AliveCor, maker of the Kardia ECG smartphone attachment to detect Atrial Fibrillation, may be a big winner in a plan by the British National Health Service (NHS).
Dr. David Albert, AliveCor founder, said the British plan opens the door to the NHS buying AliveCor devices for all 2 million atrial fibrillation patients in England.
The NHS has announced plans to give millions of patients free health apps & connected health devices in a bid to promote self-management of chronic diseases.
The plan is expected to “save money and lives by preventing strokes.” About 20 percent of British A-Fib patients have strokes. The program will start in April 2017.
The AliveCor Kardia, cleared for use in the US by the FDA, attaches to Android and Apple Devices and by pressing the sensors with your fingers (or thumbs), capture single-lead, medical-grade EKGs in just 30-seconds. Instantly you know if your heart rhythm is normal or if atrial fibrillation (A-Fib) is detected in your EKG. Data can be captured and sent to your doctor.
Request to Our Readers
Is anyone using the latest AliveCor® version, ‘Kardia™ Mobile’? (Model 1141, out since Feb. 2016) I want to update our Feb. 2015 review.
How do you typically use it? Are you satisfied with the performance? Do you transfer the data to your doctor?
Will you share your product experiences with me? Just shoot me an Email with your impressions.
AF Symposium 2016
Two Challenging, Difficult Catheter Ablation Cases with LAA Closure
by Steve S. Ryan, PhD
One of the most interesting and practical sessions was “Challenging Cases in Catheter Ablation and LAA Closure for AF”. Featured were a panel with some of the world’s ‘master’ Electrophysiologists (EPs). Each presented one or two cases of their most challenging and difficult cases from the past year. The panelists were:
• Dr. David Keane, St. Vincent’s University Hospital, Dublin, Ireland (Moderator).
• Dr. Moussa Mansour, Massachusetts General Hospital, Boston, MA.
• Dr. Andrea Natale, Texas Cardiac Arrhythmia Institute, Austin, TX
• Dr. Douglas Packer, Mayo Clinic, Rochester, MN
• Dr. Vivek Reddy, Mount Sinai Hospital, New York, NY
• Dr. Miguel Valderrabano, Houston Methodist Hospital, Houston, TX
• Dr. David Wilber, Loyola University Medical Center, Chicago, IL
Two cases of Persistent A-Fib stood out as significant for readers of A-Fib.com. To learn why, see my ‘Take Away’ comments that follow each case description.
Electrically Dead Left Atrium
Dr. Valderrabano presented the case of a 48-year-old female patient with symptomatic Persistent A-Fib. She had been cardioverted several times and had tried several antiarrhythmic drugs including amiodarone. She had had Pulmonary Vein Isolations (PVI) by other EPs before being referred to Dr. Valderrabano.
Her left atrium was enlarged. Dr. Valderrabano ablated her again but couldn’t isolate her Left Atrial Appendage (LAA) where A-Fib signals were still coming from. He used the Lariat (SentreHeart, Inc.), a noose-like suture delivery device, to close off and electrically remove her LAA.
After these steps, she had a leak from her closed-off LAA which had to be plugged. She was A-Fib free but developed Atrial Flutter which had to be ablated.
After all these ablations, she was finally in sinus rhythm. But at what cost? All the extensive ablations and scarring had made her Left Atrium electrically dead and unable to contract normally (“Stiff Left Atrium”).
The patient knew she might lose contraction of her left atrium, but was most happy to be in sinus rhythm after years of symptomatic A-Fib.
TAKE-AWAYS FOR PATIENTS
Lariat to Prevent A-Fib Signals from the LAA: The Lariat is an occlusion device, and like the Watchman, is normally used for closing off the Left Atrial Appendage (LAA) to prevent A-Fib clots breaking loose and causing a stroke. It’s particularly useful for people who can’t or don’t want to take anticoagulants.
In this case, the LAA was the source of non-Pulmonary Vein (PV) signals (and often is). By removing it, patients can often be restored to sinus rhythm. (Master EPs now consider the LAA the most important source of non-PV triggers. Unfortunately, many EPs are unaware of the LAA’s importance and don’t check it for non-PV triggers during an ablation.)
Stiff Left Atrium: No one wants to lose their Left Atrium’s ability to contract and pump. But in extreme cases, this may happen.
I talked to one of the most experienced EPS in the world who has had to do several ablations which restored a patient to sinus but also rendered their left atrium electrically dead and unable to contract normally. [Note: the Left Ventricle does most of the heavy-duty pumping work.]
His patients, even though they knew the risks, were overjoyed to finally be in normal sinus rhythm. After years of symptomatic A-Fib, they had their life back again.
FIRM Advantages and Problems
Dr. Vivek Reddy presented the case of a 63-year-old male in Persistent A-Fib who had had several ablations before being referred to him. After wearing a Holter monitor for one-week, the data showed an A-Fib burden of 27%, i.e., his A-Fib was very symptomatic and burdensome.
Dr. Reddy did a FIRM-guided ablation, but the patient was still in A-Fib.
