Basic cellular mechanisms of coronary bypass graft disease.

Abstract

The internal mammary artery (IMA) grafts have a higher patency than the saphenous vein (SV) grafts. The biological properties of the arterial and venous grafts (i.e. endothelial and smooth muscle cell function) are crucial determinants of graft function. The endothelial cells in arterial grafts release larger amounts of endothelium-derived nitric oxide formed from the precursor amino acid L-arginine in response to several vasoactive hormones than do venous grafts. In IMA, platelet-derived adenosine nucleotides activate the endothelium to release nitric oxide, thereby causing vascular relaxation, while in the saphenous vein this important protective mechanism is absent. Therefore, platelet-derived thromboxane A2 and serotonin evoke marked vasoconstriction in the saphenous vein in spite of an intact endothelium. Smooth muscle cell growth plays a significant part in intimal thickening and vascular occlusion of bypass grafts, in particular, SV grafts. Mechanical forces such as pulsatile stretch and platelet-derived growth factor are potent mitogens for SV but not IMA smooth muscle proliferation. Hence, the different endothelial and smooth muscle cell function of IMA and SV may contribute considerably to the different graft functions in patients with coronary artery disease.