"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

"Your book [Beat Your A-Fib] is the quintessential most important guide not only for the individual experiencing atrial fibrillation and his family, but also for primary physicians, and cardiologists."

Jane-Alexandra Krehbiel, nurse, blogger and author "Rational Preparedness: A Primer to Preparedness"


"Steve Ryan's summaries of the Boston A-Fib Symposium are terrific. Steve has the ability to synthesize and communicate accurately in clear and simple terms the essence of complex subjects. This is an exceptional skill and a great service to patients with atrial fibrillation."

Dr. Jeremy Ruskin of Mass. General Hospital and Harvard Medical School

"I love your [A-fib.com] website, Patti and Steve! An excellent resource for anybody seeking credible science on atrial fibrillation plus compelling real-life stories from others living with A-Fib. Congratulations…"

Carolyn Thomas, blogger and heart attack survivor; MyHeartSisters.org

"Steve, your website was so helpful. Thank you! After two ablations I am now A-fib free. You are a great help to a lot of people, keep up the good work."

Terry Traver, former A-Fib patient

"If you want to do some research on AF go to A-Fib.com by Steve Ryan, this site was a big help to me, and helped me be free of AF."

Roy Salmon Patient, A-Fib Free; pacemakerclub.com, Sept. 2013

Technology & Innovations

A-Fib Technology & Innovations

AliveCor Kardia May be Big Winner in Britain’s NHS Plan

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).

AliveCor sensor with screen and smartphone 400 x 270 pix at 300 res

AliveCor Kardia attached to a smartphone

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.

Resource for this article

Wearables in Healthcare: You can Help Develop A-Fib App

It’s early days for wearables in healthcare, but there’s a lot of potential.

In the near future, an Apple Watch or Android Wear could detect if the wearer is experiencing Atrial Fibrillation. A preliminary algorithm (app) to detect A-Fib has been developed by researchers at UCSF and engineers at Cardiogram, Inc.

Sample of A-Fib app on Smart Watch

Sample of A-Fib app on Smart Watch

The mRhythm Study: You Can Help Develop the Smart Watch App

The researchers need your help now. If you have an Apple Watch or Android Wear—regardless of whether you have A-Fib—you can contribute your data to help make the algorithm more accurate.

The mRhythm Study is being run with the UCSF Health eHeart Study, using Cardiogram to train a deep learning algorithm to detect atrial fibrillation.

To Participate in the Study: Visit the mRhythm Study website and scroll down the page and look for ‘We Need Your Help.’ At the bottom of the page, you can then read answers to ‘Frequently Asked Questions’.

See How the System Works: To see the graphic displays of how the system works, go to Cardiogram, Inc. or see the Apple Watch graphics in particular.

mrhythm graphic 400 x 175 pix at 300 res

What atrial fibrillation and normal heart rhythm look like when measured on a watch.

What This Means for Patients

Each year, more than 100,000 strokes are caused by A-Fib. But all too often, their A-Fib is “silent” with no obvious or noticeable symptoms. In these cases, their A-Fib is undiagnosed until they have a stroke. Only then do they find out they have A-Fib (…if they survive). About 50% will have a disabling stroke.

Apple Watch owners—regardless of whether you have A-Fib—you can contribute your data to help develop this app. 

If the Smart Watch algorithm app works as intended, anyone with an Apple Watch or Android Wear will be alerted if they are experiencing Atrial Fibrillation.

For the undiagnosed, their A-Fib will be ‘visible’ and no longer be “silent.” They will know if they are at risk of an A-Fib stroke and can get the proper preventive treatment.

Today patients rely on an ECG in a doctor’s office or the use of a Holter monitor to detect A-Fib. Instead, a Smart Watch with the A-Fib app can extend a patient’s monitoring period to a year (between doctor’s visits) or on an on-going basis.

Amazing! Think of all the lives saved and debilitating strokes avoided! The A-Fib Smart Watch app has the potential to revolutionize the field of A-Fib monitoring.

References for this article


My 2015 Top Five List: Advancements in the Treatment of A-Fib

Looking back over 2015, I found five significant developments for those ‘living’ with A-Fib and those seeking their ‘cure’. My ‘Top Five List’ focuses on the Watchman device, a Pradaxa antidote and research findings about lifestyle choices, and reducing fibrosis.

1. FDA Approves the Watchman Device

The Watchman occlusion device

The Watchman is positioned via catheter

Anticoagulant Alternative: Because A-Fib patients are at high risk of stroke and clots, a blood thinner (anticoagulant) like warfarin is often prescribed. If you can’t or don’t want to be on blood thinners, you had few options.

That was until March 2015 when the US Food and Drug Administration (FDA) approved the Watchman device. There’s now an option to blood thinners! The Watchman device (Boston Scientific) is inserted to close off the Left Atrial Appendage (LAA), the origin of 90%-95% of A-Fib clots.

To read my complete Top Five List…go to My 2015 Top Five List: A Review of Advancements in the Treatment of A-Fib->.