Upon closer examination and manual mapping, the ‘renegade’ A-Fib signal source was found and ablated, which restored the patient to sinus rhythm.
Dr. Reddy had discovered the A-Fib signal in the area where the FIRM basket catheter didn’t map. As mentioned in other Symposium presentations, due to design problems, the FIRM basket catheter maps only slightly more than ½ of the left atrium. (New basket catheters to correct this problem are being developed by the manufacturer, Abbott/Topera.)
TAKE-AWAYS FOR PATIENTS
Limited but Extensive Data with Fast Results: Even though the FIRM mapping and ablation system seems to currently have built-in limitations, master EPs still use the FIRM basket mapping catheter because it provides a great deal of important information very quickly. It is especially useful in cases of Persistent A-Fib where it identifies non-PV triggers such as rotors and focal drivers. As Dr. Reddy stated earlier, this is the future of A-Fib ablation.
Choose an EP Who Can Compensate for FIRM Limitations: When choosing an EP to do your ablation, it isn’t enough to select someone who uses the FIRM system. You need an EP who knows the limitations of the FIRM system and how to find and ablate non-PV triggers the FIRM system may miss. The fact that an EP uses the FIRM system is not a guarantee you will have a successful ablation.
The two cases I chose to write about were the most informative for those A-Fib patients seeking to understand the most current treatment options. This Saturday afternoon session was the last of the 2016 AF Symposium.
For more about the Lariat occlusion device, see my brief article: Lariat II Suture Delivery Device.
For more about the FIRM mapping system, see my brief article: FIRM Mapping System—Should Ablation Patients Avoid It?
If you find any errors on this page, email us. Y Last updated: Monday, February 15, 2016
AF Symposium 2016
Bordeaux New ECGI Ablation Protocol—Re-Mapping During Ablation
by Steve S. Ryan, PhD
Why should patients be interested in a new mapping and ablation technique that isn’t yet available worldwide and in the US?
Why ECGI/ECVUE is Important
ECGI/ECVUE is probably the most significant, game changing improvement in treating A-Fib (along with Contact Force sensing catheters), particularly for people with persistent A-Fib.
ECGI will not only change the ways mapping and ablations are done, but possibly how you and I are examined and diagnosed in our doctor’s office.
Image a Future Physical Without an EKG
Imagine when you go in for a physical that, instead of getting an EKG, you simply put on an ECGI vest which tells the doctor where and how many A-Fib producing potentials you have in your heart, all without you having to be in A-Fib. Admittedly, this is pie-in-the-sky speculation right now. But the ECGI vest has tremendous potential to change the way A-Fib is diagnosed and treated.
Dr. Michel Haissaguerre & New Uses of ECGI/ECVUE
Dr. Michel Haissaguerre of Central Hospital, Bordeaux, France presented new developments in how the Bordeaux group now uses ECGI/ECVUE Cardio Insight body surface mapping for persistent A-Fib. His talk was entitled “Monitoring of AF Drivers During Catheter Ablation for Persistent AF.” (For a detailed description and discussion of the ECGI system, see 2013 BAFS: Non-Invasive Electrocardiographic Imaging [ECG]). See also How ECGI Works.)
Patient Prep with the ECGI Vest
Typically, the day before an ablation, a technician (it doesn’t have to be the EP ablationist) uses a ECGI vest to map and identify sites in the heart producing A-Fib signals (rotors and focal sources). The next day, using this map combined with a CT scan which produces a very detailed 3D color map of the heart, the EP ablates and isolates these sites.
What’s New: Bordeaux Group Also Re-Maps Using the ECGI Vest
What’s brand new about how the Bordeaux group is using ECGI is that, if a patient’s A-Fib has not been terminated after the ablation, they then re-map using the ECGI vest. This often reveals missed, changed or new A-Fib drivers. They then ablate/isolate these regions.
The ideal or goal is for A-Fib to terminate into sinus rhythm or Atrial Tachycardia (AT). Atrial Tachycardia (a heartbeat that is in sinus rhythm but faster than normal) can then also be mapped and ablated into Normal Sinus Rhythm (NSR). (Atrial Tachycardia, for the average persistent patient, feels a lot better than being in A-Fib.)
If after re-mapping and ablation, the patient is still in A-Fib, they use Electrocardioversion to try to shock the patient back into sinus.
See the AF Symposium Live Case Presentations: Dr. Mélèze Hocini of the Bordeaux group ablated a 40-year-old male with persistent A-Fib. She found four areas of rotor/focal activity in his heart. After ablating the third area, the patient’s persistent A-Fib terminated. Dr. Hocini did not have to re-map or ablate the fourth area.)
Slides of Before and After ECGI Ablation
Dr, Haissaguerre showed slides of before and after an ablation using ECGI. Ablation at a driver region transformed rapid, complex signals into slower, organized signals.
In the AFACART study in which eight different centers used the ECGI system, ablations in driver regions varied from 38 to 98 minutes of cumulative RF energy delivery time per center despite similar patients and targets (indicating the current lack of standardized ablation techniques). (For more on the AFACART study, see AF Symposium 2015: AFACART Clinical Trial.)
