Atrial Fibrillation (AF) is the most frequent sustained cardiac arrhythmia. It is well known that several risk factors are associated with AF, such as hypertension, diabetes mellitus and metabolic syndrome, smoking, alcohol, coronary artery disease (CAD), obstructive sleep apnea, myocardial infarction (MI), heart failure (HF) and obesity. Furthermore, several pieces of evidence suggest the implication of epicardial adipose tissue (EAT) in the onset of AF. EAT is the visceral fat depot of the heart, located between the visceral pericardium and the myocardium. In physiologic conditions, EAT represents a source of antiatherogenic and anti-inflammatory adipokines, shows thermogenic properties, provides energy, and acts as an immune barrier.
However, in pathologic conditions, EAT may contribute to the anatomical cardiac substrate for the development of AF. In fact, EAT can produce and secrete pro-inflammatory cytokines, activin A, matrix metalloproteinases-MMPs, and reactive oxygen species, that are all factors potentially contributing to atrial collagen deposition, fibrosis, and scar formation. Furthermore, EAT may penetrate the myocardium and generate atrial fatty infiltrates that in turn may alter the atrial electrophysiological properties.
This review aims to analyze the main mechanisms underlying the role of EAT in the pathogenesis of AF, and the potential therapeutic strategies targeting the cardiac visceral fat.