17th BOSTON AF SYMPOSIUM, January 12-14, 2012 “Atrial Fibrillation: Mechanisms and New Directions in Therapy”
The annual international Boston A-Fib Symposium is one of the most important conferences on A-Fib in the world. It brings together researchers and doctors who share the latest information. However, if you haven’t read and understood most of A-Fib.com, it may be difficult reading.
The overall mood of the 17th Boston Atrial fibrillation Symposium seemed to be one of confident anticipation. Many presenters expanded on how, by next year, there will likely be four new anticoagulants approved by the FDA (dabigatran [Pradaxa] already FDA approved, rivaroxaban (Xarelto—FDA approved Nov. 4, 2011), apixaban, and edoxaban). Doctors and patients will finally have alternatives to warfarin!
The dominant theme of this year’s Symposium was improved stroke prevention. On Friday, January 13, there were no less than nine presentations on stroke prevention, and the Thursday panel discussion of “Difficult Cases” mostly focused on anticoagulation problems.
The second most discussed topic was Pulmonary Vein Reconnection after ablation—(the most urgent topic of greatest concern for A-Fib doctors and researchers).
Editor’s comment: The author also launched our new book “Beat Your A-Fib: The Essential Guide to Finding Your Cure” at this year’s Symposium. It is available both as a print book (see Amazon.com for reviews) and in a .PDF version. Visit our book site at www.BeatYourA-Fib.com for more info.
This year’s Symposium featured a number of mini-symposia and individual presentations focusing on topics such as:
- The role of rotors in experimental and human A-Fib (very divergent opinions).
- Basic science topics related to A-Fib.
- Advances in the management and treatment of persistent A-Fib.
- Lesion monitoring during catheter ablation.
- A-Fib Guidelines and regulatory issues. The newest Guidelines were released at this year’s Symposium.
- Surgical ablation and surgical stroke prevention.
- New technology and methods of treating A-Fib.
- Pharmaceutical and non-pharmaceutical strategies for stroke prevention.
- In addition to live satellite case transmissions where the attendees could watch actual ablations being performed, there were also pre-recorded teaching cases. These sessions were among the most popular among attendees. They showcased the most advanced technologies in the rapidly evolving field of A-Fib treatment.
- Advances in antiarrhythmic drug therapy.
- Minimizing and managing complications in A-Fib ablation.
- Advances in antiarrhythmic drug therapy.
- Minimizing and managing complications in A-Fib ablation.
- Update about current ongoing clinical trials.
- Reviews of selected basic and clinical science papers on A-Fib which came out in 2011.
- The use of Registries (detailed open-book record keeping) in clinical practice.
- Panel and audience discussion of challenging cases in A-Fib ablation. (This session, late Saturday afternoon, though not as well attended as the previous day’s which saw over 1,200 attendees, showcased some of the best, most experienced A-Fib doctors illustrating and discussing some of their most difficult cases.)
Editor’s comment: The author is especially indebted to Dr. Peter Stevenson, the Editor of the Boston AF Symposium News, the official newspaper of the Symposium. This is the first year the Symposium published a newspaper. The news, interviews, advertisements and session coverage was amazingly well done and informative. (I have to admit to being jealous of Dr. Stevenson’s ability to stay up all night producing spot-on summaries of important presentations and get them printed by the next morning.)
The Symposium also featured a great degree of presenter/audience interaction and participation. Each attendee had a remote clicker with 1 through 5 choices. A presenter would, for example, pose a case and give five different treatment options, then allow time for everyone to vote. The percentage of attendees voting for each choice would be almost immediately shown on screen. The presenters and audience would then discuss the results.
In a presentation on the Surgical Management of the Left Atrial Appendage, Dr. Ralph Damiano, Jr. of Barnes Jewish Hospital in St. Louis, MO discussed, among other subjects, a disturbing case where a catheter-based occlusion device was inserted onto the Left Atrial Appendage (LAA) from inside the heart, but the insertion was unsuccessful. Part of the occlusion device was left protruding from the LAA into the Left Atrium with bare metal wires exposed.
In another disturbing incident at the Symposium, the live satellite presentation from Milan, Italy showed a different LAA occlusion device being inserted into a patient’s LAA. Though we saw in the pre-op how the catheter was flushed out with saline to prevent air bubbles from leaking into the Left Atrium, that’s exactly what happened during the live case.
