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Get in Rhythm. Stay in Rhythm.™ View Replays from Atrial Fibrillation Patient Conference Aug 4-6, 2017, in Dallas, TX
Get in Rhythm. Stay in Rhythm.™ View Replays from Atrial Fibrillation Patient Conference Aug 4-6, 2017, in Dallas, TX

Day 2 Boston AF symposium: Late morning and afternoon notes

Guest Post by Dr. John Mandrola

January 13, 2012

Guest post by Dr. John Mandrola

The late-morning sessions addressed the possible mechanism(s) of AF. Many ask what causes AF. The assumption holds that if we can ablate AF, we must know what causes it. This would not be true. One line of thinking holds that disorganized electrical conduction throughout the atria plays an important role–not just focal drivers and initiators from the pulmonary veins. These sites of rotation are called rotors. People are interested in rotors because targeting these sites for ablation might help increase success rates.

Again my commentary is in italics. And remember, these are rough notes; I’m no reporter.

Dr Jalife started the session with the basic science of rotors. Such is hard to translate.

Dr Sanjiv Narayan presented his research on electrical rotors, focal beats, their relationship to complex fractionated electrograms (CFAE) and their role in causing AF. He has become the chief spokesman for FIRM (Focal Impulse and Rotor Modulation)-guided AF ablation. This novel kind of ablation uses a proprietary tool to identify such sites in AF. When ablation is performed at these critical sites, AF often terminates and then stays away. What’s exciting about his research is the ability to find these rotor sites. Ablationists have longed looked for such critical sites by analyzing sites of complex fractionated signals (CFAE), but thus far there has not been a good correlation between burning at CFAE sites and AF termination.

This work is the most talked about study in AF ablation today. The idea that a basket catheter and software can detect a focal target for AF excites people. We will see. (Of note, Dr Narayan’s recorded case yesterday was withdrawn because of CME conflict issues.)

Next…

Dr Pierre Jais (Bordeaux) presented on the role of non-invasive mapping of AF. His task was to provide insights into AF mechanisms. Non-invasive electrical maps are recorded from vests (of electrodes) that a patient wears. A CT scan provides the anatomy while the vest gives the electrograms. Meshing them together is tough to understand.

Dr Shih-Ann Chen then presented his data on rotors: His main question is whether sufficient evidence exists for rotors in human AF. He thinks so, and believes the similarity of signals and the presence of dominant frequency are the two characteristics that define rotors. In his work, only 17% of persistent-AF patients had rotors. All these patients, however, had successful termination of AF with ablation at these focal sites.

For years, AF experts have searched for techniques that better target the actual causes of AF, rather than just anatomically ablating the pulmonary veins. Dr Narayan’s work comes closest to achieving this lofty goal.

Next…

Dr Douglas Packer chaired a session on AF guidelines and regulatory issues:

Dr Hugh Calkins presented, for the first time, a [new] HRS Consensus Document on AF ablation: The paper is quite long, but he highlighted some of the important changes: The definition of paroxysmal AF was tweaked; the indications for AF ablation loosened; and the role of surgical ablation was addressed more specifically. On AF ablation techniques, demonstrating PV isolation and waiting at least twenty minutes was emphasized. On how much ablation to do in advanced cases of AF, they used the word, “consider”…doing more ablation–beyond PVI–in these patients.

There is absolutely no consensus on how much ablation is enough, or too much, in advanced cases of AF. The word ‘consider’ reflects this gap in knowledge.

On blood-thinning around the ablation procedure: Trans-esophageal echos (TEEs) are no longer emphasized as strongly, especially in patients with adequate blood thinning.

IMHO, this is good. I have long felt that adequate blood-thinning around the time of the procedure prevents stroke better than doing extra imaging studies like TEEs.

He left us with this important notion: Stopping blood-thinning after ablation depends not on symptoms of patients (asymptomatic AF can occur post ablation) but on the patient’s stroke risk as determined by the CHADS-VASC score.

