Epicardial and perivascular adipose tissue expansion and inflammation in obesity and metabolic syndrome contribute to cardiac contractile and vascular dysfunction through altered adipokine secretion.
Abstract Introduction Fat depots around the heart and vasculature Physiological function of epicardial adipose tissue Visualization of epicardial adipose tissue Epicardial fat thickness as diagnostic marker Visualization of perivascular adipose tissue Expression and secretion of fatty acids and adipokines from epicardial and perivascular fat depots Cross‐talk between secretory products from EAT and the myocardium Cross‐talk between secretory products from PVAT and the vasculature 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.
Ouwens et al. (Tue,) conducted a review in Cardiovascular disease, obesity, type 2 diabetes, metabolic syndrome. Epicardial and perivascular adipose tissue expansion and inflammation in obesity and metabolic syndrome contribute to cardiac contractile and vascular dysfunction through altered adipokine secretion.