Editor’s Comments: Even though inserting the Watchman device, for example, is a relatively simple procedure with a high success rate and relatively few complications, if a problem or mistake does happen, it can have a catastrophic result for a patient. For example, a device improperly inserted will most likely have to be removed by major heart surgery. An air bubble inside the heart can potentially cause an embolism, clot and stroke.
This editor in the past thought that the Watchman occlusion device was a wonderful development for an A-Fib patient who couldn’t or didn’t want to be on warfarin. It also was more effective than warfarin in reducing the risk of stroke.
But installing a foreign object inside the heart seems inherently dangerous. Unlike a catheter ablation which has a low risk of adverse events that usually can be corrected without any lasting damage, a mistake or problem inserting an occlusion device inside the heart can cause disastrous problems for patients.
And there are now other options for patients such as a wider choice of anticoagulants or devices that close off the LAA from outside the heart such as the surgical AtriClip or the Lariat II. Patients should not have an occlusion device installed unless the doctor can guarantee a 100 percent success rate without complications. Anything less may result in catastrophic complications for patients.
This editor predicts that, with the many different options now available to A-Fib patients, the FDA will not approve occlusion devices inserted from within the heart. Even though the failure risk is small, a failure can result in complications devastating for patients.
(Added January, 2017. I admit to being completely wrong about this prediction. The Watchman Device has received FDA approval and is in wide use with very few complications. It’s a great benefit for patients who can’t tolerate or don’t want to take anticoagulants.)
Dr. Stanley Nattel from the University of Montréal Canada made an insightful scientific research presentation on “Obesity and Obstructive Apnea— Mechanisms of AF Promotion in Experimental Models” at the 2012 Boston A-Fib Symposium. It’s well known that obesity and obstructive sleep apnea increase the risk of developing A-Fib. But what isn’t known is what specific mechanisms promote A-Fib, such as hypoxia, autonomic imbalance, left ventricular dysfunction, intravascular volume change, and/or strongly negative intrathoraic pressures.
Experiment With Rats Bred to be Fat
In a brilliant experiment Dr. Nattel studied rats bred to be fat. These Zucker obese rats weighed almost twice as much as the normal lean rats in the experiment. Both the obese and lean rats were subjected to either obstructive sleep apnea or non-obstructive sleep apnea, versus a control group of both lean and obese rats not subjected to apnea. The obstructive sleep apnea generated a strong negative chest pressure caused by forced inhalation against the closed airway, while in the non-obstructive sleep apnea group the rats could still get some air through a side port. He then induced A-Fib by pacing in all the rats.
Sleep Apnea Produces A-Fib
No rats had inducible A-Fib in the absence of apnea, indicating that, at least in this experiment, obesity by itself did not result in inducible A-Fib. Also, it was impossible to cause A-Fib in the obese or lean rats that had an open side port airway. But almost all the obese rats subjected to obstructive sleep apnea exhibited A-Fib. A small number of the lean rats subjected to obstructive sleep apnea also developed A-Fib.
From this experiment one can possibly conclude that obstructive sleep apnea substantially increases A-Fib Inducibility, and significantly more so in obese rats. If we can apply the results of this experiment to humans, we can conclude that obstructive sleep apnea combined with obesity makes someone significantly more at risk of developing A-Fib. On the other hand, just being obese may be a less significant factor in developing A-Fib.
What Mechanisms Induce A-Fib?
Dr. Nattel went further and tried to identify the actual A-Fib mechanisms behind obstructive sleep apnea and obesity. Some of the rats were subjected to pharmacological autonomic blockade while others received muscle relaxants. Some of the rats who received the pharmacological blockade could no longer be induced into A-Fib, but a majority could. One can conclude that, “autonomic nervous system changes contribute to A-Fib promotion, but only account for a part of it.”
But the rats who received the muscle relaxant did not develop A-Fib. This may be because they didn’t experience the negative pressure generated in obstructive sleep apnea when the airway is closed off.
Left Atrial Enlargement
But why was A-Fib more inducible in the obese rats? The left atrial dimensions of the obese and lean rats control group were not significantly different, but with progressive apnea there was an almost two-fold increase in atrial dimensions which increased more in the obese rats than in the lean ones. Dr. Nattel tried to prevent this left atrial dilation by inserting a balloon catheter into the inferior vena cava thereby reducing venous blood return.
