COMMENTARY

10 Highlights from the 10th Annual Western AF Symposium

John Mandrola, MD

Disclosures

March 06, 2017

Dr Nassir Marrouche (University of Utah, Salt Lake City) has nurtured the Western AF symposium into one of the biggest gatherings of global experts in atrial fibrillation (AF). I've been honored to attend as a faculty member.

Here are 10 points that stood out in my mind. Italics represent my editorial thoughts.

Big Themes in AF

1. Prof John DiMarco (University of Virginia, Charlottesville) predicted that the efficacy of AF ablation will hit a ceiling. He said the next big development will be in AF prevention.

Think of the public-health implications. Measures that prevent AF have excellent side effects: better blood pressure and lipid levels on fewer meds and lower platelet reactivity and markers of inflammation. [1,2]

2. Prof Prash Sanders's (University of Adelaide, Australia) work has changed the three pillars of AF care to four: stroke prevention, rate control, rhythm control, and risk-factor treatment.

I believe risk-factor treatment can also include stress management. The point is to look for the cause; AF usually comes from something. Modify that something. Stop seeing AF as a disease; see it as a result of the atria under duress.

AF-Mapping Troubles

3. Prof Ulrich Schotten (Maastricht University, the Netherlands) presented evidence that phase analysis of electrograms identifies lines of block not rotating wave fronts. This is disruptive because phase analysis of filtered signals is the secret sauce of present-day rotor-mapping systems. What's more—and this is crucial—Dr Schotten commands the highest respect in the field.

4. In a biomedical engineering tour de force, Dr Olaf Doessel (Karlsruhe Institute of Technology, Germany) dismantled the current mapping systems because of major flaws in the way they process electrograms. Don't map during AF, he suggested.

As Dr Harvey Feigenbaum, the father of modern echocardiography, used to say about echo interpretation, if you can't see it, don't call it. Seems we should apply the same rules to electrograms. Essentially: bad input leads to bad output.

AF and Stroke

5. Stroke researcher Dr Hooman Kamel (Weill Cornell Medicine, New York) presented on his seminal paper[3] calling for a new way of thinking about AF and stroke. Look beyond the surrogate marker of AF episodes to risk factors and left atrial disease, he said. For instance, he showed data from numerous cohort studies suggesting P-wave terminal forces measured in lead V1 on the surface ECG correlated with future stroke while AF episodes did not.

You can't listen to Dr Kamel explain the relationship of stroke and left atrial health and not be concerned about extensive AF ablation. Does the iatrogenic scar and impaired atrial contractility after ablation ultimately help patients? (See point 9.) More and more, AF episodes alone are looking like a poor surrogate marker of future stroke.

6. Numerous presenters explained that the predictive ability of the CHA2DS2-VASc score for stroke in patients with AF is hardly better than a coin flip. What's more, CHA2DS2 -VASc performs better in patients without AF.

Early studies on biomarkers show we could do much better with stroke prediction.[4] And with the advent of big data, stroke prediction should improve. The biggest impediment: researcher's attachment to old ideas. Also, it's (literally) crazy that doctors are being graded and compensated on adherence to a quality measure ( CHA2DS2-VASc) that hardly beats a coin flip.

7. Dr Mintu Turakhia (Stanford University, CA) suggested long-term stroke prediction may be the wrong lens to assess stroke risk, given that AF is modifiable. He suggests a much shorter time frame for stroke prediction. Say 1 year in the future.

This is important because if a person with AF loses weight, uses her continuous positive airway pressure (CPAP) device, and gains fitness, she may no longer have hypertension and diabetes and thus she is at lower risk of stroke. Lower baseline risk of stroke decreases the net benefit from anticoagulation.

Subclinical AF

8. Dr Suneet Mittal (Valley Medical Group, New Jersey) earned the breaking-news award with his slide showing (yet-unpublished data) that nearly all the strokes in the ASSERT trial[5] occurred in patients with subclinical AF episodes lasting greater than 24 hours.

SCAF=subclinical atrial fibrillation. Courtesy of Dr Mittal. [to view a larger image, click here]

This is big news. The data in support of anticoagulation in patients with AF comes from patients with "clinical" AF. That is, AF recorded on a 12-lead ECG in a symptomatic patient. Knowing what to do with short-duration asymptomatic (or subclinical) AF episodes recorded from devices is of vital importance. It might not be the same; look up the term "heterogeneous treatment effects."

I worry about both undertreatment and overtreatment of short AF episodes. If Dr Mittal's data are published and confirmed, it would argue for reserving use of anticoagulation for longer AF episodes. There are ongoing trials looking into this important question.

AF Ablation

9. Ablation success is defined as freedom from symptomatic or asymptomatic AF, atrial tachycardia, or atrial flutter lasting 30 seconds or longer 12 months following ablation. Numerous presenters argued for getting rid of this arbitrary 30-second rule. They suggested the more realistic goal of improving AF burden and symptoms.

I get this. I don't do a lot of searching for AF episodes in postablation patients who report improved quality of life. But at tens of thousands of dollars per procedure and substantial risk of serious complications, AF ablation is an aggressive means for palliation. If you believe palliation of symptoms is the only goal of ablation, remember, we've never compared it with a sham control . Most of us had hoped for a bit more than palliation from such an extensive procedure.

NOAC/DOAC Drugs

10. In his deep dive into the new/direct oral anticoagulant (NOAC/DOAC) trials, pharmacologist Paul Dobesh (University of Nebraska, Lincoln) made it clear that variability in trial designs render it impossible to pick the superior nonwarfarin agent. He also spoke strongly on the lack of evidence for combining antiplatelet drugs and NOACs in patients without a clear indication for both.

This talk exposed the dangers of not reading beyond the abstracts of major trials. I'm almost sure our embrace of the NOAC drugs is the right call. Opening the databases of these trials for confirmation would improve my confidence.

JMM

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