larger 28 mm balloon. 75% of Paroxysmal patients were A-Fib free after 18 months. Fluoroscopy time was around 40 minutes. Ablations times averaged 100 minutes less than RF. There were 26 Phrenic Nerve Palsy cases, 24 of those cases used the smaller 24 mm balloon catheter (the smaller balloon may penetrate too deeply into the vein and get too close to the Phrenic Nerve).

Coping with Reconnection

Dr. Hans Kottkamp of the Hirslanden Heat Center in Zurich, Switzerland, discussed how to recognize and deal with PV reconnection. “How to Identify Early Reconnection After Acute PV Isolation.” He showed how measuring Entrance Block alone may not reveal gaps in ablation lines. Both Entrance and Exit block (bidirectional block) are necessary to reveal gaps. He discussed studies in which doctors waited either 30 minutes or 60 minutes after an ablation to check for reconnection. 1/3 of early reconduction can be found if one waits 60 minutes to map for bidirectional block and close any gaps. Clinical outcomes are better if one waits 60 minutes rather than only 30.

Editor’s comment: The author wonders how practically doctors can afford to leave a patient for 6o minutes. Conscious sedation would be impossible. Would an extra hour of general anesthesia be good for a patient? Such a policy might cause serious problems for smaller operations, hospital administrators, and insurance companies who would have to pick up the tab for this extra ablation laboratory time. Larger operations with multiple laboratories might be able to schedule a 60 minute break for patients. But it seems unrealistic to expect most A-Fib ablation doctors to wait 60 minutes after an ablation to check for reconnection.

But Dr. Kottkamp pointed out that bidirectional conduction block is just a functional end point. It cannot differentiate between reversible and irreversible tissue excitability after ablation. He suggested that adenosine might be used to identify reversible tissue damage after ablation. “Adenosine restores PV LA conduction by hyperpolarizing PV cells and thereby enhancing sodium current availability.” It may reveal potentially reversible tissue injury which will react differently than tissue with permanent injury. He pointed out that RF tissue change including edema (swelling), and perhaps inflammation may contribute to late reversibility and reconnection. Strategies to Prevent Atrial-Esophageal FistulaDr. Vivek Reddy of Mount Sinai Medical Center in New York discussed different strategies to avoid Atrial-Esophageal Fistula (A Fistula is an abnormal duct or passage, in this case between the esophagus and the left atrium heart wall). 1. Minimizing power at the posterior wall when ablating. But we don’t know what the amount of power is that would minimize damage. Even applying 10 Watts can heat up the esophagus, because the posterior wall of the left atrium can be very thin in spots, and the esophagus can be found right next to the posterior wall of the left atrium. He showed a slide indicating the maximum temperatures where ulceration was seen and the maximum temperatures where ulceration was not seen. The marks overlapped. There was no “safe” threshold. Another study recommends limiting RF energy to under 20 Watts for less than 15-20 seconds when ablating in a region next to the esophagus.5 Temperature monitoring. Dr. Reddy cited studies which showed that using temperature monitors does reduce damage to the esophagus. Endoscopies of the esophagus were performed on each patient after their ablation to determine damage. But the type of temperature probe is very important. A temperature probe with a surrounding plastic sheath (like a stethoscope) can take 40 seconds to show a significant temperature rise. If you strip away the plastic cover, the temperature goes up in only a few seconds. In a typical ablation when the medical staff sees a temperature rise, they stop the ablation. But the temperature will continue to rise. After a 30 second ablation, it may take an additional 80 seconds for the temperature to come back down. Is this temperature rise causing damage to the esophagus? Temperature monitoring isn’t perfect. Where the temperature probe is located will change the readings. He cited animal studies where they inserted a balloon with many temperature probes into an esophagus. If the temperature probe was on the side where one was ablating, the rise in temperature was almost immediate. But if it was on the other side, there was a slow rise; and when the ablation was stopped, the temperature continued to rise before eventually falling. He cited a small study from Brazil where an catheter with a temperature probe was placed in the esophagus and moved side to side depending on where the heart ablation catheter was positioned. This system produced no ulceration. 3. Moving the esophagus. The esophagus can move spontaneously during an ablation. Can it be moved manually away from where a catheter is ablating? Using barium paste to identify the location of the esophagus, he showed an experimental system using a soft plastic tube with a stylet (a slender medical probe) to move the esophagus. But prospective randomized studies need to be done to determine if this system actually protects the esophagus. Can moving the esophagus cause other problems?

Editor’s Note: Moving the esophagus (combined with temperature monitoring) seems like an amazingly simple, practical method of avoiding damage to the esophagus. In fact, one of the vendor booths at the Symposium demonstrated such a system that was trying to get FDA approval.