This prevented A-Fib in 80% of the previously inducible rats. He concluded that there is, “strong, suggestive evidence that it is in fact left atrial distension that is responsible for the A-Fib susceptibility of the obese rats during obstructive apnea.” “A-Fib promotion is primarily due to acute left atrial enlargement, caused by forced inhalation against a closed airway, combined with left ventricular diastolic dysfunction and obesity.”
Dr. Nattel’s innovative experiment showed how sleep apnea is highly likely to cause A-Fib primarily by enlarging and remodeling the left atrium particularly in the obese but also in lean subjects as well.
If you or someone you know snores and/or stops breathing while sleeping and particularly if they are obese, it’s almost guaranteed they are remodeling and harming their heart and will eventually develop A-Fib. They need to have a sleep apnea study done ASAP and correct their breathing problem.
Genetic research in A-Fib, though in its preliminary stages, has the potential to be a game changer for patients with A-Fib.
Dr. Patrick Ellinor of Mass General, Boston gave a presentation on the “Genetics of A-Fib: How Will We Translate GWAS Findings to Clinical Practice?”
A-Fib Is Inheritable
“If you have any immediate family with A-Fib, you have a 40% increased risk of developing A-Fib yourself. And the younger that someone in your family gets A-Fib, the more likely you are to have A-Fib.”
Screen for A-Fib?
If someone has A-Fib, should all their immediate family members be screened for A-Fib? Since in the US alone over three million people have A-Fib, it isn’t possible or practical to screen all family members for A-Fib. And even if we could screen everyone, we don’t yet have the means to prevent A-Fib from developing or even to identify patients with pre-A-Fib.
Editor’s Comments: If anyone in your immediate family has A-Fib, you are very likely to develop A-Fib yourself. You have to be more aware and vigilant than the average person. If, for example, you feel palpitations or a racing heart rate, take it very seriously. Don’t hesitate or delay in going to an Electrophysiologist (EP) to have yourself checked out. Make sure you tell your EP or Cardiologist that your relative has A-Fib.
Specific Genetic Chromosomes Associated With A-Fib
Dr. Ellinor identified the specific genetic chromosomes currently found to be associated with A-Fib:
- and particularly 4q25
People with a particular combination of 3 genetic variants on chromosome 4q25 are six times more likely to develop A-Fib.
Further Research Needed
But current research has only revealed “associations.” Further research is needed to determine:
- Are these chromosomes associated with and/or do they cause an increased risk of A-Fib stroke, heart failure and death?
- Are these genetic variants associated with or do they indicate that a certain treatment should be used or that a certain outcome is more likely?
- How important are these genetic variants in the development of A-Fib?
- How do these genetic variants affect what types of arrhythmia develop? Do Paroxysmal A-Fib, Permanent A-Fib, or A-Flutter have different genetic profiles?
- And most importantly, how do these genetic variants work? What Is the mechanism behind the association?
“Right now all we have is an association.” “We don’t have a fundamental understanding as to how the variants themselves lead to the (A-Fib) disease.”
If you have A-Fib, you must warn all your immediate family members that they have a good chance of getting it also. Even though we don’t know yet how to definitively prevent A-Fib, there are some precautions your family members can take:
- Avoid binge drinking and heavy partying.
- Avoid antihistamines and anything that can stimulate or trigger A-Fib. (see A-Fib Triggers) (This doesn’t necessarily include coffee. Some research indicates coffee may prevent A-Fib.)
- Be more attentive to overall health. Obesity, for example, is often a contributing factor to A-Fib. Sleep apnea is known to lead to A-Fib.
- Check for deficiencies in essential minerals (electrolytes) like magnesium or potassium? Are calcium levels too high (which may be a trigger for A-Fib)?
- Avoid or learn to cope with stress (not always possible).
There is a tendency in all of us to not tell others if we are ill, perhaps because we perceive it as somewhat humiliating and a weakness in ourselves. But no one should be ashamed of having A-Fib. Most likely it isn’t anything we brought on ourselves. It’s genetic! It’s nobody’s fault!
We are not being fair to our family members by not telling them about our A-Fib. Don’t just mention it in passing. Sit down with them and tell them what A-Fib is like, and that they are at risk. If you love your family, you owe it to them. This applies particularly to your brothers and sisters with whom you may have a loving but somewhat competitive relationship. Anyone in your immediate family must be warned.
