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Objectives: Vein graft disease is a major drawback of coronary artery bypass grafting. However, histopathologic studies of old human aortocoronary grafts are scarce., Methods: We screened patients undergoing redo coronary artery bypass grafting at three university hospitals and selected those with at least one excisable old vein graft. Native non-grafted saphenous veins were also obtained as controls. Clinical and angiographic data were separately documented., Results: We evaluated 117 segments from 29 veins. All but 4 old graft segments showed degrees of luminal narrowing and fibrointimal proliferation. Moreover, 61 segments demonstrated atherosclerotic plaques. Such plaques were typically concentric and, compared with other segments, more frequently represented necrosis, calcification and giant cells (p < 0.001 for all comparisons) and had a higher inflammatory cell count, predominantly of lymphocytic origin. Native saphenous veins frequently showed fibrosis, but no calcification or active inflammation. Angiographic findings showed moderate correlation with the histological degree of luminal stenosis (Spearman's ρ = 0.564, p < 0.001)., Conclusions: Human vein graft atherosclerosis and arterial atherosclerosis share many features; however, we found lymphocytes to be the dominant inflammatory cells within plaques. Conventional angiography underestimated the atherosclerosis burden in vein grafts. Improved understanding of disease pathophysiology could lead to the development of novel interventions that reduce costly and suboptimal repeat revascularizations., (Copyright © 2012 S. Karger AG, Basel.)

Aortocoronary saphenous vein bypass grafting relieves anginal pain in patients with coronary artery disease. However, its effectiveness is limited due to graft failure; the 10-year patency rate is 50%-60%. Early, 1-year and late graft failure may be due to thrombosis, fibrointimal hyperplasia and atherosclerosis, respectively. There is general agreement that vein graft atherosclerosis differs from arterial lesions in terms of temporal and histological changes. Vein graft atherosclerosis is more rapid, with diffuse concentric changes and a less noticeable fibrous cap, making venous plaques more vulnerable to rupture and subsequent thrombus formation. Despite progress in understanding the pathophysiology, some aspects of vein graft atherosclerosis need to be clarified. This review focuses on the pathophysiologic aspects of this widespread, costly and disabling disease, with emphasis on late graft occlusion and distinctions between arterial and venous atherosclerosis in terms of histology, pathophysiology and risk factors.