Vascular Effects of Peripheral Versus Coronary PVAT

Coronary perivascular adipose tissue (PVAT) is a visceral adipose tissue of mesothelial origin that normally surrounds the major coronary arteries on the surface of the heart. Coronary PVAT is functionally distinct from the adipose tissue found on the surface of the myocardium, which is defined as myocardial epicardial adipose tissue. In addition to adipocytes and preadipocytes, coronary PVAT contains fibroblasts, macrophages, leukocytes, as well as blood vessels and autonomic nerves. With no fascia separating PVAT from the coronary circulation and myocardium, these essential components of the heart share the same microcirculation. Originally perceived as a relatively ubiquitous and benign tissue that largely provides structural support and insulation, it is becoming clear that factors derived from PVAT (adipokines) are capable of influencing a variety of key (patho)physiological parameters. In particular, recent data support that cardiac adiposity expands with obesity, that atherosclerotic plaques occur predominately in coronary arteries that are encased in PVAT, and that coronary PVAT volume is positively associated with underlying plaque burden. Patients with high myocardial epicardial adipose tissue volume have also been shown to have a higher incidence of atrial fibrillation, independent of left atrium enlargement. As such, cardiac adiposity has been identified as an independent risk factor for coronary artery disease and a predictor of future coronary events. Although specific adipokines can serve to promote vascular health and integrity, evidence is mounting in support of marked upregulation of proatherogenic mRNA and protein expression profiles in coronary PVAT and myocardial epicardial adipose tissue in the setting of obesity. This aberrant regulation of coronary PVAT also correlates with underlying vascular dysfunction and disease in obesity. Thus, there is growing evidence to support the hypothesis that local alterations in PVAT-derived factors contribute to the initiation, progression, and expansion of coronary disease, independent of changes in visceral adipose tissue and systemic adipokine levels that may occur in the setting of obesity. The purpose of the present review is to outline current data about the cardiovascular effects of coronary PVAT and the potential mechanisms by which adipose-derived factors may influence coronary endothelial and smooth muscle function and the progression of atherogenesis.