Dr. Eric Prystowsky of the Care Group presented the Best Clinical Science Papers on AF for 2011. He started with an initial literature search of 886 articles, then whittled them down to 52 articles which he reviewed in detail.
In a study of the blood thinner Rivaroxaban versus Warfarin (ROCKET AF), Rivaroxaban was “noninferior” to Warfarin and actually was somewhat better at reducing stroke risk. (Patel MK et al. NEMJ 2011; 365:883-91)
In a study of the blood thinner Apixaban versus Warfarin (ARISTOTLE), Apixaban was better than Warfarin both in reducing stroke risk and in reducing major bleeds. (This is better than “noninferiority.”) (Granger CB et al. NEMJ 2011; 365:981-92) (Apixaban seemed to test better than Rivaroxaban and Dabigatran. Dr. Prystowsky said he was “very much looking forward to using it.”)
In a study of Irbesartan’s effectiveness as an antiarrhythmic med (ACTIVE I), it wasn’t significantly different than a placebo. (Irbesartan is an “angiotensin II receptor antagonist” which blocks the action of certain natural substances that tighten blood vessels, allowing blood to flow more smoothly and the heart to pump more efficiently.) (ACTIVE I Investigators NEMJ 2011; 364: 928-38) Dr. Prystowski suggested that drugs like Irbesartan need to be applied much earlier as preventive medicine (“upstream therapy”) rather than after patients already have A-Fib.
In a study of Dronedarone in high-risk patients with permanent A-Fib (PALLAS), patients taking dronedarone were dying at more than twice the rate of those on a placebo. The ratio of stroke and hospitalization for heart failure was also more than twice as high. (See Time to Stop Taking Dronedarone (Multaq)? and No One with A-Fib Should Be Taking Dronedarone.) (Connolly SJ NEMJ 2011; 365: 2268-76)
Several studies involved Ablation and Pulmonary Vein Reconnection. One study of 831 patients who had a Pulmonary Vein Isolation in 2005 by Hussein (and Natale) was encouraging for patients. The recurrence/reconnection rate was low (less than 10%) and in a five year study there was no recurrence/reconnection after 36 months. (Hussein AA (Natale) Circ Arrhythmia Electrophysiol 2011; 4:271-8) This study took place at many different A-Fib centers, though they all used similar Pulmonary Vein Antrum Isolation procedures. Instead of making encircling lesions around each of the pulmonary veins, wider ablations encircle each of the two left and two right pulmonary veins in the Antrum area around the veins.
In a small but important study by Yamane, each PV was checked 30 minutes after the ablation with the stimulant ATP. If reconnected, the PV was ablated again where the reconnection occurred. This process was repeated every 30 minutes until 90 minutes.92% of patients were free of A-Fib recurrence without antiarrhythmic drugs after 370 days (a little over a year).
This may be a major medical breakthrough. This simple technique of waiting 30 minutes and retesting seems to nearly eliminate the problem of recurrence/reconnection and produces a very high success rate. [Several later presentations presented different techniques of waiting 30 or 60 minutes for retesting.] The mean procedure time was only around 3 hours. In practice, doctors can do other important tasks, even work on other patients, during this 30 minute wait time. Any procedure that achieves an over 80% success rate is a major improvement for patients. (Yamane T et al. Circ Arrhythm Electrophysiol 2011; 4: 60-68)
A study by Akoum presented the Utah 4 Stages of Fibrosis Recurrence Rates as determined by DE-MRI. (See A-Fib News: Magnetic Resonant Imaging Applied to A-Fib.) Recurrence rates were significantly higher in patients with Stage 4 (the most or highest) levels of fibrosis/remodeling. (Akoum N et al. J Cardiovasc Electrophysiol 2011; 22:16-22)
Three studies by Gaita, Siklody, and Deneke found that, using MRI, subliminal small lesions or clots, undetectable except with MRI, did occur in the brain after a Pulmonary Vein Isolation procedure primarily when using a Multielectrode Phased-RF Catheter. (See A-Fib News:Silent Clots from Multielectrode Phased-RF Ablation Catheters.) But these silent lesions detected by MRI were not linked to any neurologic defect or cognitive decline, and most (94%) reversed over time. (Gaita F et al. J Cardiovasc Electrophysiol 2011; 22: 961-68. Siklody CH et al. J Am Coll Cardiol 2011; 58: 651-8. Deneke T et al. Heart Rhythm 2011; 8: 1705-11)
In a study by Lomuscio, patients were given Acupuncture after a Cardioversion. Specific needle points were identified. 80 patients with persistent A-Fib were randomized into four groups: Acupuncture, Sham Acupuncture, Amiodarone and No Treatment. The patients receiving Acupuncture or Sham Acupuncture had 10 sessions of 15-20 minutes weekly starting within 48 hours of cardioversion.
