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At first sight, clopidogrel appears to be undesirable for cardiac surgeons: antiplatelet therapy can increase the risk of bleeding during coronary artery bypass graft surgery (CABG).1 Traditionally, many surgeons have felt that, with impeccable technique, their personally constructed grafts would be nearly ‘immune’ to thrombosis, even without antiplatelet therapy. However, it could theoretically reduce the risk for early vein graft failure, which is predominantly thrombosis related.
There are three different principal mechanisms that play a role in vein graft failure during postoperative periods2:
Early (<1 month): thrombosis; this is related to technical factors such as small size of the target vessel resulting in poor distal runoff, size mismatch between the graft and the target vessel creating turbulent flow, graft ischaemia and disruption of the endothelial layer as a result of mechanical trauma and manual distention, or suturing mishaps. Most saphenous vein grafts (SVG) experience endothelial injury during harvesting and exposure to arterial pressure. The loss of the endothelial layer can promote platelet adhesion and thrombosis as well as vasospasm resulting from decreased nitric oxide levels.
Intermediate period (1 to 12 months): intimal hyperplasia; platelet adhesion to the intimal surface is also the initial event in the development of intimal hyperplasia. After adhering to the intima, platelets release mitogenic proteins, stimulating smooth muscle cell migration, resulting in intimal proliferation and hyperplasia. Concentric intimal thrombus is converted into fibrous plaque. Intimal hyperplasia is also a result of the graft's adaptation to higher arterial pressures.
Later postoperative period (>12 months): accelerated atherosclerosis; As in native coronary arteries, vein graft atheromas can rupture and cause thrombotic occlusion of the graft. Vein graft atheromas are more diffuse and concentric than those in native vessels. They are less …
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