Perivascular adipose tissue and coronary vascular disease

Abstract

Coronary perivascular adipose tissue is a naturally occurring adipose tissue depot that normally surrounds the major coronary arteries on the surface of the heart. Although originally thought to promote vascular health and integrity, there is a growing body of evidence to support that coronary perivascular adipose tissue displays a distinct phenotype relative to other adipose depots and is capable of producing local factors with the potential to augment coronary vascular tone, inflammation, and the initiation and progression of coronary artery disease. The purpose of the present review is to outline previous findings about the cardiovascular effects of coronary perivascular adipose tissue and the potential mechanisms by which adipose-derived factors may influence coronary vascular function and the progression of atherogenesis.

Keywords: adipokines; adipose tissue; obesity.

Figure 1

Schematic diagram outlining known alterations in coronary PVAT-derived adipokines and potential downstream effector mechanisms in endothelium and vascular smooth muscle. Leptin released from coronary PVAT diminishes eNOS activity, preventing nitric oxide mediated dilation of vascular smooth muscle via activation of K⁺ channels and contributes to the recruitment of macrophages and retention of foam cells in the extravascular space. Calpastatin and an unknown adipose-derived constricting factor(s) (ADCF) increase vasoconstriction via Ca_V1.2 channels and may function to increase RhoA activity in healthy coronary smooth muscle. Other adipokines implicated in other vascular beds may also play a role in promoting coronary vascular endothelial and smooth muscle dysfunction, including, but not limited to: increases in resistin, chemerin, osteoglycin, osteoprotegerin, and decreases in adiponectin production.