Novel strategies for the prevention of vein graft failure

Abstract

Autologous saphenous vein continues to be the most widely used conduit for coronary artery bypass grafting (CABG) worldwide. However, early vein graft failure due to thrombosis occurs in as many as 18% of cases within the first postoperative week [1, 2]. Up to 50% of the patients may require reoperation by 10 years after CABG to alleviate symptoms and treat graft occlusion [1, 2]. Vein graft thickening (increased medial thickening and neointima formation) is the main cause of late failure [3], a process mediated by the proliferation and migration of vascular smoothmuscle cells (Fig. 40.1). Superimposed on neointima formation is atherogenesis, which ultimately leads to plaque rupture and graft occlusion [1, 2]. Apart from lipid lowering therapy [4], no intervention has hitherto proved clinically effective in preventing late vein graft failure [5]. This clearly constitutes a major clinical and economic problem that needs to be urgently resolved. The pathophysiology of vein graft failure is complex, involving disparate factors that include adhesion of platelets and leukocytes, rheological forces, metalloproteinase expression, proliferation and migration of vascular smooth muscle cells, neointima formation and oxidative stress. In this chapter, we will briefly summarize the diverse etiology of vein graft disease and then consider novel approaches to prevent late vein graft failure which include external sheaths, the endothelin-1A (ETA) receptor antagonists, nitric oxide (NO) donating aspirin, cytostatic drugs and antioxidants. © 2006 Springer-Verlag Berlin Heidelberg.