My 2015 Top Five List: A Review of Advancements in the Treatment of A-Fib

2015 in Review at A-Fib.comWith the beginning of a new year, we often look back and measure how far we’ve come. In 2015, I found five significant advancements in the treatment of Atrial Fibrillation.

1. FDA Approves the Watchman Device

The Watchman occlusion device

The Watchman is positioned via catheter

Anticoagulant Alternative: Because A-Fib patients are at high risk of stroke and clots, a blood thinner (anticoagulant) like warfarin is often prescribed. If you can’t or don’t want to be on blood thinners, you had few options.

That was until March 2015 when the US Food and Drug Administration (FDA) approved the Watchman device. There’s now an option to blood thinners! The Watchman device (Boston Scientific) is inserted to close off the Left Atrial Appendage (LAA), the origin of 90%-95% of A-Fib clots.

It’s not an absolute guarantee you will never have a stroke―but neither is taking warfarin or the newer anticoagulants. For more, see Watchman Device: An Alternative to Blood Thinners.

2. Research: Watchman Better Than a Lifetime on Warfarin

Warfarin - Coumadin tablets various dosages

Warfarin (Coumadin)

The Watchman device isn’t simply an alternative to taking warfarin, clinical trials show it’s actually better. Patients with the Watchman had fewer hemorrhagic strokes and less bleeding compared to patients on warfarin. (Warfarin and other anticoagulants work by causing bleeding and are inherently dangerous.)

It’s too early to say the same about the newer anticoagulants like Pradaxa, Xarelto, Eliquis and Savaysa/Lixiana with their short history but one would expect the same general principles to apply. For more, see Watchman Better Than Warfarin.

3. Antidote for Pradaxa

Praxbind - antidote to Pradaxa

Praxbind: Pradaxa antidote

Up to now, patients on Pradaxa have been bleeding to death in the emergency room while doctors were powerless to stop their bleeding and could only stand by and watch them die. See Stop Prescribing or Taking Pradaxa.

In October 2015, the FDA granted “accelerated approval” to Praxbind, the reversal agent (antidote) to Pradaxa (Boehringer Ingelheim). Praxbind (idarucizumab) is given intravenously to patients and reverses the anticoagulant effect of Pradaxa within minutes.

Note: The reversal agent, Andexanet Alfa, is on FDA fast track and is expected to be approved by mid-2016 as an antidote for Xarelto and Eliquis (Factor Xa inhibitors).

4. Life Style Changes Can Make Some People A-Fib Free



Weight Loss: A weight loss program and counseling in Australia has worked so well that some patients have become A-Fib free.

In his Adelaide clinic, Dr. Prashanthan Sanders convinces his overweight A-Fib patients to buy into the program, lose weight, and keep it off.  This holistic approach to health has also been successfully applied to other A-Fib contributing factors such as diabetes, sleep apnea, hypertension, binge drinking and smoking. See Weight Loss Key to Reverse Atrial Fibrillation, Improve Ablation Success.



Exercise: But not everyone can lose weight and keep it off. And other risk factors like hypertension and diabetes are more difficult to permanently change.

The same Australian researchers found that exercise improves A-Fib (even obese A-Fib patients benefit from exercise). Supervised aerobic and strength exercises reduced A-Fib by 84%.

Combine for Best Results: Exercise and weight loss together produced the best results. An astounding 94% of obese patients who both lost weight and exercised regularly were A-Fib free after rhythm control therapy (i.e., antiarrhythmic drugs and/or catheter ablation).

Couch Potato Warning: If you don’t exercise regularly, you’re almost guaranteed to stay in A-Fib. Even with rhythm control (antiarrhythmic drugs and/or ablation), 83% of the low-fitness obese patients had A-Fib.

5. Research Studies: Preventing Fibrosis

Fibrotic cells - 2008 Boston A-Fib Symposium Kottkamp

Fibrotic cells

A-Fib produces fibrosis, and up to now, was considered permanent and irreversible. Fibrosis is fiber-like scar tissue that stiffens and weakens the heart muscle which reduces pumping efficiency and leads to other heart problems.  (See Fibrosis and A-Fib).

Dr. Jose Jalife’s experimental studies with sheep found that a Gal-3 inhibitor (GM-CT-01) actually reduced or prevented fibrosis. Better yet, instead of having to wait years for possible FDA approval, a natural supplement, Pecta-Sol C (Modified Citrus Pectin) works like a Galectin-3 inhibitor.

For A-Fib patients, this may provide the means to avoid fibrosis or repair fibrotic heart tissue. (See Galectin-3 Inhibitor Prevents A-Fib).

A Personal Prediction

WATCHMAN device at A-Fib.com


On a personal note, I’m excited about the great potential of the Watchman device to significantly reduce or eliminate the threat of strokes—especially in the elderly―even if they don’t have A-Fib.

Imagine a world where stroke risk could be eliminated by a simple 20-30 minute procedure. The Watchman device (and other occlusion devices) may change the way elderly medicine is practiced.

If you find any errors on this page, email us. Y Last updated: Thursday, January 21, 2016

Should the Left Atrial Appendage (LAA) be Removed in Patients With A-Fib?