The most freedom from recurrence occurred with the Amiodarone group. The Acupuncture group came in second but approximated the results of the Amiodarone group. The No Treatment group had significantly more recurrence, while the Sham Acupuncture group had the worst recurrence rate.
Acupuncture, though not quite as effective as Amiodarone, might be a welcome option for patients who can’t tolerate or don’t want to risk the toxic side effects of Amiodarone. Cardioversion has a notoriously high recurrence rate. “50 to 75 percent of patients eventually develop Atrial Fibrillation again.”1 Ten weekly Acupuncture sessions seems a small price to pay to avoid going back into A-Fib.
But one surprising result of this study was the poor results of the Sham Acupuncture group. One would expect a placebo effect from these ten Sham Acupunctures. But instead the misdirected Acupuncture needle pricks produced more recurrence than No Treatment. The lesson to be learned is for patients to make sure their Acupuncturist knows what spots to hit and has a proven track record in treating A-Fib. Unfortunately these Acupuncturists are hard to find. (Lomuscle A et al. J Cardiovasc Electrophysiol 2011; 22: 241-7)
In a study by Schmidt, freedom from recurrence after a cardioversion related to higher levels of GFR (Glomerular Filtration Rate). GFR is a measurement of how well the kidneys function or the stage of kidney disease. (Schmidt M J Cardiovasc Electrophysiol 2011; 22: 1092-8)
In a related study by Baber, Chronic Kidney Disease (CKD) was associated with A-Fib in adults (REGARDS study). (Baber U et al. Circ Arrhythm Electrophysiol 2011; 4: 26-32)
This is an important medical breakthrough observation for patients. Kidney disease can be added to the list of causes or triggers of A-Fib.
One doctor in the question-and-answer session said that kidney disease is associated with fibrosis, inflammation and the release of factors in the blood which affect other organs, and may be why kidney disease is associated with A-Fib.
(This is not at all surprising. People with A-Fib have 5-6 times more chance of having a stroke [unless treated]. But what is needed is more long term monitoring. One can’t always expect an A-Fib stroke to occur right after an A-Fib episode.) (Daoud EG Heart Rhythm 2011; 8: 1416-23)
It isn’t clear why, since blacks have more risk factors for A-Fib such as hypertension. Genetic research might someday explain why this occurs. (Huxley RR Circulation 2011;123: 1501-8)
In a related study Rader found that, after cardiac surgery Whites developed A-Fib more than Blacks (1.74 ratio). (Rader Circ Arrhythmi Electrophysiol 2011; 4: 644-52)
It’s well recognized that someone with heart failure, for example, has a greater risk of dying during non-cardiac surgery (9.3%), and that both patients and surgeons in these cases must be aware of this added risk. But what this study shows is that patients with A-Fib also have a high risk of death (6.4%).This is a major medical breakthrough observation for A-Fib patients. Anyone with A-Fib and their surgeons should be made aware of this added risk. But few A-Fib patients now receive this warning. As a reference point, people with CAD (Coronary Artery Disease) have a risk of death of 2.9%.
Perhaps the most disturbing part of this study was the risk of death for minor outpatient procedures. For heart failure it was 4.1%. If one has A-Fib, the risk of death from minor outpatient procedures is 2.2%!!!
This study did not speculate about why having A-Fib adds more risk.
Caveat about this study: This study did not compare the risk of having A-Fib to that of a normal healthy person’s risk. The editor has written the authors of this study to see if these figures are available.)
(Diepen et al. Circulation 2011; 124: 289-96)
Dr. Peter Kowey of Lankenau Medical Center gave a detailed analysis of the various clinical trials of dronedarone. Dronedarone is not simply “amiodarone lite,” but is a unique med with its own characteristics and uses.
Unlike amiodarone, dronedarone is not characterized by “Iodine Moiety (part or component)” or Thyroid safety issues. While amiodarone is 65% successful in suppressing A-Fib, dronedarone is 50%. Dronedarone is taken twice a day with meals, while amiodarone is taken once a day after loading. Unlike amiodarone, dronedarone may have only a minor interaction with warfarin. Dronedarone is probably as efficacious as other antiarrhythmics like sotalol or class 1C drugs.
