The role of epicardial and perivascular adipose tissue in the pathophysiology of cardiovascular disease

Introduction Fat depots around the heart and vasculature Definitions Epicardial adipose tissue Perivascular adipose tissue Pericardial adipose tissue Physiological function of epicardial adipose tissue Visualization of epicardial adipose tissue Epicardial fat thickness as diagnostic marker Association of epicardial fat with insulin resistance and T2DM Association of epicardial fat with cardiovascular dysfunction Association of epicardial fat with the metabolic syndrome Association of epicardial fat with adipokines Effect of weight loss on epicardial adipose tissue Visualization of perivascular adipose tissue Expression and secretion of fatty acids and adipokines from epicardial and perivascular fat depots Fatty acids Adipokines Cross-talk between secretory products from EAT and the myocardium Cross-talk between secretory products from PVAT and the vasculature Vasorelaxation Vasoconstriction Vascular remodelling Alterations in obesity and insulin resistance Perspectives and conclusions Obesity, insulin resistance and the metabolic syndrome, are characterized by expansion and inflammation of adipose tissue, including the depots surrounding the heart and the blood vessels. Epicardial adipose tissue (EAT) is a visceral thoracic fat depot located along the large coronary arteries and on the surface of the ventricles and the apex of the heart, whereas perivascular adipose tissue (PVAT) surrounds the arteries. Both fat depots are not separated by a fascia from the underlying tissue. Therefore, factors secreted from epicardial and PVAT, like free fatty acids and adipokines, can directly affect the function of the heart and blood vessels. In this review, we describe the alterations found in EAT and PVAT in pathological states like obesity, type 2 diabetes, the metabolic syndrome and coronary artery disease. Furthermore, we discuss how changes in adipokine expression and secretion associated with these pathological states could contribute to the pathogenesis of cardiac contractile and vascular dysfunction.