Persistent A-Fib Case: In the case of a 48-year-old female in Persistent A-Fib for four months, four target areas were identified: the inferior Left Atrium (LA), the LA Septum, the anterior of the LPV (Left Pulmonary Vein) to the LAA, and the posterior area of the RPV (Right Pulmonary Vein). (They divide the left and right atria into seven general physical areas.) A-Fib continued after these driver areas were ablated. On re-mapping, the septum area was found to be still active. After 2 more minutes of RF delivery to that septum area, A-Fib terminated into normal sinus rhythm.
Ablation Failure From Thicker Atrial Tissue?
Dr. Haissaguerre pointed out that ablation failure happens particularly in the right and left atrial appendages because of thicker atrial tissue. He showed a slide where he ablated one driver area, then six months later ECGI showed a new driver region at the LAA ridge.
Right Atrium Drivers Reduced After Left Atrium Ablation
Next, he showed slides where the ECGI mapping system initially showed driver activity in the Right Atrium (RA). But after Left Atrium (LA) ablation, this driver activity was greatly reduced. He suggested that RA drivers might mirror or be a projection of LA drivers.
(This is a new research finding that may be very important and may change the way the right atrium is ablated in persistent A-Fib cases.)
ECGI After Prior Extensive PVIs
Dr. Haissaguerre showed slides of patients who had had two or three prior PVIs. ECGI clearly showed where there were still driver regions. Each patient’s persistent A-Fib was terminated into normal sinus rhythm.
Mapping of Atrial Tachycardias (ATs)
The ECGI system can also map Atrial Tachycardias (AT). Dr. Haissaguerre found that half the ATs found were focal ATs, “mostly localized reentry”; 68% were from driver regions previously ablated; 32% were from new sites.
The other half of the ATs were “Macroreentries” and required linear ablations to terminate.
Limitations of ECGI NonInvasive Driver Mapping
According to Dr. Haissaguerre:
• Body filtering (ECGI) may miss small local AF Signals, while showing the main propagating waves in a panoramic scope
• Extensive ablation may affect egm (electrogram) quality and analysis
• Besides ‘drivers’, other mechanisms of AF perpetuation may coexist, particularly in longer lasting (>1 year) AF
Dr. Haissaguerre’s Conclusions
• Remapping can confirm elimination or persistence of drivers or show new drivers (requiring further ablation)
• This dynamic information will probably increase the rate of AF termination
• Further improvement expected with rapid mapping of Atrial Tachycardias
What Patients Need to Know
The ECGI/ECVUE Cardio Insight body surface mapping seems like a major improvement and development, particularly for patients in persistent A-Fib, usually the hardest to cure.
This ECGI system is being carefully developed in eight centers in Europe (AFACART clinical trial). It was recently purchased by Medtronic and is headquarted in Dublin, Ireland.
(No one at the Medtronic booth at the AF Symposium exhibit hall could tell me when the ECGI system will be available for examination and use in the US and worldwide. I’ll update this report when I know.)
Re-Mapping a Major Improvement in ECGI: We’re grateful to Dr. Haissaguerre and the Bordeaux group for developing the technique of re-mapping during an ablation. It’s certainly a major improvement in what was already a very good mapping and ablation system.
Mapping and Ablating Atrial Tachycardias (ATs): From a patient’s perspective, it’s great to know that ECGI can be used to identify and ablate atrial tachycardias (fast heart rates).
A-Fib termination can result in normal sinus or ATs which are a form of sinus rhythm. For most people, ATs are certainly better than being in A-Fib. But they can be annoying and disruptive. It’s good to know they can be mapped and ablated just like A-Fib signals.
ECGI May Miss Small Local ATs and A-Fib Signals: ECGI isn’t perfected yet. Dr. Haissaguerre showed that many of the local ATs found came from driver regions previously ablated.
DR. MICHEL HAÏSSAGUERRE
Dr. (Prof.) Michel Haïssaguerre, Central Hospital, Bordeaux, France, and his colleagues invented pulmonary vein catheter ablation for A-Fib (PVA/I). The Bordeaux Group is considered one of the top A-Fib centers in the world and noted for their cutting edge research in the treatment of Atrial Fibrillation. Interesting fact: I (Steve Ryan) was their first US patient in 1998.
If you find any errors on this page, email us. Y Last updated: Thursday, February 11, 2016
A-Fib patients sometimes use consumer ‘DIY” Heart Rate Monitors (HRM) when exercising or performing physically demanding activities (For specific models and options, see our article, DIY Heart Rate Monitors & Handheld ECG Monitors Part I.)
How Do DIY Heart Rate Monitors Work?
Basic HRMs use a chest strap to pick up the electrical signals from the heart. However, due to the inherent design of the chest strap, the accuracy is somewhat limited and is no replacement for the signals recorded by a Holter or Event Monitor.
