Epicardial adipose tissue accumulation promotes adverse electrophysiological and fibrotic remodeling through a proinflammatory secretome, increasing the risk of cardiac arrhythmias.
Obesity is associated with higher risks of cardiac arrhythmias. Although this may be partly explained by concurrent cardiometabolic ill-health, growing evidence suggests that increasing adiposity independently confers risk for arrhythmias. Among fat depots, epicardial adipose tissue (EAT) exhibits a proinflammatory secretome and, given the lack of fascial separation, has been implicated as a transducer of inflammation to the underlying myocardium. The present review explores the mechanisms underpinning adverse electrophysiological remodeling as a consequence of EAT accumulation and the consequent inflammation. We first describe the physiological and pathophysiological function of EAT and its unique secretome and subsequently discuss the evidence for ionic channel and connexin expression modulation as well as fibrotic remodeling induced by cytokines and free fatty acids that are secreted by EAT. Finally, we highlight how weight reduction and regression of EAT volume may cause reverse remodeling to ameliorate arrhythmic risk.
Patel et al. (Fri,) conducted a review in Cardiac arrhythmias. Epicardial adipose tissue (EAT) accumulation was evaluated. Epicardial adipose tissue accumulation promotes adverse electrophysiological and fibrotic remodeling through a proinflammatory secretome, increasing the risk of cardiac arrhythmias.