Smooth Muscle Cell Proliferation Responses in Organ Cultures of Human Saphenous Vein
Occlusion of saphenous vein coronary artery bypass grafts remains a major limitation to the clinical benefits of the procedure, despite more than 25 years of experience . Early occlusion rates can be minimized by optimizing techniques for surgical preparation  and anastomosis and by the use of perioperative and early post-operative antithrombotic therapy . Unfortunately, no modification of technique or drug regime has been shown to reduce late vein graft occlusion . This is known to result from excessive proliferation of vascular smooth muscle cells (VSMCs) and the superimposition of atheroma on the resulting thickened intima . The relationship of intimal thickening to the conditions of implantation has been investigated in animal models. Briefly summarized, intimal thickening occurs only after implantation into a high-pressure (arterial) location and is not related to adventitial disruption [6, 7]. Qualitative and quantitative time course studies [8, 9] indicate also that intimal thickening occurs progressively long after the restoration of a morphologically intact endothelium and the termination of measurable platelet and leucocyte adhesion. These observations imply that intimal thickening is an intrinsic response of the vessel wall itself to the altered haemodynamics . Understanding the mechanisms underlying this response may be helpful in developing strategies to reduce vein graft occlusion.
KeywordsCholesterol Migration Aspirin Heparin Adenosine
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