Tuesday, August 23, 2011

Tutorials in the Tetons 2011---what's new in the epidemiology of atrial fibrillation?

Teton view from the terrace behind the conference center

Atrial fibrillation is never been a mundane topic at this conference. So what could possibly be exciting about a fib? Dr. Bernard Gersh from Mayo Clinic presented this year's update.

There are some fascinating new insights about its changing epidemiology, based on pathogenesis. It's no surprise that the incidence is increasing. But there's a substantial component of this rise that's not accounted for by aging of the population. The short version is that it's the epidemic of obesity. Here are some primary sources which explain the association:

The mechanisms? In addition to the obvious associations with sleep apnea and hypertension, obesity is associated with neurohormonal disturbances, inflammation, LVH and diastolic dysfunction. The latter lead to increased LA size.

Finally, pericardial fat deposition, which is associated with obesity and has proinflammatory properties, is associated with atrial fibrillation independent of the usual risk factors.

LV diastolic dysfunction showed a powerful association with incident AF in this study.

Obesity's association with AF operates in part via the correlation between weight gain and vascular stiffness. Vascular stiffness, a consequence of atherosclerosis, over time leads to increased LA size. LA size, according to the speaker, is the “hemoglobin A1C” of many aspects of cardiovascular disease. (For more about the importance of LA size and its assessment via electrocardiography see here).

What about lone atrial fibrillation? This paper has a wealth of information on its natural history and demonstrates event free survival similar to that of the general population over many years, until vascular risk factors supervene (at which time it is no longer “lone” AF).

What does this all mean? It appears that two diseases, with some overlap, are represented in the spectrum of AF. Lone AF, purely an electrical disorder, has a benign course. The stroke risk is similar to the general population until years later when vascular risk factors and/or structural heart disease develop. The more ordinary atrial fibrillation, which hospitalists more often see, appears to be a marker of vascular and structural heart disease. The correlation with atherosclerosis explains why aspirin has a modest effect in stroke prevention---it doesn't prevent cardioembolism but does prevent some of those strokes that come from the vascular disease that underlies the more common type of AF.

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