Next…

Dr John Camm talked about what AF registries can teach us. He spoke a great deal about a number of registry studies (all with acronyms): RECORD AF (JACC), REALISE-AF, AFFECTS (Am J Cardiol), Global AF Registry (ESC 2011), EuroHeart Survey (EuroPace online), RHYTHM-AF (ESC 2011), AF-Ablation Pilot Registry (ESC 2011).

Registries provide useful information on the real-world strategies for treating AF: rate-control versus rhythm-control, use of blood-thinning meds, international differences in treatment, cardioversion techniques and of course, AF ablation.

What do these registries tell us? Real-world therapy of AF frequently diverges from guidelines and varies widely depending on geography. Yes, in speaking about the treatment of AF, variability sums it up well.

Next…

Dr Randall Brockman from the FDA presented a regulatory update on surgical ablation technology. FDA recommends randomized clinical trials, but recognizes difficulties with surgical ablation strategies. Control groups, for example, represent a problem: should the control group be medical therapy or catheter ablation? Also, how does one sort out the risks and benefits of surgical ablation when used as a stand-alone procedure versus when used as an adjunct to other heart surgery (CABG or Valve).

Dr Brockman seemed to be speaking to makers and users of surgical devices. Basically, he laid out how a trial of surgical ablation should be designed.

As an AF ablationist, I am conflicted about surgical ablation. That said, however, though the upfront risks are greater with surgery, the success rates are encouraging. Worries about surgical ablation beyond the immediate risks include how well the atrium will contract. Remember, regular electrical rhythm is good, but you also want the atria to transport blood to the ventricle. Medical people call this the mechanical function of the atria.

The entire afternoon session dealt with stroke prevention in AF:

The session was chaired by Dr Daniel Singer. He started with a blood-thinner 101 lesson, nicely highlighting all the mega trials on blood thinners–up to apixaban. He gave a great review.

One interesting note: post-hoc analysis of elderly patients treated with dabigatran showed advanced age increased overall bleeding risk, but the lower risk of brain bleeding with dabigatran was preserved.

When the trials of novel blood thinners are combined, more than 50,000 patients have been studied. That’s a lot of patients. The data consistently shows these drugs confer favorable stroke prevention, equivalent-to-better bleeding risks and trends for lower mortality. Costs, patient adherence and the lack of an antidote remain barriers to more widespread acceptance. It’s only a matter of time.

Next…

Dr Chris Granger highlighted the AVERROES and ARISTOTLE trials: The bottom line was that apixaban looked great. It was superior to warfarin in reducing stroke, was associated with much less bleeding and even conferred lower mortality rates. AVERROES compared apixaban to aspirin in patients felt unsuitable for warfarin. Here as well, apixaban was superior. He emphasized that all the new blood-thinners had favorable trends towards lower mortality.

Dr Granger hit on some important questions that come up with all three of the novel blood thinners:

  1. How do these drugs compare to skillful use of warfarin? Dr Granger emphasized the fact that the available data suggests these drugs have benefit even when warfarin is well-managed.
  2. Should we switch patients doing well with warfarin? He thought the data supports strong consideration for switching.
  3. Are the novel blood-thinners cost effective? Much evidence, including a recent analysis by the British regulatory agency, NICE, suggested that dabigatran is cost-effective. This makes sense because taking care of people with strokes gets very expensive.

Next…

Dr Jeffrey Weitz presented on practical implications of the recent trials of the novel agents:

Smartly, he started his talk by noting patients thought not to be candidates for the novel blood thinners: Those doing well on warfarin, those with impaired kidney function, (he was concerned even when the GFR gets below 50), those with mechanical heart valves and those not compliant with warfarin. Message: pick the right patients. (Grin.)

He mentioned that the Hemoclot test can tell us about dabigatran concentration. I don’t know much about the Hemoclot test; neither did more than 90% of the audience. I’m going to look that one up.

Dr Weitz refuted recent talk about reversal agents for rivaroxaban. There are no antidotes for any of these agents at this moment.

It was a really good talk.

Next…

Dr Michael Gold clarified the often-confusing issues with using blood-thinners around the time of cardioversions or implantable devices.