Dr. Dhanunjaya Lakkireddy

Dr. Dhanunjaya Lakkireddy

AF Symposium 2015

Should the Left Atrial Appendage (LAA) be Removed in Patients With A-Fib?

by Steve S. Ryan, PhD

Leading doctors and researchers have pointed out the importance of the Left Atrial Appendage (LAA) particularly when ablating persistent A-Fib. In the Bordeaux group’s Five-Step Ablation Protocol for Chronic A-Fib, after isolating the Pulmonary Veins (PVs), their next step is to look for A-Fib signals coming from the LAA. In 2010, Dr. Andrea Natale and his colleagues showed that in 30% of A-Fib patients, the LAA was the only structure that had A-Fib signals. (Circulation 2010.)

In his presentation, Dr. Dhanunjaya Lakkireddy from the Un. of Kansas Hospital in Kansas City, MO, confirmed these findings. After the PVs, “the LAA is the most common source of (A-Fib) focus triggers and other A-Fib signals.”

In Older Patients the PVs Have No A-Fib Signals

He further stated that in patients over 70 years old, especially women, the LAA plays a more important role so much so that the PVs are often silent.

How Removing the LAA Affects Left Atrium Pumping Volume

Removing or closing off the LAA reduces the pumping volume of the left atrium by 15% to 30%. But after the LAA is removed, the overall left atrium volume improves.

Removing The LAA Reduces Natriuretic Peptides―But The Heart Compensates Over Time

The LAA is responsible for neuroharmonal changes such as natriuretic peptide levels (i.e., regulates the amount of sodium in the urine) which are important for bodily functions such as thirst. When the LAA is removed, natriuretic peptide levels go down. But Dr. Lakkireddy’s research shows that over time these levels normalize. Other heart areas such as the right atrium compensate and produce more natriuretic peptides to make up for what the LAA used to produce.

Removing the LAA Lowers Blood Pressure

Removing or closing off the LAA often improves blood pressure by dropping epinephrine (adrenaline) levels and lowering (“down-regulating”) the

renin-angiotensin system (hormone system that regulates blood pressure and fluid balance).

Removing the LAA Improves Recurrence Rates

Dr. Lakkireddy found that removing or closing off the LAA at the same time as a catheter ablation for A-Fib reduces recurrence rates by 29%.

Editor’s Comments:
Why LAA A-Fib Signal Sources in Older People—Why Do PVs Go Silent?
One of the most important findings of Dr. Lakkireddy’s research is that in older people the LAA is the most important source of A-Fib signals, so much so that the PVs are often silent. This is counter-intuitive and hard to understand. If, as we know from years of previous research, A-Fib usually starts and is most often found in the PVs, why do the PVs go silent and A-Fib activity mostly move to the LAA in older people? What is the physical or chemical mechanism that causes this major change?
Sea-Change in Ablation Strategy
Dr. Lakkireddy’s presentation was the most important and ground-breaking for older A-Fib patients. It should change the way ablations are performed on older people. If you are over 70 years old, in persistent A-Fib and aren’t very active, you must seek out EPs and centers who understand and ablate the LAA. Most EPs don’t even look at the LAA as possible A-Fib signal sources. Don’t rely on your local EP to learn about this research and adopt any requisite new ablation strategies.
In Older A-Fib Patients the LAA Should be Removed
It certainly looks like, in the case of older people with A-Fib, the LAA should be removed by an occlusion device (either the Lariat or by surgery [AtriClip]). In addition to the known benefit of reducing A-Fib stroke risk (90%-95% of A-Fib clots come from thee LAA), the LAA is a major and often the only source of A-Fib signals in older people.
Little Downside to Removing the LAA
And according to Dr. Lakkireddy, there is very little downside to removing the LAA.
Blood pressure goes down, over time natriuretic peptide levels return to their pre-LAA levels as the heart compensates, the lost LA pumping volume does improve, and recurrence rates are reduced when the LAA is removed.
Older people who are less active may not even notice the loss of LAA pumping volume or the reservoir or surge effect of the LAA. (On the other hand, an active athletic senior may be affected by the loss of pumping volume if the LAA is removed.)
LAA Can Be Removed Before or After an Ablation
In the case of a catheter ablation for A-Fib, it may not be necessary to remove the LAA at the time of the ablation. Since it is a safer procedure than even an A-Fib ablation, the LAA could be removed three months before or after a catheter ablation.

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Last updated: Friday, March 6, 2015


Obesity Produces Fibrosis, But Getting Lean Reverses Fibrosis (in Sheep)

AF Symposium 2015

Dr. Prashanthan Sanders 150 pix at 96 res

Dr. Prashanthan Sanders

Obesity Produces Fibrosis, But Getting Lean Reverses Fibrosis (in Sheep)

by Steve S. Ryan, PhD

In a fascinating experimental study with sheep, Dr. Prashanthan Sanders from Royal Adelaide Hospital in Australia, overfed sheep so that they developed sustained obesity for 72 weeks. Their fibrosis increased. Their atria were damaged by fibrotic tissue replacing normal atria muscle. As the sheep moved from being overweight to obese, it was progressively easier to induce A-Fib.

