Cellular cross-talk between epicardial adipose tissue and myocardium in relation to the pathogenesis of cardiovascular disease.

Epicardial and perivascular fat depot size is considered an index of cardiac and visceral obesity. The functional and anatomic proximity of epicardial adipose tissue (EAT) to myocardium has drawn increasing attention in recent years among researchers attempting to elucidate its putative role as an endocrine organ. This includes the role of EAT as a lipid storing depot and as an inflammatory tissue secreting cytokines and chemokines under pathogenic conditions such as cardiovascular diseases. In this review, we discuss the current state of knowledge regarding the potential EAT mediators of inflammation and the paracrine cross-talk between EAT and the underlying myocardium. We also highlight the most recent findings on the causes and correlates of myocardial steatosis/cardiac lipotoxicity and its association with cardiac dysfunction.