ANDROMEDA Study Clinical Trials
The ANDROMEDA study was terminated early, because there was a 2-fold increase in mortality in the dronedarone group.
In the ATHENA study dronedarone significantly reduced Cardio Vascular (CV) hospitalizations by 37%.
The PALLAS study was terminated early due to excess deaths, strokes and heart failure hospitalization. It was intended to assess the efficacy and safety of dronedarone in patients with permanent A-Fib. Patients taking dronedarone were dying at more than twice the rate of those on a placebo. The ratio of stroke and hospitalization for heart failure was also more than twice as high. (See A-Fib News: Time to Stop Taking Dronedarone (Multaq)? and A-Fib News: No One with A-Fib Should Be Taking Dronedarone.)
New Drugs In Clinical Trials
Dr. Kowey described new drugs being tested in clinical trials as amiodarone congeners (similar to amiodarone).
- Benzofuran derivatives (Budiodarone)
- Atrial specific agents (vernakalant, IKach, IKur blockers
Dr. Kowey realistically appraised the expected future use and utility of dronedarone:
“Dronedarone’s promise as a safe and simple drug that could be used by a broader group of physicians will not be realized.”
“Dronedarone’s use should be restricted to cardiologists and electrophysiologists who are accustomed to intensive patient monitoring for efficacy and safety.”
One of the most interesting sessions at the Boston A-Fib Symposium is always the “Difficult Cases in AF Management–Antiarrhythmic Drugs, Anticoagulation, and Clinical Decision Making.” In this panel doctors Jeremy Ruskin, A. John Camm, Hans Kottkamp, Kevin Heist, Peter Kowey, Eric Prystowsky, and Albert Waldo described individual cases and discussed what were the best treatment options for these particular patients.
The first case was presented by Dr. Kowey and involved a 76-year-old man with shortness of breath and tiredness. He was found to be in A-Fib with rates of around 100 bpm. He was on the rate control med atenolol and had moderate high blood pressure. His labs were normal.
The options the audience could vote to treat Patient #1 were: rate control with blood thinners, cardioversion, or “refer for catheter ablation.” Most of those voting picked cardioversion. Some picked rate control.
In the discussion it was pointed out that patient #1 needed to be on rate control meds because his heart beat was high. But he was already on atenolol which did not help his shortness of breath and tiredness. The general consensus was to do a cardioversion.
But one Dr. pointed out that it would be wrong to wait too long, because A-Fib is likely to become progressively worse over time. If the cardioversion didn’t work or didn’t last very long and his symptoms were still bad, he could then be referred for a catheter ablation within a relatively short period of time. Most of the participants agreed that patient #1 needed to be on blood thinners for life unless his circumstances changed. One doctor stressed how all patients need to be involved in the decision process and need to understand the advantages and disadvantages of each treatment option.
What Actually Happened to Patient #1
Dr. Kowey said that patient #1 was given an anti-hypertensive drug and an oral anticoagulant. The beta-blocker atenolol was stopped and was substituted by the antiarrhythmic med sotalol which has beta-blocker characteristics. Patient #1 was cardioverted successfully, and then continued taking sotalol. However, after two months patient #1’s A-Fib recurred, but he did not have any symptoms, and his blood pressure was now well-controlled. When asked to vote on his changed condition, most of the participants voted that patient #1 continue on rate control and warfarin or rate control and dabigatran/rivaroxaban.
Patient #1 was taken off of sotalol and started on dronedarone. He continued on blood thinners. He continues to do fine without significant symptoms and no hospitalizations.
Dr. Eric Prystowsky presented the case of an 86-year-old woman who came in to have her pacemaker checked. Her pacemaker showed that she had silent A-Fib, the longest episode being 2.4 hours.
85% of the attendees voted to put her on a blood thinner. (Current guidelines recommend that anyone experiencing A-Fib episodes longer than 48 hours be put on blood thinners.)
Several doctors and audience members had divergent views on this important subject. One doctor pointed out that elderly women have a greater risk of having a hemorrhagic stroke from blood thinners than from an A-Fib ischemic stroke. (The newer blood thinners like dabigatran might work better than warfarin in reducing the risk of a hemorrhagic stroke.) Another doctor said that data showed that A-Fib episodes shorter than 24 hours had little chance of causing a stroke.2 But another doctor cited a study where an A-Fib episode as short as 6 minutes could produce a 2.5 risk of stroke.