A HRM keeps track of your heart’s R-R interval or the time between R peaks. Without getting too technical, the R peak on a generic ECG waveform (see the diagram) corresponds to the ventricle beat (depolarization) and has the largest amplitude (height) of the complete waveform.
When the amplitude (picked up as a voltage differential) exceeds a certain threshold, a “beat” is picked up by the chest strap and transmitted wirelessly to the HRM. It is the time between these R peak “beats” that is used by the HRM to determine instantaneous heart rate. It is only going to pick up episodes of arrhythmia as are manifested in ventricle beats (the R on the waveform).
Learn more about the EKG signal, see Steve’s article: “Understanding the EKG (ECG) Signal“.
Learn more about the EKG signal, see Steve’s article: “Understanding the EKG (ECG) Signal“.
This is one of the fundamental differences in how data is recorded by HRMs (R-R interval) versus Holter/Event Monitors (actual waveform).
In fact, this is what Polar has to say:
Polar products are not designed to detect arrhythmia or irregular rhythms and will interpret them as noise or interference. The computer in the wrist unit will make error corrections, so that arrhythmia beats are not included in the averaged beats per minute. The blinking heart symbol in the face of the unit, however, will continue to show all heart beats received.
In most cases the Polar products will work fine for persons with arrhythmia.
HRM Recording Capability
Most HRMs provide some internal storage recording capability. While lower cost HRMs simply record low, high and average heart rate, upper end models allow you to download heart rate data to your PC.
App-enabled smartphones are changing how this data is viewed, collected and saved for future review.
How To Setup and Use an HRM
On most of the HRMs, you can set a heart rate zone, and the watch monitor (or app-enabled smartphone) will record how long you stayed in that zone.
You could then program a high heart rate zone which you might only enter if you were in A-Fib. That way you could record how long you stayed in A-Fib and what your max heart rate was. This data could be reviewed on the watch monitor (or app-enabled smartphone) without having to download it to a PC.
On HRMs with PC interface capability, you can view data in a graphic form (on some watches/smartphones you can view the graphic data but with lower resolution.) This analyses could tell you when you were at a higher heart rate—A-Fib—and how long you stayed there. Of course these kinds of features require some PC skills, but typically the programs are pretty user friendly. (See the above graphic example of a Polar PC program).
For more, see our article, DIY Heart Rate Monitors & Handheld ECG Monitors.
Return to Index of Articles: Diagnostic Testing
Last updated: Tuesday, April 14, 2015
AF Symposium 2015
The Virtual Heart Computerized Simulation
by Steve S. Ryan, PhD
The most hopeful, promising research of the 2015 AF Symposium was presented by Dr. Natalia Trayanova of Johns Hopkins Un., Baltimore, MD. She described the “virtual heart”—a computerized model to simulate an individual patient’s heart.
A Computerized Model
The idea is to build computerized models that can be used to guide an individual patient’s therapy. She previously simulated a heart attack in a specific region of an individual heart and how it affected the dynamics of that specific heart.
Using the virtual heart computerized simulation, she can, for example, program in not only how much fibrosis an individual heart has but its structure. (Is the fibrosis circularly-distributed? Does it have a complex shape or is it patchy?)
The Bordeaux Group Patient Data
Dr. Trayanova is rapidly developing more atria data and experience. The Bordeaux group is providing her patient data from their ECGI body surface potential mapping system (CardioInsight). She has done approximately a dozen retrospective studies using the virtual heart technology (as of January 2015).
How it Works
Dr. Trayanova and her team start by doing an MRI scan. Then they hyper-enhance segments which correspond to areas of fibrotic remodeling.
The next step is to develop a computational mesh that incorporates representations of ion channels, calcium cycling and other electrophysical aspects of an individual’s atria. All this is incorparated into patient-specific geometry of the model.
What the Model Can Reveal
Then they let the model run and see what the arrhythmia looks like. Does the fibrotic substrate anchor rotors in particular locations? What are the spatial characteristics of the regions where they are located? Can these spatial metrics guide where the proper ablation should be?
Dr. Trayanova’s team merges these virtual atria with a CARTO map to predict where the catheter should ablate.
The potential of Dr. Trayanova’s research for A-Fib patients is incredible! Imagine getting an MRI and knowing where your A-Fib is coming from, how your A-Fib affects and works in your heart both now and in the predictive future, how various A-Fib drugs can be expected and predicted to affect your heart, how much and what kind of fibrosis you have, how you can expect your fibrosis to progress and affect you over time, what therapies should be done in your particular case, if you need a catheter ablation, where exactly in your heart the EP needs to ablate, and to be able to accurately predict whether or not or how fast you will progress from paroxysmal to persistent A-Fib based on computer models that mirror your own heart.
Dr. Trayanova’s research has the potential to radically change the way A-Fib is treated. Almost all the uncertainties EPs and A-Fib patients now have to deal with can potentially be eliminated with the virtual computer reconstruction of individual A-Fib hearts.
Last updated: Thursday, April 16, 2015
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.
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)
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.)
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 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.”