4. Force monitoring. Force applied seems to make a difference, whether or not one uses temperature monitoring. 5. Conscious Sedation vs. General Anesthesia. Dr. Reddy describes studies by Dr. Natale in which 48% of patients under General Anesthesia (completely unconscious) had esophagus ulceration versus only 4% of patients under Conscious Sedation. 6. Protecting the Esophagus. Dr. Reddy described experimental studies in which a cooling balloon was positioned in the esophagus to protect it from heat from the ablation catheter. This decreased the chance of ulcer formation in the esophagus. But the cold might attenuate lesion formation by the RF catheter. 7. Cryo Ablation. Editor’s Note: Small studies have indicated that Cryo (Freezing) Focal Ablation at regions near the esophagus is safe. Cryo “can cause transmural injury to the esophagus but may be less likely to result in deep ulceration and fistula formation.”5However, this strategy involves removing an RF Catheter and inserting a Cryo Catheter which lengthens and complicates the ablation procedure. Hospital administrators and insurance companies may not approve of this strategy because of the added costs. 8. Proton Pump Inhibitors. Not discussed in Dr. Reddy’s talk that was limited to 10 minutes was a strategy to avoid esophageal fistula after, rather than during, an ablation. Most centers now put patients on Proton Pump Inhibitors like Nexium for 2-3 weeks after an ablation. Even if there is ulceration in the esophagus from the heat of an ablation catheter, the Proton Pump Inhibitors prevent gastric acids for backing up into the esophagus in case of Gastroparesis (weak stomach not emptying its contents) or GERD (Gastroesophageal Reflux Disease). Atrial-Esophageal Fistula usually occur 2-3 weeks after an ablation. It takes that long for gastric acids to burn through the esophagus areas structurally weakened by catheter heat from inside the heart. Some centers also treat patients for 2-3 week after an ablation with sucrafate (Carrafate), a medicine used to heal ulcers. Please be advised that Atrial-Esophageal Fistula is a very rare complication [approximately 1/1000+ cases] that is becoming even more rare because of the use of preventive strategies. Because Atrial-Esophageal Fistula is such a rare complication, it may be difficult for doctors to determine which of the above strategies is the best and most essential to be used. But from this patient’s perspective, anyone interested in getting a catheter ablation for A-Fib should ask their doctor what precautions they take to prevent Atrial-Esophageal Fistula.)

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Return to AF Symposiums by Year

Return to Index of Articles: AF Symposium: Steve’s Summary Reports

Last updated: Friday, August 28, 2015

References    (↵ returns to text)
  1. http://www.theheart.org/article/1142899.do
  2. Ibid.
  3. http://www.stopafib.org/newsitem.cfm/NEWSID/317/fibrosis from atrial remodeling/atrial fibrillation stroke risk
  4. http://www.nmh.org./nm/af+treatments-hybrid+maze+procedure
  5. Bahnson, Tristram D. “Strategies to Minimize the Risk of Esophageal Injury During Catheter Ablation for Atrial Fibrillation.” Pacing and Clinical Electrophysiology, 2009;32(2):248-260. http://www.medscape.com/viewarticle/587908?src=emailthis
  6. Bahnson, Tristram D. “Strategies to Minimize the Risk of Esophageal Injury During Catheter Ablation for Atrial Fibrillation.” Pacing and Clinical Electrophysiology, 2009;32(2):248-260. http://www.medscape.com/viewarticle/587908?src=emailthis

Boston AF Symposium – 2012

17th BOSTON AF SYMPOSIUM, January 12-14, 2012 “Atrial Fibrillation: Mechanisms and New Directions in Therapy”

The annual international Boston A-Fib Symposium is one of the most important conferences on A-Fib in the world. It brings together researchers and doctors who share the latest information.  However, if you haven’t read and understood most of A-Fib.com, it may be difficult reading.

2012 BAFS – Steve at Entrance

Overview/Highlights

The overall mood of the 17th Boston Atrial fibrillation Symposium seemed to be one of confident anticipation. Many presenters expanded on how, by next year, there will likely be four new anticoagulants approved by the FDA (dabigatran [Pradaxa] already FDA approved, rivaroxaban (Xarelto—FDA approved Nov. 4, 2011), apixaban, and edoxaban). Doctors and patients will finally have alternatives to warfarin!

The dominant theme of this year’s Symposium was improved stroke prevention. On Friday, January 13, there were no less than nine presentations on stroke prevention, and the Thursday panel discussion of “Difficult Cases” mostly focused on anticoagulation problems.
The second most discussed topic was Pulmonary Vein Reconnection after ablation—(the most urgent topic of greatest concern for A-Fib doctors and researchers).

Editor’s comment: The author also launched our new book “Beat Your A-Fib: The Essential Guide to Finding Your Cure” at this year’s Symposium. It is available both as a print book (see Amazon.com for reviews) and in a .PDF version. Visit our book site at www.BeatYourA-Fib.com for more info.

This year’s Symposium featured a number of mini-symposia and individual presentations focusing on topics such as:

  • The role of rotors in experimental and human A-Fib (very divergent opinions).
  • Basic science topics related to A-Fib.
  • Advances in the management and treatment of persistent A-Fib.
  • Lesion monitoring during catheter ablation.
  • A-Fib Guidelines and regulatory issues. The newest Guidelines were released at this year’s Symposium.
  • Surgical ablation and surgical stroke prevention.
  • New technology and methods of treating A-Fib.
  • Pharmaceutical and non-pharmaceutical strategies for stroke prevention.
  • In addition to live satellite case transmissions where the attendees could watch actual ablations being performed, there were also pre-recorded teaching cases. These sessions were among the most popular among attendees. They showcased the most advanced technologies in the rapidly evolving field of A-Fib treatment.
  • Advances in antiarrhythmic drug therapy.
  • Minimizing and managing complications in A-Fib ablation.
  • Advances in antiarrhythmic drug therapy.
  • Minimizing and managing complications in A-Fib ablation.
  • Update about current ongoing clinical trials.
  • Reviews of selected basic and clinical science papers on A-Fib which came out in 2011.
  • The use of Registries (detailed open-book record keeping) in clinical practice.
  • Panel and audience discussion of challenging cases in A-Fib ablation. (This session, late Saturday afternoon, though not as well attended as the previous day’s which saw over 1,200 attendees, showcased some of the best, most experienced A-Fib doctors illustrating and discussing some of their most difficult cases.)
Editor’s comment: The author is especially indebted to Dr. Peter Stevenson, the Editor of the Boston AF Symposium News, the official newspaper of the Symposium. This is the first year the Symposium published a newspaper. The news, interviews, advertisements and session coverage was amazingly well done and informative. (I have to admit to being jealous of Dr. Stevenson’s ability to stay up all night producing spot-on summaries of important presentations and get them printed by the next morning.)

The Symposium also featured a great degree of presenter/audience interaction and participation. Each attendee had a remote clicker with 1 through 5 choices. A presenter would, for example, pose a case and give five different treatment options, then allow time for everyone to vote. The percentage of attendees voting for each choice would be almost immediately shown on screen. The presenters and audience would then discuss the results.