(The author is not familiar with this study and has written this doctor for more info.)
The Symposium attendees then voted on whether they currently use a 24 hour or 48 hour long episode to determine the need for anticoagulation. 38% said they used 24 hour, 62% said they used 48 hour.
Dr. Prystowsky pointed out the importance of discussing and documenting in the patient’s folder all the anticoagulation options and how patients could be affected by each. This should be done not only for the patient’s benefit, but as a protection from law suits. Another doctor pointed out that patients often have a hard time determining when exactly an A-Fib episode started or how long it actually lasted (unlike this elderly woman whose pacemaker revealed the duration of her A-Fib episodes).
The general consensus was that the duration of an A-Fib episode that causes a risk of stroke is contested. There needs to be more hard data and studies developed to resolve this issue.
Editor’s Comments: Doctors do the best they can to protect patients from having an A-Fib stroke. But taking blood thinners is not an absolute guarantee that one will never have an A-Fib stroke. Warfarin reduces the risk of an A-Fib stroke by 60%-70%.3But that isn’t 100%. There is that 30-40% you still have to worry about. And with many blood thinners there is an increased risk of bleeding, GI problems, and developing an hemorrhagic stroke.
The only guarantee of not having an A-Fib stroke is to no longer have A-Fib, or to perhaps have one’s Left Atrial Appendage (LAA) closed off or removed. 90%-95% of A-Fib clots come from the LAA.
Dr. A. John Camm presented a case of a 45-year-old male competitive endurance athlete in great shape who used to run 70-75 miles/week but who experienced sudden palpitations in his heart. His EKG showed he had A-Flutter.
The choices of treatment presented to the Symposium voters were:
- Beta-blocker – bisoprolol
- Atrial flutter Right Atrium ablation procedure
Most voted for an atrial flutter ablation. That’s what was done for patient #3.
But Dr. Camm presented data from a study which showed that endurance athletes don’t have as good results and, if they continue to run after ablation, don’t do as well as patients in other sports or no sports patients. (Heidbuchel H. et al. Int J Cardiol 2006; 107:67-72)
What happened to patient #3
Now aged 50 his EKG showed A-Fib and nocturnal pauses, probably brought on by his running. He also had a large left atrium. In the discussion doctors pointed out that telling a runner to stop running doesn’t work. Running is an important part of their life. What you have to tell them is they risk developing A-Fib. (See A-Fib News: Vigorous Exercise and A-Fib.)
Dr. Camm pointed out that endurance athletes have five times more risk of developing Lone A-Fib, that 5%-10% of middle age endurance athletes will develop A-Fib. Runners develop increased vagal tone, and the pressure and volume overload they apply produce atrial stretch and dilation, inflammation, and atrial fibrosis.
Several doctors pointed out that A-Fib often lurks in the background, is a part of A-Flutter, or often develops after an A-Flutter ablation.
Editor’s comment: From this patient’s perspective, a patient having an A-Flutter ablation should also have an A-Fib ablation at the same time. A Flutter ablation is a relatively simple procedure compared to A-Fib ablation. It can usually be done at the end (or at the beginning) of an A-Fib ablation. See Flutter Ablation should be Combined with Left Atrium A-Fib Ablation.
Some doctors said they would never do an A-Fib ablation when only A-Flutter is present. Others said they routinely do both Flutter and A-Fib ablation at the same time, particularly in the case of athletes.
Dr. Kottkamp pointed out that the size of the left atrium wasn’t a problem, that he was more interested in the overall health of the left atrium as shown in an EKG. The bigger atrium is not always more sick than the smaller atrium. He does ablations if the left atrium is 50 or 52 mm.
Dr. Hans Kottkamp presented a case of a 60-year-old male in long-standing persistent (chronic) A-Fib with dilated cardiomyopathy. (He hadn’t seen a cardiologist in three years.) He was diagnosed with A-Fib nearly twenty years ago. He had a low ejection fraction (25-30%), worsening heart failure, shortness of breath during minimal exercise, and peripheral edema (swelling).
