Abstract
Obesity is associated with an increased risk of atrial and ventricular arrhythmias, including life-threatening ones. Epicardial adipose tissue (EAT) is located deep under the visceral pericardium (epicardium) and is therefore in direct contact with the underlying myocardium. In pathological conditions, EAT undergoes a phenotypic transition from a neighbor with protective properties to a substrate that secretes many substances that change the electrophysiology of cardiomyocytes by modulating ion currents that disrupt intercellular electrical connections and stimulate fibrosis. An excess of EAT can cause atrial and ventricular conduction disturbances, which are already evident with standard electrocardiography, predispose to the occurrence of the re-entry phenomenon and cardiac arrhythmias. Among the mechanisms of arrhythmogenesis under the influence of EAT, modulation of ion channels and gap junctions, fibrous remodeling and fatty infiltration are more often considered. However, most of these mechanisms have been studied in experimental studies and cannot easily be extrapolated to humans. There is convincing evidence of a direct relationship between EAT volume and the severity of atrial fibrillation, as well as the clinical benefit obtained from weight loss in patients with this arrhythmia. It is likely that the benefits of weight loss may extend to ventricular arrhythmias.