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
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.)
- Narrow therapeutic window. Insufficient anticoagulation (INR less than 2) may result in stroke. Over-anticoagulation (INR over 4) increases the risk of bleeding.
- Late onset and offset. A patient has to be taking warfarin for a while for it to reach a therapeutic level.
- Unpredictable dose response. Genetic and other factors may influence how individuals react to warfarin.
- Drug-drug interactions. Certain drugs (and some supplements) interfere with warfarin.
- Drug-food interactions. People taking warfarin must limit foods containing vitamin K (like broccoli or some leafy vegetables)
- 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.
- 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.
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.)
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 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)|
(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 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.)
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.
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.
Return to Index of Articles: AF Symposium: Steve’s Summary Reports
Last updated: Friday, January 1, 2016
- 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↵
- Turpie, “New oral anticoagulants in atrial fibrillation.” European Heart Journal advanced publication 12/19/07↵
- The Center for Shared Decision Making. http://www.dartmouth-hitchcock.org/medical-information/decision_making_help.html↵
- Turpie, “New oral anticoagulants in atrial fibrillation.” European Heart Journal advanced publication 12/19/07↵
- Turpie, “New oral anticoagulants in atrial fibrillation.” European Heart Journal advanced publication 12/19/07↵
- 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.↵
- 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↵
- 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.↵
When I think about the field of atrial fibrillation in 2013, several thoughts come to mind. There were technical advancements, some new drug therapies, and additions to our understanding of Atrial Fibrillation (and a few accomplishments for our A-Fib.com website).
Heart Imaging And Mapping Systems
Perhaps the most important technical innovations in 2013 for A-Fib patients were the introduction of two new heart imaging and mapping systems. A third system, the Bioelectronic Catheter, represents a whole new technology with tremendous potential for A-Fib patients.
The ECGI System
The ECGI system, combined with a CT scan, produces a complete 3-D image of your heart along with identifying all the A-Fib-producing spots. Think of it as an ECG with 256 special high resolution electrodes rather than 12. It greatly reduces your ablation time and your radiation exposure.
A day before your ablation, you simply don a special vest with 256 electrodes covering your upper torso, and lay down. The 3-D image created is a road map of your heart with all the focal and rotor areas (A-Fib-producing spots) identified. During your ablation your EP simply ablates the “guilty” areas. Read more of my article…
The FIRM System
The FIRM system uses a different approach to mapping the heart and the A-Fib producing spots. It uses a basket catheter inside the heart to map large areas in a single pass and reveal the location of foci and rotors. Read more of my article…
Why are these two technologies important? ECGI allows your imaging & mapping to be performed the day prior to your ablation, rather than during your ablation. This shortens the length of your ablation procedure. In addition it reduces your radiation exposure and produces remarkably accurate 3D images of your heart and identifies where A-Fib signals are coming from. The FIRM system, though performed during an ablation rather than before it, may be a significant improvement over the Lasso catheter mapping system now in current use. Both systems may mark a new level of imaging/mapping for A-Fib.
Stretchable Electronics Meets the Balloon Catheter
The merging of living systems with electronic systems is called “bioelectronics”. Key is a flexible, pliable circuit made from organic materials—the carbon-based building blocks of life. Bioelectronics have entered the EP lab with a prototype of a ‘bioelectronic catheter’, the marriage of a pliable integrated circuit with a catheter balloon.
In a mapping application, the deflated bioelectronic balloon catheter is slipped into the heart, then pumped up. The inflated integrated circuit conforms to the heart’s grooves and makes contact with hard-to-reach tissue. It can map a hundred electrical signals simultaneously, across a wider area and in far greater detail than had been previously possible. And it’s being developed to function in reverse. For ablation applications, instead of detecting current, it can apply precise electrical burns. This is a potentially breakthrough technology that may well change the way catheter mapping and ablation are performed. (Thanks to David Holzman for calling our attention to this ground-breaking research article.)
This is a remarkable time in the history of A-Fib treatment. Three very different technologies are poised to radically improve the way A-Fib is detected, mapped and ablated. We’ll look back at 2013 as a watershed year for A-Fib patients.
Three New Anticoagulants
In 2013 we saw three new anticoagulants, a welcome development for A-Fib patients. Note: the new anticoagulants are very expensive compared to the proven anticoagulant warfarin.
How do they compare to warfarin?
Warfarin seems to have a slightly higher chance of producing intracranial bleeding.
In general stay away from Pradaxa. There are horrible ER reports of patients bleeding to death from even minor cuts, because there is no antidote or reversal agent. Read more about my Pradaxa warning…
Eliquis, in general, tested better than Xarelto in the clinical trials, but it’s so new we don’t have a lot of real-world data on it yet. And, as with Pradaxa, neither have antidotes or reversal agents.
In addition, there was what some consider a major problem with the clinical trials comparing the new anticoagulants to warfarin. ‘Compliance’ rates by warfarin users were poor (many either weren’t taking their warfarin or weren’t in the proper INR range). Did this skew the results?