Catheter-Based Occlusion

In a presentation on the Surgical Management of the Left Atrial Appendage, Dr. Ralph Damiano, Jr. of Barnes Jewish Hospital in St. Louis, MO discussed, among other subjects, a disturbing case where a catheter-based occlusion device was inserted onto the Left Atrial Appendage (LAA) from inside the heart, but the insertion was unsuccessful. Part of the occlusion device was left protruding from the LAA into the Left Atrium with bare metal wires exposed.

In another disturbing incident at the Symposium, the live satellite presentation from Milan, Italy showed a different LAA occlusion device being inserted into a patient’s LAA. Though we saw in the pre-op how the catheter was flushed out with saline to prevent air bubbles from leaking into the Left Atrium, that’s exactly what happened during the live case.

Editor’s Comments: Even though inserting the Watchman device, for example, is a relatively simple procedure with a high success rate and relatively few complications, if a problem or mistake does happen, it can have a catastrophic result for a patient. For example, a device improperly inserted will most likely have to be removed by major heart surgery. An air bubble inside the heart can potentially cause an embolism, clot and stroke.

This editor in the past thought that the Watchman occlusion device was a wonderful development for an A-Fib patient who couldn’t or didn’t want to be on warfarin. It also was more effective than warfarin in reducing the risk of stroke.

But installing a foreign object inside the heart seems inherently dangerous. Unlike a catheter ablation which has a low risk of adverse events that usually can be corrected without any lasting damage, a mistake or problem inserting an occlusion device inside the heart can cause disastrous problems for patients.
And there are now other options for patients such as a wider choice of anticoagulants or devices that close off the LAA from outside the heart such as the surgical AtriClip or the Lariat II. Patients should not have an occlusion device installed unless the doctor can guarantee a 100 percent success rate without complications. Anything less may result in catastrophic complications for patients.
This editor predicts that, with the many different options now available to A-Fib patients, the FDA will not approve occlusion devices inserted from within the heart. Even though the failure risk is small, a failure can result in complications devastating for patients.

Presentations

TOPICS DOCTOR TITLE OF PRESENTATION
Obesity, Sleep Apnea & A-Fib Nattel Obesity and Obstructive Apnea – Mechanisms of AF Promotion in Experimental Models
Genetics of A-Fib—40% Increased Risk of Developing it if Relative Has A-Fib Ellinor Genetics of AF: How Will We Translate GWAS Findings to Clinical Practice?
Best Clinical Science Papers on A-Fib
Listed By Topics:

  1. Rivaroxaban versus Warfarin
  2. Apixaban versus Warfarin
  3. Irbesartan
  4. Dronedarone
  5. Ablation and Pulmonary Vein Reconnection (Natale)
  6. Waiting 30 Minutes to Check PV Ablations
  7. Utah 4 Stages of Fibrosis Recurrence Rates
  8. MRI-Detected Subliminal Lesions
  9. Acupuncture after a Cardioversion
  10. Kidney Disease Leads to Recurrence After Cardioversion
  11. Chronic Kidney Disease associated with A-Fib in adults
  12. Temporal relationship between A-Fib and strokes
  13. Whites develop A-Fib more than Blacks
  14. After cardiac surgery Whites develop A-Fib more than Blacks
    Danger for A-Fib patients undergoing non-cardiac surgery and even minor outpatient procedures
Prystowsky Best Clinical Science Papers on AF for 2011
Dronedarone Clinical Trials Analysis Kowey Antiarrhythmic Use in Clinical Practice: Focus on Clinical Trials of Dronedarone
Difficult Cases in A-Fib Management
Listed by Patient Cases:
1. 76-year-old man in A-Fib 100 bpm feeling tired & with shortness of breath
2. 86-year-old woman with silent A-Fib & short A-Fib episodes
3. 45-year-old male endurance runner with A-Flutter
4. 60-year-old male in chronic A-Fib for 12 years with cardiomyopathy
5. CHADS2 scores of 0-1 and still suffered strokes (10 different patients)
Aspirin not effective or safe
Ruskin Difficult Cases in AF Management – Antiarrhythmic Drugs, Anticoagulation, and Clinical Decision Making
Yoga & Stress Reduction in A-Fib Lakkireddy Roll of Yoga and Stress Reduction Techniques in the Management of AF

Obesity, Sleep Apnea and A-Fib

Dr. Stanley Nattel from the University of Montréal Canada made an insightful scientific research presentation on “Obesity and Obstructive Apnea— Mechanisms of AF Promotion in Experimental Models” at the 2012 Boston A-Fib Symposium.  It’s well known that obesity and obstructive sleep apnea increase the risk of developing A-Fib. But what isn’t known is what specific mechanisms promote A-Fib, such as hypoxia, autonomic imbalance, left ventricular dysfunction, intravascular volume change, and/or strongly negative intrathoraic pressures.

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 Experiment With Rats Bred to be Fat

In a brilliant experiment Dr. Nattel studied rats bred to be fat. These Zucker obese rats weighed almost twice as much as the normal lean rats in the experiment. Both the obese and lean rats were subjected to either obstructive sleep apnea or non-obstructive sleep apnea, versus a control group of both lean and obese rats not subjected to apnea. The obstructive sleep apnea generated a strong negative chest pressure caused by forced inhalation against the closed airway, while in the non-obstructive sleep apnea group the rats could still get some air through a side port. He then induced A-Fib by pacing in all the rats.

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Sleep Apnea Produces A-Fib

No rats had inducible A-Fib in the absence of apnea, indicating that, at least in this experiment, obesity by itself did not result in inducible A-Fib. Also, it was impossible to cause A-Fib in the obese or lean rats that had an open side port airway. But almost all the obese rats subjected to obstructive sleep apnea exhibited A-Fib. A small number of the lean rats subjected to obstructive sleep apnea also developed A-Fib.