First message: bridging with heparin is problematic. There is very good data showing the safety of performing device surgery (pacemaker/ICDs) without interrupting warfarin therapy. Secondly, cardioversion with dabigatran appears to be safe. Thirdly, from the RE-LY data, dabigatran and warfarin have similar bleeding rates around the time of surgical procedures.

I have never been a fan of bridging strategies, and, I have felt it safe (and preferred) to implant devices without interrupting warfarin in patients at high risk of blood clotting problems. Dr Gold emphasizes this data every year. EP doctors get it, but most cardiologists and surgeons have yet to embrace this strategy.

Dr Natale presented data on how to use blood-thinners around the time of AF ablation: He has long advocated the strategy of doing AF ablation with uninterrupted warfarin treatment and no TEEs. Many centers adopted this strategy and all has been well. Strokes have approached zero without an increased risk of bleeding. (It’s worked for our center too. We have done ablation in this way for years.) That is, until dabigatran came along. Now, many patients referred for AF ablation are taking dabigatran.

He reviewed their recent data (first presented at AHA) on dabigatran versus warfarin during AF ablation.

Dabigatran looked worse than warfarin. They had 3 of 145 patients on dabigatran suffer strokes, compared to 0 of 145 on warfarin. This caused them to go back to using warfarin before ablation.

The issue of dabigatran use before and after AF ablation is controversial. There are other centers that feel differently. I don’t think the issue is settled.

The next sets of talks included non-medical means to prevent stroke. This task entails addressing how best to deal with clots that form in the left atrial appendage. An important prologue should include assessment of the assumption that all (or most) strokes in AF come from the left atrial appendage. This is a matter of some debate.

Dr Zoltan Turi presented on catheter-based approaches to stroke prevention. The PROTECT-AF trial (800 patients) looked at warfarin-eligible patients with AF who were randomized to a left atrial appendage occlusion device or warfarin. The device looked favorable in efficacy, but the Achilles heel was the complications around the implantation. Strokes, perforation of the heart, and bleeding were all significant problems after implant. When just patients with successful occlusion of the LAA were included, stroke risk was greatly lowered. This suggests the concept of percutaneously closing the LAA has merit.

But…Devices to close the LAA have a long, long, long way to go.

Next…

Dr Damiano (St Louis) reviewed surgical management of the left atrial appendage. He makes surgical closure look pretty easy, though I suspect it’s not. Only small trials are available, so knowing where this is going is hard to say.

Next…

Dr Camm reviewed the TRENDS, ASSERT and IMPACT trials. These studies address the sticky issue of what to do when non-symptom-causing episodes of AF are detected during pacemaker follow-up. This is an extremely common finding. Remember, patients that get pacemakers often have risk factors for AF–they are usually older, with high blood pressure and intrinsic heart disease. Also remember that most of us think stroke risk in AF has more to with the condition of the patient rather than amount of AF.

As he always does, Dr Camm comprehensively reviewed the many studies in this area, the most recent of which was the ASSERT trial, published in NEJM this week. (I have not yet reviewed this trial.) What I took from the talk was that the presence of non-symptomatic atrial-high-rate episodes predicted stroke.

Though the data is hard to decipher, it seems likely that these episodes are not benign. And, that they warrant strong consideration of beginning stroke prevention strategies. The threshold duration of the arrhythmia episode remains unknown.

Dr Thomas Arentz (Germany) went over the issue of brain lesions after AF ablation. He mostly talked about PVAC, which as we know was associated with an excess of brain lesions. In the end, the significance of non-symptomatic brain lesions is unknown. Interestingly, he pointed out that other well accepted heart procedures, like coronary angiograms, are associated with brain lesions as well. He also showed a beautiful MRI image of a non-contracting left atrium in a patient who had multiple extensive left atrial ablations, which highlights the idea that aggressive ablation strategies have downsides.

Further studies and enhanced surveillance will help clarify this important issue.

Afternoon Panel: (Whoa, I am tired.)

Dr. Mandrola is a cardiac electrophysiologist who blogs at Dr. John M

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Last Modified January 16, 2012

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