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Baltimore, MD

Doctors & patients are saying about 'Beat Your A-Fib'...

"If I had [your book] 10 years ago, it would have saved me 8 years of hell.”

Roy Salmon, Patient, A-Fib Free,
Adelaide, Australia

"This book is incredibly complete and easy-to-understand for anybody. I certainly recommend it for patients who want to know more about atrial fibrillation than what they will learn from doctors...."

Pierre Jaïs, M.D. Professor of Cardiology, Haut-Lévêque Hospital, Bordeaux, France

"Dear Steve, I saw a patient this morning with your book [in hand] and highlights throughout. She loves it and finds it very useful to help her in dealing with atrial fibrillation."

Dr. Wilber Su,
Cavanaugh Heart Center, 
Phoenix, AZ

"...masterful. You managed to combine an encyclopedic compilation of information with the simplicity of presentation that enhances the delivery of the information to the reader. This is not an easy thing to do, but you have been very, very successful at it."

Ira David Levin, heart patient, 
Rome, Italy

"Within the pages of Beat Your A-Fib, Dr. Steve Ryan, PhD, provides a comprehensive guide for persons seeking to find a cure for their Atrial Fibrillation."

Walter Kerwin, MD, Cedars-Sinai Medical Center, Los Angeles, CA

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, it may be difficult reading.


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.)


EPs & Surgeons’ Consensus Statement on A-Fib  Catheter Ablation Approved as First Line Treatment for A-FibCalkinsThe 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 StrokeCammOral Anticoagulation: A Review of the Data
Catheter Ablation Far Superior to Current Antiarrhythmic Drugs KottkampIs 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. MoradyLesions Learned: Providing Guidance for the Next (and Current) Generation of Ablationists
How to Prevent Atrial-Esophageal Fistula  NakagawaImproving 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 PapponeBiatrial Catheter Ablation for Chronic Atrial Fibrillation
The Watchman Device to Close off the Left Atrial Appendage ReddyNovel 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.


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 FailureScore = 1
“H” HypertensionScore = 1
“A” Age over 75Score = 1
“D” DiabetesScore = 1
“S2″ Previous Stroke or TIAScore = 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


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.”


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.


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.)


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


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.)


  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.


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®)


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.


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 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. 


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.)

Pulmonary VeinsPulmonary Veins & Left Atrial AppendagePulmonary Veins
Pulmonary Vein-Mitral Valve Isthmus Line
Left Atrium RoofLeft Atrium RoofCFAEs
Posterior WallLeft Atrium Roof
Coronary SinusCoronary Sinus & Inferior left AtriumMitral Isthmus Block Line
Septal AreaAreas 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 PVCoronary Sinus
Accessory Pathways (between Left Atrium & Left Ventricle)Right Atrium-Cavotricuspid Isthmus (for Flutter)

(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:

Avoid RF Near the EsophagusNot EffectiveEspecially in complicated cases of A-Fib, it’s often necessary to ablate near the Esophagus
Low Power for only 5-10 seconds near the EsophagusNot EffectiveUncertainty about what is the maximum safe power
Probe to Monitor Esophageal TemperatureNot EffectiveEven with a small rise in temperature, there are still lesions
Monitor for Bubbles with ICENot EffectiveNot viable
Monitor for PainNot EffectiveSedation may mask pain, or the patient may not feel any pain
Displace (move) the Esophagus Away from the Spots to be AblatedNot EffectiveNot yet practicable
Cryoablation (freezing) for Sites Near the EsophagusEffective
Post-Ablation Carafate/Proton Pump Inhibitor 2-Week ProgramEffective

(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.
  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.

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