Coronary vein graft disease: pathogenesis and prevention

Abstract

Not long after coronary artery bypass grafting surgery was described, several reports presented follow-up angiographic data on large cohorts of patients, demonstrating that approximately one-half of saphenous vein grafts fail within 10 to 15 years of surgery and that graft failure is associated with worse clinical outcomes. Three processes are responsible for vein graft failure. Thrombosis, intimal hyperplasia and accelerated atherosclerosis contribute to graft failure in the acute, subacute and late postoperative periods, respectively. Studies have shown that perioperative antiplatelet therapy can reduce early thrombosis and graft failure. As in native coronaries, intensive lipid lowering can attenuate the process of atherosclerosis in vein grafts. Intimal hyperplasia in the vein graft is thought to be an adaptation of the vein to higher pressures in the arterial circulation. This process is further promoted by the loss of inhibition from the endothelial layer, which is injured during surgery. A new 'no-touch' technique for harvesting grafts may be effective in preventing disruption to the endothelial layer, and subsequent intimal hyperplasia and graft loss. Off-pump surgery and endoscopic vein harvesting, which are known to reduce surgical morbidity, have been shown to be no worse than on-pump surgery and open vein harvesting, respectively, in terms of vein graft patency. Various gene therapies can prevent intimal hyperplasia in animal models, but human data obtained so far have been disappointing. Placing an external stent around a vein graft may reduce tangential wall stress and subsequent intimal hyperplasia.