The choices of treatment presented to the voters at the Symposium were:
- Electrical cardioversion
- Catheter ablation (both PV Isolation & substrate modification)
- AV-Node ablation + pacemaker
- AV-Node ablation + CRT-D (Cardiac Resynchronization Therapy with Defibrillator (regular biventricular pacing paces the right atrium and right ventricle, CRT pacing also paces the left ventricle to keep both in sync)
What happened to patient #4
Because patient #4 had been in long-standing persistent A-Fib for so long and had developed cardiomyopathy (and probably because he wasn’t likely to accept and cooperate with intensive monitoring), he was given an AV-Node ablation + CRT-D.
Three months after the AV Node ablation his heart was significantly improved. His ejection fraction improved to 45-50%.
Patient #5 (actually 10 different cases) CHADS2 scores of 0-1 and still suffered strokes
Dr. Jeremy Ruskin presented sobering, discouraging cases for doctors and patients. Ten A-Fib patients with low CHADS2 scores (0-1) all suffered CVAs (Cerebrovascular Accidents—strokes), TIAs (Transient Ischemic Attacks—mini-strokes), or Embolic MI (Myocardial Infarction—heart attack).
Editor’s Comments: One of the cases Dr. Ruskin cited was a young man only 35 years old who suffered an A-Fib stroke. Is this a wake-up call for doctors and patients? Should anyone who has A-Fib be on a serious blood thinner (not aspirin which isn’t very effective)? It’s hard to think of this 35-year-old having to take warfarin for the rest of his life. How would taking warfarin for so long affect him?
But maybe the newer oral anticoagulants [dabigatran, rivaroxaban, apixaban] might lend themselves to daily dosage over a longer period of time. Could these new anticoagulants replace aspirin as a recommended blood thinner for A-Fib patients with low CHADS2 scores/supposedly low risk of stroke?
Dr Albert Waldo cited studies that “aspirin at 150-200 mg/day is neither effective nor safe.” (Sato H et al. Stroke 2006;37:447-51.) Aspirin was no better than a placebo and caused a marginally increased risk of major bleeding.
In a Danish registry study of 132,372 A-Fib patients followed for 12 years, “the use of aspirin to prevent stroke in patients with A-Fib remains very poorly justified…Aspirin alone did not decrease the risk of TE (Thromboembolism stroke) compared to no treatment.” (Olesen JB et al. Thromb Haemost 2011;106:739-49)
One study showed Apixaban to be much better in reducing stroke risk than aspirin. (Connolly SJ et al. N Engl J Med. 2011 364:806-17)
Perhaps apixaban, if FDA approved, might be a welcome substitute for aspirin in patients at low risk of an A-Fib stroke.
Dr. Dhanunjaya Lakkireddy of the University of Kansas School of Medicine talked about the calming effect of yoga.
Dr. Lakkireddy noticed that a couple of his patients wearing heart-rate monitors became A-Fib free when they were taking yoga classes. “I wouldn’t have believed until I saw it.” He initiated a study to monitor a group of A-Fib patients for three months to assess the frequency of their A-Fib episodes, and their anxiety, depression, and quality of life. Then he switched them to yoga for three months. Yoga reduced their A-Fib episodes and improved their emotional well-being.
Dr. Lakkireddy researched the therapeutic effects of yoga. A-Fib is often triggered by an imbalance in the activity of the nervous system. Yoga can improve this imbalance. Yoga can also improve heart and body inflammation which is a known trigger of A-Fib. But though yoga helps, it doesn’t cure A-Fib, “it only makes it less burdensome.”
Editor’s Comments: Though everyone would prefer to be cured of their A-Fib, that isn’t always possible. For those living with A-Fib, yoga may make the A-Fib burden more bearable and improve one’s quality of life.
Return to Index of Articles: AF Symposium: Steve’s Summary Reports
Last updated: Thursday, January 26, 2017
- www.intelihealth.com (by Aetna)/atrial fibrillation/treatment.↵
- Capucci, A et al. “Monitored Atrial Fibrillation Duration Predicts Arterial Embolic Events in Patients Suffering From Bradycardia and Atrial Fibrillation Implanted With Antitachycardia Pacemakers” Journal of the American College of Cardiology Volume 46, Issue 10, 15 November 2005, Pages 1913–1920↵
- Chatterjee, S. et al. “Left Atrial Appendage Occlusion: Lessons Learned From Surgical and Transcatheter Experiences.” Ann Thorac Surg 2011;92:2283-92. doi: 10.1016/j.athoracsur.2011↵