Atrial fibrillation (AF) is the most frequently observed arrhythmia in the clinic, affects ≈2 to 6 million people in the United States, and is known to increase the risk of stroke, heart failure, and sudden death.1 Epidemiological studies have identified multiple factors that enhance risk for susceptibility to AF, including age, coronary artery disease, heart failure, hypertension, and, more recently, obesity. The increase in the incidence of obesity is at alarming proportions; more than one third of the adult population in the United States is classified as obese, an observation that is expected to affect AF incidence. Several mechanisms have been proposed to underlie the observed association between obesity and AF, including increased left atrial dimensions, impaired diastolic function, and inflammatory processes, as well as enhanced fibrosis and fatty infiltration of the myocardium and associated comorbidities such as obstructive sleep apnea. All such events lead to electrophysiological and structural remodeling of the atrium and predispose to AF induction and maintenance. In this brief viewpoint article, we will focus on the emerging evidence showing the importance of adipose tissue in increasing the risk of AF in obesity and outline possible molecular/ionic mechanism(s) involved.
CITATION STYLE
Pandit, S. V., Anumonwo, J., & Jalife, J. (2016, May 13). Atrial Fibrillation Susceptibility in Obesity. Circulation Research. Lippincott Williams and Wilkins. https://doi.org/10.1161/CIRCRESAHA.116.308686
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