And finally, unlike warfarin where effectiveness can be measured with INR levels, we don’t have any way to measure how effectively the new blood thinners actually anticoagulate blood. Read more of my article “Warfarin vs. Pradaxa and the Other New Anticoagulants“.
Keep in mind: ‘New’ doesn’t necessarily mean ‘better’ or ‘more effective’ for You.
High Blood Pressure with Your A-Fib? Is Renal Denervation a solution?
As many as 30% of people with A-Fib also have high blood pressure which can’t be lowered by meds, exercise, diet, etc. There was hope that Renal Denervation would help.
With Renal Denervation, an ablation catheter is threaded into the left and right arteries leading to the kidneys, then RF energy is applied to the nerves in the vascular walls of the arteries, hopefully reducing ‘Sympathetic Tone’, lowering high blood pressure and reducing A-Fib. For many people Renal Denervation seemed the only realistic hope of lowering their high blood pressure. However, the Medtronic Simplicity-3 trial indicated that renal denervation doesn’t work. Read more of this article… For 2014 news on this topic, read more…
A Study of Obesity and A-Fib: A-Fib Potentially Reversible
Obesity is a well known cause or trigger of A-Fib, probably because it puts extra pressure and stress on the Pulmonary Vein openings where most A-Fib starts.
In 2013 A research study report focused on obese patients with A-Fib. Those who lost a significant amount of weight also had 2.5 times less A-Fib episodes and reduced their left atrial area and intra-ventricular septal thickness.
Good news! Losing weight can potentially reverse some of the remodeling effects of A-Fib. Related article: Obesity in Young Women Doubles Chances of Developing A-Fib.
Obstructive Sleep Apnea and A-Fib
Obstructive Sleep Apnea (OSA) is another well recognized cause or trigger of A-Fib. Anyone with A-Fib should be tested for sleep apnea.
Earlier studies have shown approximately two-thirds (62%) of patients with paroxysmal or persistent A-Fib suffer from sleep apnea. In 2013, research reports showed that the worse one’s sleep apnea is, the worse A-Fib can become. In addition, sleep apnea often predicts A-Fib recurrence after catheter ablation.
Before an ablation, Dr. Sidney Peykar of the Cardiac Arrhythmia Institute in Florida, requires all his A-Fib patients be tested for sleep apnea. If they have sleep apnea, they must use CPAP therapy after their ablation procedure.
A-Fib.com: Our New Website’s First Year
The original A-Fib.com web site was created using the phased out software MS FrontPage. Thanks to a “no strings attached” grant from Medtronic, A-Fib.com was reinvented with a more up-to-date but familiar look, and features more functionality (built on an infra-structure using Joomla and WordPress). We can now grow the site and add features and functions as needed.
It involved a tremendous amount of work. A special thanks to Sharion Cox for building the new site and for technical support. My wife, Patti Ryan, designed the look and all graphics. (I can’t thank Patti enough; I’m so lucky!)
Update the Directory of Doctors & Facilities
Back when I started A-Fib.com in 2002, there were less than a dozen sites performing ablations for A-Fib. Today our Directory of Doctors and Facilities lists well over 1,000 centers in the US, plus many sites worldwide.
Increasingly, doctors were writing me asking why they weren’t included, or why their info was incorrect since they had moved, etc. To update our records and our service to A-Fib patients, starting in July 2013, we prepared and mailed letters to over 1,000 doctors/facilities. We asked each to update/verify their listing (and include a contact person for our use).
The response to our bulk mailing was great. The data input started in October and continued for several months (as time allowed). Recently, we cut over to the ‘new’ Directory menu and pages.
What’s Ahead for A-Fib.com in 2014
2014 Boston AFib Symposium Reports: Check out my new reports from the 2014 Boston A-Fib Symposium (BAFS) held January 9-11, 2014 in Orlando FL.
The first two reports are posted. Look for more reports soon. I usually end up with 12-15 reports in total.
Our a-Fib.com Directory of Doctors & Facilities: Work on updating our listings is still underway. We need to contact those who did not respond to our request for verification or updating of their listing. (Shall we write again or maybe make phone calls?)
Amazon Best Sellers list: Our book sales continue to grow. Did you know that our book ‘Beat Your A-Fib’ has been on Amazon’s Best Sellers list continually in two categories (Disorders & Diseases Reference and Heart Disease) since its debut in March 2012? Visit Amazon.com and read over 40 customer reviews.
Help A-Fib.com Become Self-sustaining: We plan to step up our efforts to make A-Fib.com a self-sustaining site. (Since 2002, Steve and Patti Ryan have personally funded A-Fib.com with an occassional reader’s donation.)
In our efforts toward sustainabiliy, several years ago we added a PayPal ‘Donate’ button (you don’t need a PayPal account to donate) and invited donations toward our onlline maintenance costs.
Our newest effort is our ‘A-Fib can be Cured! shop with T-shirts and more at Spreadshirt.com. With each shirt purchase $2 goes to support A-Fib.com. (We will roll out new designs every quarter or so).
