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Towards a solution for saphenous vein graft failure

The Asia Pacific Heart Journal
Publication Date
DOI: 10.1016/s1328-0163(97)90004-x
  • Biology
  • Economics
  • Medicine
  • Pharmacology


Abstract The saphenous vein is the most commonly used conduit for coronary revascularisation due to its ready availability, ease of harvesting, and favourable surgical handling. Its limitation, however, lies in the subsequent progressive decline in graft patency in a large proportion of cases, resulting either from early thrombotic occlusion or from the later development of vein graft disease. By 10 years, less than 50% of grafts are patent, with the remainder showing angiographic evidence of significant graft disease. Vein graft thickening involves medial vascular smooth muscle cell (VSMC) proliferation, VSMC migration across the internal elastic lamina into the intima, and further proliferation at this site where they form a neointima. This cell layer continues to secrete extracellular matrix proteins and undergoes atherogenic changes resulting in progressive narrowing of the vessel lumen, a reduction in graft flow, and an increased risk of thrombotic occlusion. Although the triggers for neointima formation have not been clearly defined, the process undoubtedly involves complex interactions between VSMCs, endothelial cells, platelets and leukocytes. Given the enormous economic and human considerations, the finding of an effective treatment for late vein graft failure is a matter of some urgency. Treatment options include surgical, pharmacological and molecular biological interventions aimed at ameliorating the problem. Combination drug therapy, or phased therapy (involving targetting of different stages in the development of graft disease) may offer the greatest potential for pharmacological intervention. External stenting represents a promising non-pharmacological intervention that is clinically feasible but needs assessment in human studies. However, it is the rapid advances being made in gene manipulation and therapy that may ultimately offer the best means of controlling smooth muscle cell activity. (Asia Pacific Heart J 120

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