From this experiment one can possibly conclude that obstructive sleep apnea substantially increases A-Fib Inducibility, and significantly more so in obese rats. If we can apply the results of this experiment to humans, we can conclude that obstructive sleep apnea combined with obesity makes someone significantly more at risk of developing A-Fib. On the other hand, just being obese may be a less significant factor in developing A-Fib.

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What Mechanisms Induce A-Fib?

Dr. Nattel went further and tried to identify the actual A-Fib mechanisms behind obstructive sleep apnea and obesity. Some of the rats were subjected to pharmacological autonomic blockade while others received muscle relaxants. Some of the rats who received the pharmacological blockade could no longer be induced into A-Fib, but a majority could. One can conclude that, “autonomic nervous system changes contribute to A-Fib promotion, but only account for a part of it.”

But the rats who received the muscle relaxant did not develop A-Fib. This may be because they didn’t experience the negative pressure generated in obstructive sleep apnea when the airway is closed off.

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Left Atrial Enlargement

But why was A-Fib more inducible in the obese rats? The left atrial dimensions of the obese and lean rats control group were not significantly different, but with progressive apnea there was an almost two-fold increase in atrial dimensions which increased more in the obese rats than in the lean ones. Dr. Nattel tried to prevent this left atrial dilation by inserting a balloon catheter into the inferior vena cava thereby reducing venous blood return.

This prevented A-Fib in 80% of the previously inducible rats. He concluded that there is, “strong, suggestive evidence that it is in fact left atrial distension that is responsible for the A-Fib susceptibility of the obese rats during obstructive apnea.” “A-Fib promotion is primarily due to acute left atrial enlargement, caused by forced inhalation against a closed airway, combined with left ventricular diastolic dysfunction and obesity.”

Dr. Nattel’s innovative experiment showed how sleep apnea is highly likely to cause A-Fib primarily by enlarging and remodeling the left atrium particularly in the obese but also in lean subjects as well.
If you or someone you know snores and/or stops breathing while sleeping and particularly if they are obese, it’s almost guaranteed they are remodeling and harming their heart and will eventually develop A-Fib. They need to have a sleep apnea study done ASAP and correct their breathing problem.

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Genetics of A-Fib—40% Increased Risk of Developing A-Fib If Relative Has It

Genetic research in A-Fib, though in its preliminary stages, has the potential to be a game changer for patients with A-Fib.

Dr. Patrick Ellinor of Mass General, Boston gave a presentation on the “Genetics of A-Fib: How Will We Translate GWAS Findings to Clinical Practice?”

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A-Fib Is Inheritable

“If you have any immediate family with A-Fib, you have a 40% increased risk of developing A-Fib yourself. And the younger that someone in your family gets A-Fib, the more likely you are to have A-Fib.”

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Screen for A-Fib?

If someone has A-Fib, should all their immediate family members be screened for A-Fib? Since in the US alone over three million people have A-Fib, it isn’t possible or practical to screen all family members for A-Fib. And even if we could screen everyone, we don’t yet have the means to prevent A-Fib from developing or even to identify patients with pre-A-Fib.

Editor’s Comments: If anyone in your immediate family has A-Fib, you are very likely to develop A-Fib yourself. You have to be more aware and vigilant than the average person. If, for example, you feel palpitations or a racing heart rate, take it very seriously. Don’t hesitate or delay in going to an Electrophysiologist (EP) to have yourself checked out. Make sure you tell your EP or Cardiologist that your relative has A-Fib.

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Specific Genetic Chromosomes Associated With A-Fib

Dr. Ellinor identified the specific genetic chromosomes currently found to be associated with A-Fib:

  • 1q21
  • 16q22
  • and particularly 4q25

People with a particular combination of 3 genetic variants on chromosome 4q25 are six times more likely to develop A-Fib.

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Further Research Needed

But current research has only revealed “associations.” Further research is needed to determine:

  1. Are these chromosomes associated with and/or do they cause an increased risk of A-Fib stroke, heart failure and death?
  2. Are these genetic variants associated with or do they indicate that a certain treatment should be used or that a certain outcome is more likely?
  3. How important are these genetic variants in the development of A-Fib?
  4. How do these genetic variants affect what types of arrhythmia develop? Do Paroxysmal A-Fib, Permanent A-Fib, or A-Flutter have different genetic profiles?
  5. And most importantly, how do these genetic variants work? What Is the mechanism behind the

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“Right now all we have is an association.” “We don’t have a fundamental understanding as to how the variants themselves lead to the (A-Fib) disease.”

If you have A-Fib, you must warn all your immediate family members that they have a good chance of getting it also. Even though we don’t know yet how to definitively prevent A-Fib, there are some precautions your family members can take:
  1. Avoid binge drinking and heavy partying.
  2. Avoid antihistamines and anything that can stimulate or trigger A-Fib. (see A-Fib Triggers) (This doesn’t necessarily include coffee. Some research indicates coffee may prevent A-Fib.)
  3. Be more attentive to overall health. Obesity, for example, is often a contributing factor to A-Fib. Sleep apnea is known to lead to A-Fib.
  4. Check for deficiencies in essential minerals (electrolytes) like magnesium or potassium? Are calcium levels too high (which may be a trigger for A-Fib)?
  5. Avoid or learn to cope with stress (not always possible).
    There is a tendency in all of us to not tell others if we are ill, perhaps because we perceive it as somewhat humiliating and a weakness in ourselves. But no one should be ashamed of having A-Fib. Most likely it isn’t anything we brought on ourselves. It’s genetic! It’s nobody’s fault!