Posted February 2014
Help A-Fib.com become self-sustaining! Help keep A-Fib.com independent and ad-free.
Will 2014 be the year you help support A-Fib.com?
Last updated: Wednesday, February 11, 2015
Diagnosis & Testing
Guide to DIY Heart Rate Monitors & Handheld ECG Monitors (Part I) REVISED APRIL 2015
Guide to DIY Heart Rate Monitors: How They Work For A-Fib Patients (Part II) NEW
Didn’t find what you’re looking for? Try the ‘Search our Site’ feature (top right of every page)
Return to Subject Index to A-Fib.com Articles Last updated: Tuesday, April 14, 2015
6. “Is Atrial Fibrillation curable? Or can you only treat or control it? Should I seek a cure?”
A-Fib is definitely curable. (I was cured of my A-Fib in 1998). If you have A-Fib, no matter how long you’ve had it, you should aim for a complete and permanent cure.
Currently, Catheter Ablation and the Maze/Mini-Maze operations both offer the hope of becoming A-Fib free permanently. For example, Pulmonary Veins Ablation/Isolation (PVA/I) techniques are achieving success rates of 70%-85% in making Paroxysmal patients A-Fib free. A second procedure, when required, raises the success rate to 90% or higher.
Being ‘cured’ of A-Fib is possible for more and more patients everyday. Discuss these treatment options with your cardiologist or electrophysiologist.
If your doctor is satisfied with just keeping your A-Fib “under control,” I recommend you get a second opinion.
Refer to our Finding the Right Doctor page and related readings. We step you through all you need to know to find the right doctor for you and your treatment goals.
Last updated: Tuesday, July 14, 2015
5. “Can I die from my Atrial Fibrillation? Is it life threatening?”
Most episodes of A-Fib are not life threatening. Even though you may feel awful, it’s not like having a heart attack.
The biggest danger from A-Fib is the risk of stroke. Because your heart isn’t pumping out properly, blood clots can form and travel to the brain causing stroke. If you have A-Fib, you are five times more likely to have a stroke than the general population. It’s most important to take a blood thinner like warfarin (Coumadin) or aspirin to help prevent these clots from forming.
If you’ve had A-Fib for a long time, your heart may enlarge, develop fibrosis and eventually weaken. You may become more prone to other heart problems. For example, If you have A-Fib and aren’t being treated by a doctor, you are five-to-six times more likely to have a stroke than the general population. Also, A-Fib may lead to mental deterioration. Atrial fibrillation is independently associated with senile, vascular, and alzheimer’s dementia.
For more about the physiology of A-Fib, see our Overview of Atrial Fibrillation.
Last updated: Wednesday, August 26, 2015
3. “Could my A-Fib go away on its own? I don’t want to take any medication. Can I just wait and see?”
On occasion A-Fib does go away on its own. In a process called “spontaneous remission” the body adjusts to whatever caused the A-Fib and starts beating normally without any treatment at all.
But don’t count on this happening.
You still need to be under a doctor’s care and monitoring. The biggest risk of not treating Atrial Fibrillation is increased risk of clots and stroke. If you are young and otherwise in good health, for now, you may not need any medication.
Last updated: Tuesday, July 14, 2015
Go back to FAQ for the Newly Diagnosed A-Fib Patient
2. “Did I cause my Atrial Fibrillation? Am I responsible for getting A-Fib?”
Most likely not.
We all remember our first attack of A-Fib—the shock, fear, confusion, the sense of something wrong in our body that we can’t control and the rushing to a doctor and/or emergency room.
Often there’s a tendency to blame ourselves, to feel guilt. We ask ourselves “What did I do—or not do—that caused my A-Fib?”
In general we are not responsible and didn’t cause our A-Fib. It’s different from a life-style related condition (like liver failure due to alcohol abuse).
Those newly diagnosed need to think of A-Fib as fate or karma or a life accident—rather than something we bring on ourselves. In life sometimes bad things happen to good people through no fault of their own. Think of A-Fib that way.
We need to keep saying to ourselves, “I am not responsible for my A-Fib. I did not cause my A-Fib,” like a chant or mantra whenever we start feeling guilt or blame for our A-Fib.
Last updated: Tuesday, July 14, 2015
10. “Can I drive my car if I have Atrial Fibrillation?”
In general, yes. With most types of A-Fib you can drive safely.
But if your episodes of A-Fib cause dizziness, you need a driving plan. As soon as you feel the beginning of an episode, pull off to the side of the road and stop the car. Put on your car’s hazard lights. Wait there until the episode passes.
If this happens often or if your episodes of A-Fib last a long time, you may have to stop driving entirely.
Last updated: Wednesday, July 15, 2015
4. “Is Atrial Fibrillation a prelude to a heart attack?”
In general, no, A-Fib is not like a heart attack.
A heart attack is a physical problem with your heart muscles or heart functions. For example, a blocked artery may result in what is called a “myocardial infarction” in which part of the heart tissue actually dies due to a lack of blood.
