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  • Review Article
  • Published:

Vein graft failure: from pathophysiology to clinical outcomes

Key Points

  • Thrombosis, constrictive remodelling, intimal hyperplasia, and unstable atherosclerotic lesions are the critical mechanisms contributing to vein graft failure

  • Factors associated with the surgical procedure of bypass grafting, such as vein graft harvesting and handling, and the size and condition of the conduit and target vessel, determine long-term patency

  • Experimental models have shown that inhibiting endothelial cell damage, smooth muscle migration and proliferation, and the inflammatory response contribute to the prevention of vein graft failure

  • Lipid-lowering therapy, antiplatelet therapy, and the 'no-touch' technique during surgery are clinically proven to prevent vein graft failure

  • New therapies to prevent vein graft failure, such as gene therapy and external stenting, are promising and require further study

  • Balloon angioplasty and medical therapy are the preferred revascularization strategies for uncomplicated stenotic grafts, whereas redo graft surgery might be the preferred option for old or diffusely diseased venous grafts

Abstract

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.

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Figure 1: Macroscopic and microscopic views of a human vein graft.
Figure 2: Development of vein graft failure.
Figure 3: Inflammation in vein graft failure.
Figure 4: Murine vein graft lesions in hypercholesterolaemic mice.
Figure 5: Immunohistochemical characterization of hypercholesterolaemic murine vein grafts.
Figure 6: Scanning electron microscopy photographs of saphenous veins.
Figure 7: Angiogram of an elderly patient with unstable angina.

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Acknowledgements

The authors were supported by a grant from the European Union 7th Framework Programme, Health Innovation, CARDIMMUN (Project 601728), and a grant from the Netherlands CardioVascular Research Initiative for the GENIUS project 'Generating the best evidence-based pharmaceutical targets for atherosclerosis' (CVON2011-19).

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de Vries, M., Simons, K., Jukema, J. et al. Vein graft failure: from pathophysiology to clinical outcomes. Nat Rev Cardiol 13, 451–470 (2016). https://doi.org/10.1038/nrcardio.2016.76

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