Boston AF Symposium, January 16-17, 2004

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

OVERVIEW

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

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

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

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

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

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

(Author’s Note: These summaries are dedicated to the memory of Dr. Brian McGovern of Massachusetts General and the Atrial Fibrillation Foundation who was killed April, 2003. Though I met Dr. McGovern only once, his death was like losing a best friend. I was most fortunate to have Dr. McGovern share with me over a box lunch some of the history of the Boston A-Fib Symposium and the Atrial Fibrillation Foundation. He was a charming, smart, experienced, knowledgeable, down-to-earth doctor dedicated to helping people with A-Fib. We will never forget him.

In his introductory remarks Dr. Jeremy Ruskin of Massachusetts General dedicated the Boston A-Fib Symposium 2004 in memory of Dr. McGovern. Many speakers began their talks by expressing how Dr. McGovern affected their lives and how he is missed.)

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

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

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

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

Dr. Camm cited several studies such as:

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Answering questions from the audience Dr. Nattel pointed out that not all cases of Congestive Heart Failure develop A-Fib.
¹(atrial transient-outward [I_to ], slow delayed-rectifier [I_ks], L-type Ca²⁺ [I_ca.L] ²(Na⁺ Ca⁺⁺ exchange current [I_NCX]

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

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

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

(AUTHOR’S NOTE: The great innovation of Dr. Morady and Dr. Pappone is the use of what I would call the “drop and drag” technique of making linear circular lesions. Instead of trying to make continuous, perfect linear lesions which can be difficult and time consuming, they simply drop and drag the catheter to make the linear circular lesions, even though there may be gaps left in the lesions. Though A-Fib signals may still get through these gaps and cause Atrial Flutter, over time scar tissue and fibrosis usually close these gaps. This procedure represents a major change in treating A-Fib. Instead of concentrating on the Pulmonary Veins and Pulmonary Vein Potentials, the emphasis is on creating blocking lesions in the left atrium. After this procedure Pulmonary Vein Potentials may still remain. As Dr. Morady said, “It doesn’t matter if the triggers are still there……Our focus has swung from triggers to substrate modification [changing the left atrium].”
This “drop and drag” technique may soon become the standard way of doing Pulmonary Vein Ablations. It is easier, faster, requires less operator skill, and seems to get somewhat better results than other PVA procedures.)

(In 2007 it appears that Dr. Pappone’s lesions are now very similar to linear lesions and have few or no gaps. He makes many short, overlapping passes with the catheter rather than the “drop and drag” technique.)

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

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

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

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Last updated: Sunday, February 15, 2015

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