Then Dr. Sanders made the sheep lose weight. With a 30% weight reduction, the fibrosis was no longer present! The sheep were similar to the lean sheep controls.

Dr. Sanders used activation mapping to show that in the obese sheep there was an increased delay in activation suggesting delayed conduction. It took a longer time to activate the atria. But when the obese sheep lost weight, conduction became normal. Also there were improvements in left atrial pressure, inflammatory cell counts and fibrosis, atrial TGf beta 1 and reversal of connexin-43 and ETR-beta (which contribute to fibrosis).

Hypertension and A-Fib in Sheep

Dr. Sanders also stimulated sheep into progressive hypertension for 15 weeks. As with the obese sheep above, these hypertensive sheep developed fibrosis. And activation mapping again showed delayed and abnormal conduction.

Sleep Apnea and A-Fib in Animals

Citing other research, including from Dr. Andrea Natale’s group, repetitively blocking off breathing as in sleep apnea developed increased fibrosis as well as slowed atrial conduction, increased atrial size, and induced more atrial fibrillation.

More Risk Factors Lead to Persistent A-Fib

Dr. Sanders pointed out that A-Fib patients with cardiovascular risk factors like obesity, hypertension, and sleep apnea are more likely to progress to persistent A-Fib than individuals with few or no risk factors.

Fibrosis Produces More Fibrosis

Fibrosis (interstitial fibrosis) is the main factor in changing the atrial substrate. Voltage maps of fibrotic atria show large areas of low voltage, increased areas of scarring, and a more complex electrogram resulting in abnormal conduction. According to Dr. Sanders, fibrosis produces more fibrosis. “There is clear evidence that A-Fib feeds back on itself to remodel this process, and there is even a suggestion that it may induce further atrial fibrosis.”

Editor’s Comments:
(Readers of this report may also want to read Dr. Jose Jalife’s similar experimental sheep studies where, among other findings, he proved that pacing sheep into A-Fib produces fibrosis. See Experiments in Atrial Remodeling in Sheep and the Transition From Paroxysmal to Persistent A-Fib.)
In a previous report Dr. Sanders described the great results he is achieving by having his overweight A-Fib patients lose weight, buy into the program and keep the weight off. Sometimes this life style change alone makes them A-Fib free. But not everyone can lose weight and keep it off. Other risk factors like hypertension and diabetes are more difficult to permanently change. And once A-Fib is well established, life style changes aren’t as effective. Though life style changes certainly do improve overall health and heart health.
Fibrosis is Usually Permanent and Irreversible
Unlike some of Dr. Sanders results with sheep, fibrosis in general is considered permanent and irreversible.
Life Style Changes Usually Not Effective in Lone A-Fib
Approximately half of people with A-Fib have no risk factors or co-morbidities (which used to be called “Lone A-Fib.”) I, for example, developed A-Fib at age 54 when I was in perfect health, running track and 5ks, lifting weights, etc. Life style changes aren’t always effective in cases of Lone A-Fib.
Risk Factors lead to persistent A-Fib
Why do some people with A-Fib stay Paroxysmal for years while others progress rapidly to Persistent A-Fib? Perhaps Dr. Sanders has discovered the reason. Risk factors or co-morbidities like obesity, sleep apnea, hypertension, diabetes, etc. make people more likely to transition from paroxysmal to persistent A-Fib. Patients with A-Fib risk factors should be warned of this danger.
Fibrosis Produces More Fibrosis
Here’s yet another scary thought for anyone with A-Fib. According to Dr. Sanders, fibrosis may feed upon itself producing yet more fibrosis.
Though this isn’t normally done today, anyone diagnosed with A-Fib ought to have a heart MRI to measure exactly how much fibrosis has developed in their heart and how much and how fast it is progressing.
This danger of fibrosis progression is yet another incentive to consider a catheter ablation in order to be A-Fib free with no further progression of fibrosis.

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Last updated: Friday, March 6, 2015

The Virtual Heart Computerized Simulation – Dr. Natalia Trayanova

AF Symposium 2015

Dr. Natalia Trayanova, Johns Hopkins University

Dr. Natalia Trayanova

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).

The Virtual Heart Simulation images

The Virtual Heart Simulation images

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.

Editor’s Comments:
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.
References for this article

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Last updated: Thursday, April 16, 2015

Getting FDA Approval for the Watchman Device

AF Symposium 2015

Getting FDA Approval for the Watchman Device

by Steve S. Ryan, PhD, February 2015

Vivek Reddy Mt Siani Hospital

Dr Vivek Reddy Mt Sinai Hospital

The Watchman device is in the last stages of the approval process from the FDA. This is a true “tipping point” in the development of devices to help A-Fib patients (The Watchman is approved everywhere else in the world).  If (or rather when) the Watchman is approved in the U.S., it will be because of the dedicated, thorough research of Dr. Vivek Reddy and his many colleagues and researchers.
(Added March 2015: The FDA approved the Watchman Device March 2015. See http://a-fib.com/my-2015-top-five-list-of-a-fib-advancements/)

Dr. Vivek Reddy of Mount Sinai Hospital gave a historically important talk entitled “5 Year Follow-Up Data On Watchman in Coumadin Eligible Patients.” He discussed the two major clinical trials of the Watchman device—PROTECT-AF and PREVAIL.


