Epidemiology of atrial fibrillation: emerging concepts

A recent review provided as free full text in Mayo Clinic Proceedings covered some underappreciated, though not really new, concepts about risk factors for atrial fibrillation.

Of note:

Evidence that caffeine increases risk is hard to come by. However, it is well known that alcohol does so in a dose related fashion.

Metabolic syndrome is a risk factor for atrial fibrillation as are some of its individual components including obesity. On the opposite end of the spectrum so is extreme exercise. This paradox suggests that atrial fibrillation represents two distinct diseases.

A recent post at Billy Rubin's Blog pointed me further down the trail of exercise and the heart. He cited a New York Times health blog piece concerning the paradox, which he thinks sends the wrong message to some. What concerned me more about the article was the implication that the paradox is new or controversial:

The Vasaloppet, a grueling 56-mile cross-country ski marathon held each March in northwestern Sweden, provides a convenient venue for studying the impacts of intense, prolonged aerobic exertion on the human body, and in recent years, several studies have reported on the generally enviable fitness and longevity of the racers.

But the newest Vasaloppet-related study, published in June in The European Heart Journal, is worrisome.

It's not all that controversial and certainly not new. Here are the findings of the European Heart Journal study:

Aims We aimed to investigate the association of number of completed races and finishing time with risk of arrhythmias among participants of Vasaloppet, a 90 km cross-country skiing event...

Methods and results..Primary outcome was hospitalization for any arrhythmia and secondary outcomes were atrial fibrillation/flutter (AF), bradyarrhythmias, other supraventricular tachycardias (SVT), and ventricular tachycardia/ventricular fibrillation/cardiac arrest (VT/VF/CA). Among 52 755 participants, 919 experienced arrhythmia during follow-up. Adjusting for age, education, and occupational status, those who completed the highest number of races during the period had higher risk of any arrhythmias [hazard ratio (HR)1.30; 95% CI 1.08–1.58; for greater than or equal to 5 vs. 1 completed race], AF (HR 1.29; 95% CI 1.04–1.61), and bradyarrhythmias (HR 2.10; 95% CI 1.28–3.47). Those who had the fastest relative finishing time also had higher risk of any arrhythmias (HR 1.30; 95% CI 1.04–1.62; for 100–160% vs. greater than 240% of winning time), AF (1.20; 95% CI 0.93–1.55), and bradyarrhythmias (HR 1.85; 95% CI 0.97–3.54). SVT or VT/VF/CA was not associated with finishing time or number of completed races.

The results were driven entirely by bradyarrhythmias and atrial fibrillation. The atrial fibrillation seen here was almost certainly vagally mediated atrial fibrillation, a long and well known clinical entity associated with extreme athletic conditioning. It and the vagally mediated bradyarrhythmias reported in the study can occasionally pose a clinical nuisance but for the most part are pretty benign.

But extreme vagotonia (and vagal tone is often considered a manifestation of a healthy cardiovascular system) is not the only consequence of ultra conditioning. The authors of the above review published an earlier paper in the Proceedings about structural damage that can occur:

Emerging data suggest that chronic training for and competing in extreme endurance events such as marathons, ultramarathons, ironman distance triathlons, and very long distance bicycle races, can cause transient acute volume overload of the atria and right ventricle, with transient reductions in right ventricular ejection fraction and elevations of cardiac biomarkers, all of which return to normal within 1 week. Over months to years of repetitive injury, this process, in some individuals, may lead to patchy myocardial fibrosis, particularly in the atria, interventricular septum, and right ventricle, creating a substrate for atrial and ventricular arrhythmias. Additionally, long-term excessive sustained exercise may be associated with coronary artery calcification, diastolic dysfunction, and large-artery wall stiffening.

This of course refers to a healthy population. There are those occasional individuals who have sudden events related to acute exertion because of pre-existing disease. The clinical significance, if any, of the structural changes cited above is not known.

Like other things in nature, there seems to be some optimal dose of exercise beyond which diminishing return and maybe even harm occur. We're not sure what the magic number is but the authors of the Proceedings papers seem to think it is about an hour a day.