We are not being fair to our family members by not telling them about our A-Fib. Don’t just mention it in passing. Sit down with them and tell them what A-Fib is like, and that they are at risk. If you love your family, you owe it to them. This applies particularly to your brothers and sisters with whom you may have a loving but somewhat competitive relationship. Anyone in your immediate family must be warned.

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Best Clinical Sciences Papers on A-Fib

Dr. Eric Prystowsky of the Care Group presented the Best Clinical Science Papers on AF for 2011. He started with an initial literature search of 886 articles, then whittled them down to 52 articles which he reviewed in detail.

In a study of the blood thinner Rivaroxaban versus Warfarin (ROCKET AF), Rivaroxaban was “noninferior” to Warfarin and actually was somewhat better at reducing stroke risk. (Patel  MK et al. NEMJ 2011; 365:883-91)

In a study of the blood thinner Apixaban versus Warfarin (ARISTOTLE), Apixaban was better than Warfarin both in reducing stroke risk and in reducing major bleeds. (This is better than “noninferiority.”) (Granger CB et al. NEMJ 2011; 365:981-92) (Apixaban seemed to test better than Rivaroxaban and Dabigatran. Dr. Prystowsky said he was “very much looking forward to using it.”)

In a study of Irbesartan’s effectiveness as an antiarrhythmic med (ACTIVE I), it wasn’t significantly different than a placebo. (Irbesartan is an “angiotensin II receptor antagonist” which blocks the action of certain natural substances that tighten blood vessels, allowing blood to flow more smoothly and the heart to pump more efficiently.) (ACTIVE I Investigators NEMJ 2011; 364: 928-38) Dr. Prystowski suggested that drugs like Irbesartan need to be applied much earlier as preventive medicine (“upstream therapy”) rather than after patients already have A-Fib.

In a study of Dronedarone in high-risk patients with permanent A-Fib (PALLAS), patients taking dronedarone were dying at more than twice the rate of those on a placebo. The ratio of stroke and hospitalization for heart failure was also more than twice as high. (See Time to Stop Taking Dronedarone (Multaq)? and No One with A-Fib Should Be Taking Dronedarone.) (Connolly SJ NEMJ 2011; 365: 2268-76)

Several studies involved Ablation and Pulmonary Vein Reconnection. One study of 831 patients who had a Pulmonary Vein Isolation in 2005 by Hussein (and Natale) was encouraging for patients.  The recurrence/reconnection rate was low (less than 10%) and in a five year study there was no recurrence/reconnection after 36 months. (Hussein AA (Natale) Circ Arrhythmia Electrophysiol 2011; 4:271-8) This study took place at many different A-Fib centers, though they all used similar Pulmonary Vein Antrum Isolation procedures. Instead of making encircling lesions around each of the pulmonary veins, wider ablations encircle each of the two left and two right pulmonary veins in the Antrum area around the veins.

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Waiting 30 Minutes to Check PV Ablations

In a small but important study by Yamane, each PV was checked 30 minutes after the ablation with the stimulant ATP. If reconnected, the PV was ablated again where the reconnection occurred. This process was repeated every 30 minutes until 90 minutes.92% of patients were free of A-Fib recurrence without antiarrhythmic drugs after 370 days (a little over a year).

This may be a major medical breakthrough. This simple technique of waiting 30 minutes and retesting seems to nearly eliminate the problem of recurrence/reconnection and produces a very high success rate. [Several later presentations presented different techniques of waiting 30 or 60 minutes for retesting.] The mean procedure time was only around 3 hours. In practice, doctors can do other important tasks, even work on other patients, during this 30 minute wait time. Any procedure that achieves an over 80% success rate is a major improvement for patients. (Yamane T et al. Circ Arrhythm Electrophysiol 2011; 4: 60-68)

A study by Akoum presented the Utah 4 Stages of Fibrosis Recurrence Rates as determined by DE-MRI. (See A-Fib News: Magnetic Resonant Imaging Applied to A-Fib.) Recurrence rates were significantly higher in patients with Stage 4 (the most or highest) levels of fibrosis/remodeling. (Akoum N et al. J Cardiovasc Electrophysiol 2011; 22:16-22)

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MRI-Detected Subliminal Lesions

Three studies by Gaita, Siklody, and Deneke found that, using MRI, subliminal small lesions or clots, undetectable except with MRI, did occur in the brain after a Pulmonary Vein Isolation procedure primarily when using a Multielectrode Phased-RF Catheter. (See A-Fib News:Silent Clots from Multielectrode Phased-RF Ablation Catheters.) But these silent lesions detected by MRI were not linked to any neurologic defect or cognitive decline, and most (94%) reversed over time. (Gaita F et al. J Cardiovasc Electrophysiol 2011; 22: 961-68. Siklody CH et al. J Am Coll Cardiol 2011; 58: 651-8. Deneke T et al. Heart Rhythm 2011; 8: 1705-11)

In a study by Lomuscio, patients were given Acupuncture after a Cardioversion. Specific needle points were identified. 80 patients with persistent A-Fib were randomized into four groups: Acupuncture, Sham Acupuncture, Amiodarone and No Treatment. The patients receiving Acupuncture or Sham Acupuncture had 10 sessions of 15-20 minutes weekly starting within 48 hours of cardioversion.

The most freedom from recurrence occurred with the Amiodarone group. The Acupuncture group came in second but approximated the results of the Amiodarone group. The No Treatment group had significantly more recurrence, while the Sham Acupuncture group had the worst recurrence rate.