In PROTECT-AF, patients who were followed for five years had less strokes (Primary Efficacy Endpoint) than those in the warfarin arm and there were less deaths. (Reddy, V. et al. JAMA. 312:1988 [2014])


Reddy Watchman 1 500 pix at 96 resThe PREVIAL clinical trial was a smaller study designed to confirm the results of the PROTECT-AF trial and validate the safety of the implant procedure. With regards to the Primary Efficacy Endpoint (composite of all stroke, systemic embolism, and cardiovascular/unexplained death at 18 months), “non-inferiority was not achieved.” In other words, the Watchman group performed slightly worse than the warfarin control group.

But for some reason the warfarin control group performed much better than in any other trial. The Ischemic Stroke Rate per 100 patient-years was 1.1 in PROTECT-AF, while in PREVAIL it was only 0.3. In other words, the warfarin control group in PREVAIL overperformed compared to any other clinical trial.

Dr. Reddy pointed out to the FDA panel October, 2014 that the longer-term follow-up of the PROTECT-AF trial confirmed the efficacy of the Watchman therapy, even though the PREVAIL trial trended negative compared to the warfarin control group. But this particular PREVAIL warfarin control group was “unusual” and performed much better than expected.

Looking at other adverse events, the hemorrhagic stroke rate was 0.4% for the Watchman arm and 0.7% for the warfarin control group.

The Cardiovascular Death rate was 1.4% for the Watchman vs. 2.3% for warfarin.


Reddy Watchman 2 500 pix wide by 96 resWhen you combine the PROTECT-AF and PREVAIL studies even with the “unusual” PREVAIL warfarin control arm results, “All Stroke” is non-inferior or about the same for both arms.

Also, as one would expect, after 6-months post implant, the Watchman arm had significantly less bleeding events than warfarin.

Early Safety Endpoint Achieved

The Early Safety Endpoint in PREVAIL was achieved.

• There was a significant increase in inplant success rate (95.1%) compared to PROTECT-AF (90.9%). There was no significant difference in complication rates between experienced and new implanters, demonstrating the success of the physician training program. Following successful implantation, 99.3% of patients were able to discontinue warfarin after 12 months.

• There was a 52% reduction in procedure/device related vascular complications (1.9% in PREVAIL vs, 4.0% in PROTECT-AF).

• There was a 52% reduction in pericardial effusions requiring intervention and at a rate comparable to other left atrial procedures.

Editor’s Comments:
Because of a freak statistical accident, the warfarin arm in the PREVAIL trial performed much better than expected and much better than in any previous trials. Perhaps if the PREVAIL trial were longer or had more subjects, the results might approach the longer PROTECT-AF trial. One shouldn’t interpret the results of PREVAIL as negating the conclusive results of the longer PROTECT-AF trial. In PREVIAL the Watchman device performed just as well as in PROTECT-AF. Only the warfarin control arm was different.
The most significant finding of PREVAIL was the the Early Safety Endpoints were achieved. That was the primary reason the FDA wanted the PREVAIL study in the first place.
Thanks to the excellent research and presentation by Dr. Reddy and his colleagues before the FDA, I’ll go out on a limb and predict the FDA will approve the Watchman device, probably by the middle of 2015.
The Watchman device closes off the LAA where 90-95% of A-Fib strokes come from. It’s a very low risk procedure that takes as little as 20 minutes to install. Afterward, you would usually not need to be on blood thinners. (For more, see my article, The Watchman Device: The Alternative to Blood Thinners).
If the FDA were to not approve the Watchman, this would be a major setback in the treatment of A-Fib in the US. The Watchman is approved everywhere else in the world. One would have to go to Canada or overseas to get the Watchman installed.
NOTE: Dr. Reddy also discussed this topic in February at the 2015 International Symposium on Left Atrial Appendage (ISLLA) held in Marina Del Rey, CA.

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Last updated: Friday, November 11, 2016

Closure of the LAA: Why One Patient Chose the Lariat Over the Watchman Device

By Steve S. Ryan, PhD, February 2015

When closing off the Left Atrial Appendage, a small pocket of heart tissue located above the left atrium, you are typically looking at an occlusion device such as the Lariat or the Watchman (surgical removal is also an option). The Lariat is relatively new, so, how does it compare to the Watchman?

About the Lariat

Lariat II image

The Lariat occlusion device

The Lariat device is a noose-like device which is slipped around the LAA. This ‘lasso’ is then tightened, and eventually the tissue dies and shrivels up (like a grape into a raisin). In effect, the Lariat chokes off the LAA and eliminates it as a source of A-Fib signals. (For more on the Lariat see my article: Tech & Innovations: Lariat II.)

