Epicardial adipose tissue (EAT) is metabolically active tissue that accumulates around the coronary arteries. Epicardial fat is a rich source of free fatty acids and may contribute to local inflammatory load by increased synthesis of inflammatory cytokines. Direct passage of bioactive molecules into the coronary arteries due to close contact with the vascular wall and the lack of fascia may contribute to the pathogenesis of coronary artery disease. Direct correlation between visceral fat and EAT defines the latter as an indirect marker of intra-abdominal visceral adiposity. EAT is related to anthropometric and clinical features of the metabolic syndrome (MS) and to hepatic transaminases as markers of steatohepatitis. An increase in EAT thickness is related to an increase in left ventricular mass and is correlated with atrial enlargement and impairment in diastolic filling in obesity. Echocardiographic study of EAT is an easy and reliable imaging indicator of visceral adiposity and cardiovascular risk. EAT is an independent factor strongly correlated with significant coronary stenosis. A level of EAT above an established average value can be considered a predictive marker of cardiovascular risk. We review the most recent studies proving the specific active role of EAT in the development of cardiac disease.