Reopening of the occluded saphenous vein composite grafts after coronary artery bypass grafting

Aortocoronary saphenous vein graft disease, with its increasing clinical sequelae, presents an important and unresolved dilemma in cardiological practice. During the 1st month after bypass surgery, vein graft attrition results from thrombotic occlusion, while later the dominant process is atherosclerotic obstruction occurring on a foundation of neointimal hyperplasia. Although the risk factors predisposing to vein graft atherosclerosis are broadly similar to those recognized for native coronary disease, the pathogenic effects of these risk factors are amplified by inherent deficiencies of the vein as a conduit when transposed into the coronary arterial circulation. A multifaceted strategy aimed at prevention of vein graft disease is emerging, elements of which include: continued improvements in surgical technique; more effective antiplatelet drugs; increasingly intensive risk factor modification, in particular early and aggressive lipid-lowering drug therapy; and a number of evolving therapies, such as gene transfer and nitric oxide donor administration, which target vein graft disease at an early and fundamental level. At present, a key measure is to circumvent the problem of vein graft disease by preferential selection of arterial conduits, in particular the internal mammary arteries, for coronary bypass surgery whenever possible.

Occlusive arterial disease is a leading cause of morbidity and mortality worldwide. Aside from balloon angioplasty, bypass graft surgery is the most commonly performed revascularization technique for occlusive arterial disease. Coronary artery bypass graft surgery is performed in patients with left main coronary artery disease and three-vessel coronary disease, whereas peripheral artery bypass graft surgery is used to treat patients with late-stage peripheral artery occlusive disease. The great saphenous veins are commonly used conduits for surgical revascularization; however, they are associated with a high failure rate. Therefore, preservation of vein graft patency is essential for long-term surgical success. With the exception of 'no-touch' techniques and lipid-lowering and antiplatelet (aspirin) therapy, no intervention has hitherto unequivocally proven to be clinically effective in preventing vein graft failure. In this Review, we describe both preclinical and clinical studies evaluating the pathophysiology underlying vein graft failure, and the latest therapeutic options to improve patency for both coronary and peripheral grafts.