A serious problem with the Lariat is described as “the gunny-sack effect”. The LAA heart tissue between the lariat lasso atrophies and becomes thinner. As with a gunny sack, the multiple tight folds begin to loosen and unravel slightly leaving a hole. If the hole is large enough, blood may flow into and out of the dead LAA possibly carrying with it dead tissue remnants into the blood stream which can cause clots and strokes. The number of clot/strokes reported so far is very small compared with the total Lariat cases worldwide.

Easily Fixed if Discovered

Once this hole or leak is discovered, it’s relatively easy for the EP to fix by closing it off using one of several occluder devices.

About the Watchman Device

The Watchman occlusion device

The Watchman occlusion device

The Watchman device, in contrast, is basically a plug that closes off the LAA from the inside of the LAA. It’s inserted via catheter, positioned and inflated. It ‘screens’ any clots from leaving the LAA. Eventually, heart tissue grows over the area.

But due to the typical non-symmetrical opening of the LAA, there can be leakage when the Watchman is installed due to the ‘edge effect’ (the device not always fitting perfectly). The leakage, though, isn’t generally large enough to permit clots to escape from the LAA into the heart. The incidence of leaks is around 30% to 35% depending on which research you look at.

Clots can also form on the surface of the device site. Therefore, after the Watchman is installed, patients are put on blood thinners for some time. (The risk of clot formation on the device site is around 4.5%, which is comparable to the risk of patients on oral anticoagulation.)

Eventually heart wall tissue grows over the occluded surface. Though this does not necessarily block electrical activity coming from the LAA, so the edges of the LAA may have to be ablated (which can be challenging).

Solution: Ablation First, Then Watchman

To avoid this last scenario (A-Fib triggers coming from the LAA), your EP will typically recommend you first get a catheter ablation to isolate the LAA. Later, after the ablations scars (lesions) have healed, the Watchman can then be installed, if necessary.

The Watchman device and the Lariat are FDA approved.

Why One Patient Chose the Lariat

Shannon Dickson, editor of THE AFIB REPORT, says he chose the Lariat “after already having had a successful LAA isolation ablation a year earlier which had eliminated the last remaining trigger source of a periodic LAA-based tachycardia. The reason I chose the Lariat in spite of having no more arrhythmia at all after that LAA isolation procedure, was to not only be able to stop all OAC drugs, but to add an extra measure of insurance that my LAA could never again become a source of any future arrhythmia. The prior successfully ablated LAA trigger source could never reconnect at some point and start the whole mischief again.

By fully ligating the LAA with a successful Lariat or AtriClip procedure, the added bonus of full electrical isolation of the LAA is added to the obvious vascular isolation as well.

The Watchman is designed to prevent LAA-based thromboembolic events, but does not electrically isolate the LAA. As such, any Watchman candidates who still have active LAA-based triggering should strongly consider getting an LAA isolation ablation prior to the Watchman procedure.”

Shannon considers the LAA “the most lethal appendage in the human anatomy.”

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Questions About the Lariat

The Lariat is a relatively new procedure with many questions from patients. Here are several of these questions with my thoughts after each one.

Q: “What are the long-term effects of leaving dead heart tissue to dissolve and become reabsorbed on the left atrium and in the pericardium sack?” These are yet to be fully studied. Most of the time the LAA remnant shrinks and becomes a fibrous, hardened tissue.

Preliminary data suggests that the hormones normally produced by the LAA are eventually re-produced by the Right Atrial Appendage (RAA) (it’s not talked about much, but yes, there is a Right Atrial Appendage too) and other parts of the heart.

Q: “If there is any type of hole left, will blood from the heart eventually leak into the pericardium sack once the LAA is gone?”

Most likely not. This hasn’t been an issue in all the years of surgical staple or suture ligation of the LAA. When the LAA shrinks and dissolves, it may form a permanent cap over any remaining hole. The perfect analogy here may be the umbilical cord after it is tied. The blood flow ceases and it becomes a hardened, fibrous structure.

Q: “What actually happens to the LAA when it dies and deteriorates?”

We know that the LAA shrivels up (like a grape into a raisin) and eventually disintegrates. On the inside of the heart where the LAA mouth was, heart tissue eventually grows over this now-closed mouth or opening.

Q: “How long does this process take?”

In general it takes around three to six months for heart tissue inside the heart to grow over the closed-off mouth of the LAA. On the outside of the heart, the LAA shrinks to a final-state cap over the closed-off LAA mouth in about a year or slightly longer and is somewhat variable per person.

Q: “How does this dead tissue affect the rest of the heart and body?”

Most likely this dead LAA tissue won’t have a bad effect on the rest of the heart and body. In the experience of surgical stapling or sutures to close off the LAA, there hasn’t been a body of evidence of late issues or complications. Though again, it’s too early in the experience of the Lariat procedures to say this definitively.

Q: “Some say the LAA dead tissue is simply absorbed by the body. How does this happen?”

