Abstract
Atrial fibrillation is the most frequent arrhythmia in adults, becoming more frequent with age. Recent clinical studies demonstrated that epicardial fat is linked with atrial fibrillation induction and recurrence. The arrhythmogenic mechanism consists in the fact that the epicardial adipose tissue is metabolically active, inducing local inflammation and enhancing the oxidative stress, which lead to atrial fibrillation as well as atherosclerosis. Having metabolic activity and secreting various anti- and pro-inflammatory biomarkers, the fat surrounding the heart has been linked to the complex process of coronary plaque vulnerabilization. This clinical update aims to summarize the role of epicardial adipose tissue in the pathogenesis, persistence, and severity of atrial fibrillation.