2013
DOI: 10.1097/sla.0b013e318288c38d
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Saphenous Vein Graft Failure After Coronary Artery Bypass Surgery

Abstract: Despite advances in management, VGF remains one of the leading causes of poor in-hospital and long-term outcomes after coronary artery bypass graft surgery. New developments in VGF prevention such as gene therapy, external graft support, fully tissue-engineered grafts, hybrid grafts, and synthetic conduits are promising but unproven. Future efforts to reduce VGF require a multidisciplinary approach with a primary focus on prevention.

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Cited by 308 publications
(267 citation statements)
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“…The patency rates of saphenous vein grafts were 71-87% at 1 year after surgery in previous studies [16][17][18] and up to 50% at 10 years [16][17][18][19][20][21].…”
Section: Introductionmentioning
confidence: 88%
See 1 more Smart Citation
“…The patency rates of saphenous vein grafts were 71-87% at 1 year after surgery in previous studies [16][17][18] and up to 50% at 10 years [16][17][18][19][20][21].…”
Section: Introductionmentioning
confidence: 88%
“…However, the long-term patency of SVG is reported to be poor [16][17][18][19][20][21]. The late-term SVG failure is mainly due to atherosclerotic obstruction occurring on a foundation of neointimal hyperplasia [64].…”
Section: Cabg Using Saphenous Vein Graftsmentioning
confidence: 99%
“…In a recent analysis of vein graft failure, early denudation of endothelium attributed to surgical trauma, longitudinal wall (shear) stress, and venous exposure to increased arterial pressure were found to be the primary triggers toward the development of intimal hyperplasia. 9 When a vein is exposed to arterial pressure, there is an increase in wall shear stress, triggering an adaptive response of vessel dilatation to accommodate the increased blood pressure and flow. This aggressive vessel dilatation increases wall tension, which leads to medial thickening, an additional adaptive response.…”
mentioning
confidence: 99%
“…1,2 However, several lines of evidence have suggested that about 40% of these autologous grafts are ultimately unsuccessful, as pathologic vascular restenosis and wall thickening re-occurs, a process called intimal hyperplasia (IH). [3][4][5] The pathogenesis of the intimal hyperplastic lesion is still poorly understood and no successful clinical intervention has been identified. It is believed that restenosis is a result of vascular smooth muscle cell (vSMC) proliferation and differentiation.…”
mentioning
confidence: 99%