More study needs to be done to identify and define the actual processes and time table, but previous surgical studies and autopsies indicate that the dead LAA disintegrates and is eventually re-absorbed by the body.

The Bottom Line

The Lariat’s “Gunny-sack” effect described above is relatively rare and is easily fixed. It shouldn’t be a major concern if you need to have a lariat device installed to close off your Left Atrial Appendage. Just make sure your EP checks the Lariat for leaks every three months during the first year after you get it installed. If your doctor doesn’t or won’t do that, find someone else to install the Lariat.

In spite of the small risk of clotting with the Lariat, if you can’t tolerate taking anticoagulants, it’s still the procedure of choice (the Watchman device requires 6 weeks of anticoagulants post-procedure). But it’s a more complicated procedure than installing a Watchman. You should only go to an EP experienced at installing the Lariat.

People chose the Lariat because it’s a welcome alternative to a lifetime on blood thinners (anticoagulants). 90%-95% of A-Fib clots come from the LAA. Closing off the LAA isn’t an absolute guarantee one will never have an A-Fib clot or stroke, but it comes close. (Neither are today’s anticoagulants.)

Overall, most people who have a Lariat installed are older with long-term persistent A-Fib, or with long-term paroxysmal A-Fib with the LAA as the prime driver of their arrhythmia.

If you are worried about what happens to your LAA when it dies and disintegrates, and how it might affect your body and overall health, we have no evidence or experience that it is a long-term health risk.

Which is Better―The Lariat or the Watchman?

There haven’t been any head-to-head comparisons of the Lariat and Watchman. So far, reaching conclusions about the superiority of one device versus the other cannot be made at this time. The choice of device has to be made based on the individual needs of a particular patient.

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Return to Index of Articles: Research & Innovations

Last updated: Friday, August 28, 2015

Boston AF Symposium – 2008

Boston AF Symposium, January 17-19, 2008

“Atrial Fibrillation: Mechanisms and New Directions in Therapy”

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


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

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

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

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

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

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

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


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


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.)

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

(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.)

Editor’s Comments:

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

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

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

Current Guidelines Don’t Work

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

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

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

Implications for Patient Care and Clinical Investigation.”

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

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

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

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

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

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

3. Surgical Ablation
Surgical ablation is appropriate for:

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

4. Recommend ablation techniques.

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

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

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

6. Help decide anticoagulation strategies.

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

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

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

8. Specify patient follow-up criteria.

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

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Last updated: Friday, January 1, 2016

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

Subject Index to A-Fib.com Articles for Additional Reading

Book of heart 2 Red in box 150 x 96Subject Index to A-Fib.com Articles

This index is a growing list of articles found throughout the A-Fib.com site that augment or supplement the major topics (each subject title is a link). If you have a keyword or topic, you can also use the ‘Search’ feature in the upper right corner of every page. New posts are flagged in Red.

Select a subject to browse articles:

♥  Dealing with Atrial Fibrillation

♥  Diagnosis & Testing

♥  Minerals Deficiencies & Supplements

♥  Drug Therapies & Medications

♥  Catheter Ablation, CyroBalloon and Pulmonary Veins Isolation

♥  Surgeries: Maze/Mini-Maze, Convergent, LAA Closure

  AF Symposium Articles by Year: Steve’s Summary Reports

♥  Research and Innovations

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Last updated: Monday, March 2, 2015

Article Index: Diagnostic Testing

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Diagnosis & Testing

At-Home Testing for Sleep Apnea with WatchPAT Device (Feb 2015) NEW

A Primer: Ambulatory Heart Rhythm Monitors

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

Understanding the EKG Signal

The CHADS2 Stroke-Risk Grading System UPDATED

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Return to Subject Index to A-Fib.com Articles Last updated: Tuesday, April 14, 2015

Article Index: Technology Advancements and Innovation

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Technology Advancements and Innovation

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Last updated: Friday, February 13, 2015

Article Index: Research & Innovations

Research Studies and Scientific FindingsResearch You Can Use at A-Fib.com

The Facts About Women with A-Fib: Mother Nature and Gender Bias—Or—Get Thee to an EP ASAP by Patti Ryan

By Combining RF and CryoBalloon Ablation Techniques, Do Success Rates Increase?

Israeli Study Contradicts Recent CHA2DS2-VASc Guidelines: Being Female Not a Risk Factor for Stroke

2015 International Symposium on Left Atrial Appendage (ISLAA): Brief Reports

Sleep Apnea—New At-Home Testing Option

A-Fib Hospitalizations Up Sharply since 2000

Magnesium and Long Life: Insights for Atrial Fibrillation Patients

The New CHA2DS2-VASC Guidelines and the Risks of Life-Long Anticoagulation Therapy

A-Fib and Stroke: Women Under-Diagnosed & Under-Treated, a Woman’s Perspective

Left Atrial Appendage May be Important for Heart Repair 

Obesity in Young Women Doubles Chances of Developing A-Fib 

Premature Atrial Contractions (PACs) Predict A-Fib 

FIRM (Focal Impulse and Rotor Modulation) for Catheter Ablation of A-Fib

Women in A-Fib Not at Greater Risk of Stroke!