Acupuncture, though not quite as effective as Amiodarone, might be a welcome option for patients who can’t tolerate or don’t want to risk the toxic side effects of Amiodarone. Cardioversion has a notoriously high recurrence rate. “50 to 75 percent of patients eventually develop Atrial Fibrillation again.”1 Ten weekly Acupuncture sessions seems a small price to pay to avoid going back into A-Fib.
But one surprising result of this study was the poor results of the Sham Acupuncture group. One would expect a placebo effect from these ten Sham Acupunctures. But instead the misdirected Acupuncture needle pricks produced more recurrence than No Treatment. The lesson to be learned is for patients to make sure their Acupuncturist knows what spots to hit and has a proven track record in treating A-Fib. Unfortunately these Acupuncturists are hard to find. (Lomuscle A et al. J Cardiovasc Electrophysiol 2011; 22: 241-7)

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Kidney Disease GFR (Glomerular Filtration Rate) Relates to Recurrence After Cardioversion

In a study by Schmidt, freedom from recurrence after a cardioversion related to higher levels of GFR (Glomerular Filtration Rate). GFR is a measurement of how well the kidneys function or the stage of kidney disease. (Schmidt M J Cardiovasc Electrophysiol 2011; 22: 1092-8)
In a related study by Baber, Chronic Kidney Disease (CKD) was associated with A-Fib in adults (REGARDS study). (Baber U et al. Circ Arrhythm Electrophysiol 2011; 4: 26-32)

This is an important medical breakthrough observation for patients. Kidney disease can be added to the list of causes or triggers of A-Fib.
One doctor in the question-and-answer session said that kidney disease is associated with fibrosis, inflammation and the release of factors in the blood which affect other organs, and may be why kidney disease is associated with A-Fib.

In a study by Daoud (TRENDS), they found a temporal relationship between Atrial Tachycardias/A-Fib and Cerebrovascular Events (strokes).

(This is not at all surprising. People with A-Fib have 5-6 times more chance of having a stroke [unless treated]. But what is needed is more long term monitoring. One can’t always expect an A-Fib stroke to occur right after an A-Fib episode.) (Daoud EG Heart Rhythm 2011; 8: 1416-23)

A study by Huxley (ARIC) found that Whites developed A-Fib more than Blacks.

It isn’t clear why, since blacks have more risk factors for A-Fib such as hypertension. Genetic research might someday explain why this occurs. (Huxley RR Circulation 2011;123: 1501-8)

In a related study Rader found that, after cardiac surgery Whites developed A-Fib more than Blacks (1.74 ratio). (Rader Circ Arrhythmi Electrophysiol 2011; 4: 644-52)

A study by Diepen raises serious danger for A-Fib patients undergoing noncardiac surgery and even minor outpatient procedures.

It’s well recognized that someone with heart failure, for example, has a greater risk of dying during non-cardiac surgery (9.3%), and that both patients and surgeons in these cases must be aware of this added risk. But what this study shows is that patients with A-Fib also have a high risk of death (6.4%).This is a major medical breakthrough observation for A-Fib patients. Anyone with A-Fib and their surgeons should be made aware of this added risk. But few A-Fib patients now receive this warning. As a reference point, people with CAD (Coronary Artery Disease) have a risk of death of 2.9%.

Perhaps the most disturbing part of this study was the risk of death for minor outpatient procedures. For heart failure it was 4.1%. If one has A-Fib, the risk of death from minor outpatient procedures is 2.2%!!!
This study did not speculate about why having A-Fib adds more risk.

Caveat about this study: This study did not compare the risk of having A-Fib to that of a normal healthy person’s risk. The editor has written the authors of this study to see if these figures are available.)
(Diepen et al. Circulation 2011; 124: 289-96)

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Dronedarone Clinical Trials Analysis

Dr. Peter Kowey of Lankenau Medical Center gave a detailed analysis of the various clinical trials of dronedarone. Dronedarone is not simply “amiodarone lite,” but is a unique med with its own characteristics and uses.

Unlike amiodarone, dronedarone is not characterized by “Iodine Moiety (part or component)” or Thyroid safety issues. While amiodarone is 65% successful in suppressing A-Fib, dronedarone is 50%. Dronedarone is taken twice a day with meals, while amiodarone is taken once a day after loading. Unlike amiodarone, dronedarone may have only a minor interaction with warfarin. Dronedarone is probably as efficacious as other antiarrhythmics like sotalol or class 1C drugs.

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ANDROMEDA Study Clinical Trials

The ANDROMEDA study was terminated early, because there was a 2-fold increase in mortality in the dronedarone group.

In the ATHENA study dronedarone significantly reduced Cardio Vascular (CV) hospitalizations by 37%.

The PALLAS study was terminated early due to excess deaths, strokes and heart failure hospitalization. It was intended to assess the efficacy and safety of dronedarone in patients with permanent A-Fib. Patients taking dronedarone were dying at more than twice the rate of those on a placebo. The ratio of stroke and hospitalization for heart failure was also more than twice as high. (See A-Fib News: Time to Stop Taking Dronedarone (Multaq)? and A-Fib News: No One with A-Fib Should Be Taking Dronedarone.)

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New Drugs In Clinical Trials

Dr. Kowey described new drugs being tested in clinical trials as amiodarone congeners (similar to amiodarone).

  • Benzofuran derivatives (Budiodarone)
  • Ranolazine
  • Atrial specific agents (vernakalant, IKach, IKur blockers

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Conclusions

Dr. Kowey realistically appraised the expected future use and utility of dronedarone:

“Dronedarone’s promise as a safe and simple drug that could be used by a broader group of physicians will not be realized.”

“Dronedarone’s use should be restricted to cardiologists and electrophysiologists who are accustomed to intensive patient monitoring for efficacy and safety.”

DIFFICULT CASES IN A-FIB MANAGEMENT

One of the most interesting sessions at the Boston A-Fib Symposium is always the “Difficult Cases in AF Management–Antiarrhythmic Drugs, Anticoagulation, and Clinical Decision Making.”  In this panel doctors Jeremy Ruskin, A. John Camm, Hans Kottkamp, Kevin Heist, Peter Kowey, Eric Prystowsky, and Albert Waldo described individual cases and discussed what were the best treatment options for these particular patients.