Conversely, A-Fib is primarily an electrical or rhythm problem, though it may be related to other heart problems like hypertension and Mitral Valve disease. For more about the physiology of A-Fib, see our Overview of Atrial Fibrillation.
However, A-Fib untreated over a long period of time could eventually stretch and weaken your heart, and possibly lead to heart malfunction and a heart attack.
Last updated: Wednesday, August 26, 2015
Frequently Asked Questions by Newly Diagnosed Patients
Newly diagnosed Atrial Fibrillation patients have many questions about living with A-Fib. These are answers to the most frequently asked questions by patients and their families. (Click on the question to jump to the answer)
Last updated: Monday, July 13, 2015
11. “Is drinking coffee (tea, colas, other products with caffeine) going to make my A-Fib worse or trigger an A-Fib attack?”
I used to include coffee as a trigger of A-Fib. But a recent research study suggests the opposite, that coffee and caffeine in moderate to heavy doses (2-3 cups to 10 cups/day) may not trigger or induce A-Fib.
The researchers who discovered the antiarrhythmic effects of coffee (caffeine) were somewhat surprised at their findings. They had expected to find the opposite results. Caffeine is a stimulant. It makes its consumers awake and alert, and it improves performance.
Coffee (caffeine) is commonly associated with disruption of cardiac rhythm. But does research confirm this belief? Most cardiac patients tolerate normal amounts of caffeine without difficulty.
The Danish Diet, Cancer, and Health Study which followed 50,000 middle-aged people for around six years, found that caffeine does not increase the risk for developing A-Fib. The daily consumption of caffeine from coffee, tea, cola, cocoa, and chocolate was quite high, as is usual in Scandinavia where people drink 2-10 cups of coffee per day. But researchers are currently unable to identify the mechanism(s) behind coffee’s potential antiarrhythmic effect.
The important question is, how does coffee (caffeine) affect you personally?
If you drink a cup of coffee and then have an A-Fib attack, you may have to stop drinking coffee. But for others, a blanket prohibition against drinking coffee probably isn’t justified by current research. In fact, coffee (caffeine) may have antiarrhythmic effects.
Advice from contributor ‘Allan’, cured of Persistent A-Fib after two ablations at Bordeaux, writes:
“I tried many different things both mainstream and alternative to get relief from A-Fib. I also observed and noted triggers with a great deal of intensity, so I feel compelled to comment on the latest post regarding the positive effects of Coffee/Caffeine. I never had anything other than bad effects from coffee on my A-Fib. Coffee/caffeine was a significant trigger for me…even in very small doses. So I guess my story underscores the complexity of triggers/suppressants across the general population. I do hope people reading that report don’t go out and dose up on coffee. We all know that coffee will make our hearts go faster, which is probably not good.”
Thanks to contributor Karl for calling our attention to these articles.
Last updated: Wednesday, July 15, 2015
12. “Is there any way to tell how often I get A-Fib or how long the episodes last? What kind of A-Fib monitors are available? I have silent A-Fib (A-Fib without any obvious symptoms). It was discovered by accident when I was getting an EKG during a physical.”
Your doctor may use a Holter or an Event Monitor. A Holter Monitor records your EKG continuously, usually for 24 hours; an Event Monitor can be used for up to 30 days or longer. For a more in depth discussion about Holter and Event monitors, see my report A Primer: Ambulatory Heart Rhythm Monitors.
To monitor for A-Fib yourself, try a consumer, or DIY, sports heart rate monitor available from sporting goods stores. Used by runners and other athletes, they rely on the use of a chest strap to pick up the electrical signals from the heart and transmit to a special wrist watch.
On most you can program a high heart rate zone which you might enter only if you were in A-Fib. That way you could record when and how long you stayed in A-Fib and what your max heart rate was. Some have internal storage recording that can be download to your PC to view data in a graphic form.
We like the “Polar” brand. Check out the array of Polar brand heart rate monitors on Amazon.com. Other companies include Timex, Garmin, Acumen, Nike, and Cardiosport.
17. “I care for my mom who has A-Fib. She is 94 and sees a doctor on a regular basis. She gets A-Fib attacks maybe once every two weeks and usually in the morning. But I work full time. Is there a heart rate monitor my mom can wear that would alert me when her heart rate is over a certain number? That way I can be alerted even when I’m at work.”
Yes, MyPulse by Smart Monitors, Inc. has a solution for you. This is a practical alternative to the expense of a medical monitoring service if you are just interested in simple heart rate data. Most consumer heart rate monitors rely on a chest strap which transmits heart rate data to a wristwatch. The MyPulse Long Range Monitor has a small Repeater device carried by the person wearing the chest strap. The Repeater transmits the data to a Receiver which is connected to a PC/notebook via a USB port. The MyPulse application runs on a PC and provides a graphic display of real time heart rate data.
The software can be configured to provide alerts via email or text message to multiple recipients if a preset heartbeat limit is exceeded.
(Thanks Julie Skarbeck for this important question and to Ed Webb for doing the research and writing about the Smart Monitor.)