Dabigatran (Pradaxa) Danger During Ablation—Switch to Warfarin

Stem Cells Reverse Heart Damage—(And May Repair Fibrosis and Scarring in A-Fib)

Septum Opening Plugged? You Can Still Have a Catheter Ablation to Fix your A-Fib

Testing TechnologyTechnology Advancements and Innovation

Patient Review: AliveCor Heart Monitor for SmartPhones 

Closure of the LAA: Why One Patient Choose the Lariat Over the Watchman Device

Emerging Technology: The Cyberknife & Radiosurgery

Advances in Heart Imaging And Mapping Systems

Removing or Closing Off the Left Atrial Appendage

Lariat II Suture Delivery Device

North American Arctic Front Stop-Af Trial

Laser Balloon Catheter

Multi-electrode RF Ablation Catheters

Force-Sensing Technologies

Remote Magnetic Navigation Systems by Hanson and Stereotaxis

The Watchman Device

Imaging Technologies

Rotational Angiogaphy

Balloon Catheters/Cryoballoon Catheter

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 If you find any errors on this page, email us. Y Last updated: Monday, October 3, 2016


Article Index: AF Symposium Steve’s Summary Reports

Article Index

AF Symposium Steve’s Summary Reports

♥ 2016 AF Symposium

2016 Overview Report
2016 My Reports Written for Patients

♥ 2015 AF Symposium

2015 Brief Reports
2015 My Reports Written for Patients

♥ 2014 AF Symposium

2014 Overview Report
2014 My Reports Written for Patients

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Last updated: Sunday, October 2, 2016

Article Index: Surgeries: Maze/Mini-Maze, Convergent, LAA Closure

Book of heart 2 Red in box 150 x 96Article Index

Maze/Mini-Maze Convergent, LAA Closure

2015 International Symposium on Left Atrial Appendage (ISLAA): Brief Reports (Feb 2015) NEW

Alert: Patients with Lariat Device for Left Atrial Appendage Closure NEW

Advantages of the Convergent Procedure by Andy C. Kiser, MD and Paul Mounsey, MD

Role of the LAA & Removal Issues

FAST Trial: Surgical Versus Catheter Ablation―Flawed Study, But Important Results for Patients

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Last updated: Wednesday, February 25, 2015

Article Index: Catheter Ablation, CyroBalloon and Pulmonary Veins Isolation

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Catheter Ablation, CyroBalloon and Pulmonary Veins Isolation

New Ablation Technique by Dr. Andrea Natale (Jan 2015) NEW

A-Fib Catheter Ablations: Ten-Year Success Rate is 87%

Considering a Catheter Ablation? Know Complication Rates When Choosing Your Doctor

Ablation Success Rate Much Better With Weight Control

Live Longer―Have a Catheter Ablation

Catheter Ablation Complications: In-depth Review and Comparison with AAD Therapy

Recurrence of A-Fib After Successful Catheter Ablation

Bordeaux Five-Step Ablation Protocol for Chronic A-Fib

A Cryo Ablation Primer

The Evolving Terminology of Catheter Ablation

Radiation Exposure During an Ablation Procedure: How to Protect Yourself from Damage

Risks Associated with Pulmonary Vein Procedure

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Last updated: Saturday, February 14, 2015

Article Index: Drug Therapies & Medicines

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Drug Therapies & Medicines

Eleven Things I Know About A-Fib Drug Therapy by Dr. Peter Kowey (Jan 2015) NEW

Warfarin vs. Pradaxa and the Other New Anticoagulants

Anticoagulant Therapy after Successful A-Fib Catheter Ablation: Is it Right for Me?

Amiodarone: Most Effective and Most Toxic

ATRIA Clinical Research Findings: Anticoagulants for Stroke Prevention

Watchman: the Alternative to Blood Thinners

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Last updated: Wednesday, August 26, 2015

Article Index: Minerals Deficiencies & Supplements

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Minerals Deficiencies & Supplements

Atrial Fibrillation Risk Linked with Low Serum Magnesium

Acupuncture Helps A-Fib—Specific Acupuncture Sites Identified

Alternative Remedies and Tips

Natural’ Supplements for a Healthy Heart (Updated April 2014)

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Last updated: Wednesday, March 18, 2015

Multielectrode RF Ablation Catheters

Technology & Innovations

Medtronic multielectrode ablation catheter

Medtronic multielectrode ablation catheter

Multielectrode RF Ablation Catheters

These circular and mesh array shaped catheters are also probably years away from FDA approval. Like balloon catheters they can fit into a pulmonary vein opening and isolate the opening in two or more passes.

These catheters also offer ablation at specific poles to produce pin-point ablation of A-Fib spots in the heart. Currently none of the versions offer internal or external irrigation. (Most RF catheter ablation today uses open irrigation to cool the catheter tip, which allows more energy to be delivered without the limitation of overheating the catheter tip.) (posted 2011)

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Last updated: Sunday, February 15, 2015

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