Patient #1: 76-year-old man in A-Fib 100 bpm feeling tired & with shortness of breath

The first case was presented by Dr. Kowey and involved a 76-year-old man with shortness of breath and tiredness. He was found to be in A-Fib with rates of around 100 bpm. He was on the rate control med  atenolol and had moderate high blood pressure. His labs were normal.

The options the audience could vote to treat Patient #1 were: rate control with blood thinners, cardioversion, or “refer for catheter ablation.” Most of those voting picked cardioversion. Some picked rate control.

In the discussion it was pointed out that patient #1 needed to be on rate control meds because his heart beat was high. But he was already on atenolol which did not help his shortness of breath and tiredness. The general consensus was to do a cardioversion.

But one Dr. pointed out that it would be wrong to wait too long, because A-Fib is likely to become progressively worse over time. If the cardioversion didn’t work or didn’t last very long and his symptoms were still bad, he could then be referred for a catheter ablation within a relatively short period of time. Most of the participants agreed that patient #1 needed to be on blood thinners for life unless his circumstances changed. One doctor stressed how all patients need to be involved in the decision process and need to understand the advantages and disadvantages of each treatment option.

What Actually Happened to Patient #1

Dr. Kowey said that patient #1 was given an anti-hypertensive drug and an oral anticoagulant. The beta-blocker atenolol was stopped and was substituted by the antiarrhythmic med sotalol which has beta-blocker characteristics. Patient #1 was cardioverted successfully, and then continued taking sotalol. However, after two months patient #1’s A-Fib recurred, but he did not have any symptoms, and his blood pressure was now well-controlled. When asked to vote on his changed condition, most of the participants voted that patient #1 continue on rate control and warfarin  or rate control and dabigatran/rivaroxaban.

Patient #1 was taken off of sotalol and started on dronedarone. He continued on blood thinners. He continues to do fine without significant symptoms and no hospitalizations.

Patient #2: 86-year-old woman with silent A-Fib & short A-Fib episodes

Dr. Eric Prystowsky presented the case of an 86-year-old woman who came in to have her pacemaker checked. Her pacemaker showed that she had silent A-Fib, the longest episode being 2.4 hours.

85% of the attendees voted to put her on a blood thinner. (Current guidelines recommend that anyone experiencing A-Fib episodes longer than 48 hours be put on blood thinners.)

Several doctors and audience members had divergent views on this important subject. One doctor pointed out that elderly women have a greater risk of having a hemorrhagic stroke from blood thinners than from an A-Fib ischemic stroke. (The newer blood thinners like dabigatran might work better than warfarin in reducing the risk of a hemorrhagic stroke.) Another doctor said that data showed that A-Fib episodes shorter than 24 hours had little chance of causing a stroke.2 But another doctor cited a study where an A-Fib episode as short as 6 minutes could produce a 2.5 risk of stroke.

(The author is not familiar with this study and has written this doctor for more info.)

The Symposium attendees then voted on whether they currently use a 24 hour or 48 hour long episode to determine the need for anticoagulation. 38% said they used 24 hour, 62% said they used 48 hour.

Dr. Prystowsky pointed out the importance of discussing and documenting in the patient’s folder all the anticoagulation options and how patients could be affected by each. This should be done not only for the patient’s benefit, but as a protection from law suits. Another doctor pointed out that patients often have a hard time determining when exactly an A-Fib episode started or how long it actually lasted (unlike this elderly woman whose pacemaker revealed the duration of her A-Fib episodes).

The general consensus was that the duration of an A-Fib episode that causes a risk of stroke is contested. There needs to be more hard data and studies developed to resolve this issue.

Editor’s Comments: Doctors do the best they can to protect patients from having an A-Fib stroke. But taking blood thinners is not an absolute guarantee that one will never have an A-Fib stroke. Warfarin reduces the risk of an A-Fib stroke by 60%-70%.3But that isn’t 100%. There is that 30-40% you still have to worry about.  And with many blood thinners there is an increased risk of bleeding, GI problems, and developing an hemorrhagic stroke.
The only guarantee of not having an A-Fib stroke is to no longer have A-Fib, or to perhaps have one’s Left Atrial Appendage (LAA) closed off or removed. 90%-95% of A-Fib clots come from the LAA.

Patient #3: 45-year-old male endurance runner with A-Flutter

Dr. A. John Camm presented a case of a 45-year-old male competitive endurance athlete in great shape who used to run 70-75 miles/week but who experienced sudden palpitations in his heart. His EKG showed he had A-Flutter.

The choices of treatment presented to the Symposium voters were:

  1. Beta-blocker – bisoprolol
  2. Flecainide
  3. Amiodarone
  4. Atrial flutter Right Atrium ablation procedure

Most voted for an atrial flutter ablation. That’s what was done for patient #3.
But Dr. Camm presented data from a study which showed that endurance athletes don’t have as good results and, if they continue to run after ablation, don’t do as well as patients in other sports or no sports patients. (Heidbuchel H. et al. Int J Cardiol 2006; 107:67-72)

What happened to patient #3

Now aged 50 his EKG showed A-Fib and nocturnal pauses, probably brought on by his running. He also had a large left atrium. In the discussion doctors pointed out that telling a runner to stop running doesn’t work. Running is an important part of their life. What you have to tell them is they risk developing A-Fib. (See A-Fib News: Vigorous Exercise and A-Fib.)

Dr. Camm pointed out that endurance athletes have five times more risk of developing Lone A-Fib, that 5%-10% of middle age endurance athletes will develop A-Fib. Runners develop increased vagal tone, and the pressure and volume overload they apply produce atrial stretch and dilation, inflammation, and atrial fibrosis.

Several doctors pointed out that A-Fib often lurks in the background, is a part of A-Flutter, or often develops after an A-Flutter ablation.

Editor’s comment: From this patient’s perspective, a patient having an A-Flutter ablation should also have an A-Fib ablation at the same time. A Flutter ablation is a relatively simple procedure compared to A-Fib ablation. It can usually be done at the end (or at the beginning) of an A-Fib ablation. See Flutter Ablation should be Combined with Left Atrium A-Fib Ablation.

Some doctors said they would never do an A-Fib ablation when only A-Flutter is present. Others said they routinely do both Flutter and A-Fib ablation at the same time, particularly in the case of athletes.

Dr. Kottkamp pointed out that the size of the left atrium wasn’t a problem, that he was more interested in the overall health of the left atrium as shown in an EKG. The bigger atrium is not always more sick than the smaller atrium. He does ablations if the left atrium is 50 or 52 mm.

Patient #4: 60-year-old male in chronic A-Fib for 12 years with cardiomyopathy

Dr. Hans Kottkamp presented a case of a 60-year-old male in long-standing persistent (chronic) A-Fib with dilated cardiomyopathy. (He hadn’t seen a cardiologist in three years.) He was diagnosed with A-Fib nearly twenty years ago. He had a low ejection fraction (25-30%), worsening heart failure, shortness of breath during minimal exercise, and peripheral edema (swelling).

The choices of treatment presented to the voters at the Symposium were:

  1. Electrical cardioversion
  2. Catheter ablation (both PV Isolation & substrate modification)
  3. AV-Node ablation + pacemaker
  4. AV-Node ablation + CRT-D (Cardiac Resynchronization Therapy with Defibrillator (regular biventricular pacing paces the right atrium and right ventricle, CRT pacing also paces the left ventricle to keep both in sync)

What happened to patient #4

Because patient #4 had been in long-standing persistent A-Fib for so long and had developed cardiomyopathy (and probably because he wasn’t likely to accept and cooperate with intensive monitoring), he was given an AV-Node ablation + CRT-D.

Three months after the AV Node ablation his heart was significantly improved. His ejection fraction improved to 45-50%.

Patient #5 (actually 10 different cases) CHADS2 scores of 0-1 and still suffered strokes

Dr. Jeremy Ruskin presented sobering, discouraging cases for doctors and patients. Ten A-Fib patients with low CHADS2 scores (0-1) all suffered CVAs (Cerebrovascular Accidents—strokes), TIAs (Transient Ischemic Attacks—mini-strokes), or Embolic MI (Myocardial Infarction—heart attack).

Editor’s Comments: One of the cases Dr. Ruskin cited was a young man only 35 years old who suffered an A-Fib stroke. Is this a wake-up call for doctors and patients? Should anyone who has A-Fib be on a serious blood thinner (not aspirin which isn’t very effective)? It’s hard to think of this 35-year-old having to take warfarin for the rest of his life. How would taking warfarin for so long affect him?
But maybe the newer oral anticoagulants [dabigatran, rivaroxaban, apixaban] might lend themselves to daily dosage over a longer period of time. Could these new anticoagulants replace aspirin as a recommended blood thinner for A-Fib patients with low CHADS2 scores/supposedly low risk of stroke?

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Aspirin Not Effective or Safe

Dr Albert Waldo cited studies that “aspirin at 150-200 mg/day is neither effective nor safe.” (Sato H et al. Stroke 2006;37:447-51.) Aspirin was no better than a placebo and caused a marginally increased risk of major bleeding.

In a Danish registry study of 132,372 A-Fib patients followed for 12 years, “the use of aspirin to prevent stroke in patients with A-Fib remains very poorly justified…Aspirin alone did not decrease the risk of TE (Thromboembolism stroke) compared to no treatment.” (Olesen JB et al. Thromb Haemost 2011;106:739-49)

One study showed Apixaban to be much better in reducing stroke risk than aspirin. (Connolly SJ et al. N Engl J Med. 2011 364:806-17)

Perhaps apixaban, if FDA approved, might be a welcome substitute for aspirin in patients at low risk of an A-Fib stroke.

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Yoga & Stress Reduction in A-Fib

Dr. Dhanunjaya Lakkireddy of the University of Kansas School of Medicine talked about the calming effect of yoga.

Dr. Lakkireddy noticed that a couple of his patients wearing heart-rate monitors became A-Fib free when they were taking yoga classes. “I wouldn’t have believed until I saw it.” He initiated a study to monitor a group of A-Fib patients for three months to assess the frequency of their A-Fib episodes, and their anxiety, depression, and quality of life. Then he switched them to yoga for three months. Yoga reduced their A-Fib episodes and improved their emotional well-being.

Dr. Lakkireddy researched the therapeutic effects of yoga. A-Fib is often triggered by an imbalance in the activity of the nervous system. Yoga can improve this imbalance. Yoga can also improve heart and body inflammation which is a known trigger of A-Fib. But though yoga helps, it doesn’t cure A-Fib, “it only makes it less burdensome.”

Editor’s Comments: Though everyone would prefer to be cured of their A-Fib, that isn’t always possible. For those living with A-Fib, yoga may make the A-Fib burden more bearable and improve one’s quality of life.

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Return to AF Symposiums by Year

Return to Index of Articles: AF Symposium: Steve’s Summary Reports

Last updated: Sunday, February 15, 2015

References    (↵ returns to text)
  1. www.intelihealth.com (by Aetna)/atrial fibrillation/treatment.
  2. Capucci, A et al. “Monitored Atrial Fibrillation Duration Predicts Arterial Embolic Events in Patients Suffering From Bradycardia and Atrial Fibrillation Implanted With Antitachycardia Pacemakers” Journal of the American College of Cardiology Volume 46, Issue 10, 15 November 2005, Pages 1913–1920
  3. Chatterjee, S. et al. “Left Atrial Appendage Occlusion: Lessons Learned From Surgical and Transcatheter Experiences.” Ann Thorac Surg 2011;92:2283-92. doi: 10.1016/j.athoracsur.2011

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