Saphenous Vein Graft Intervention
Saphenous Vein Graft Intervention
Saphenous vein grafts are prone to degeneration and occlusion. Vein graft disease continues to be a significant problem in maintaining long-term benefits after coronary artery bypass surgery. The neointimal hyperplasia and aggressive atherosclerosis that occur in saphenous vein grafts make interventions particularly challenging due to plaque embolization and the no-reflow phenomenon. This review discusses the pathophysiology of vein graft disease and the various percutaneous strategies that have been applied to manage vein grafts. We review the issues surrounding stent selection and various approaches to embolic protection devices. Finally, we discuss the technical steps that optimize success in treating this challenging patient subset.
Degeneration and occlusion of saphenous vein grafts (SVG) continue to be significant problems in maintaining long-term benefit in patients who have undergone coronary artery bypass graft (CABG) surgery. SVG occlusion during the first year is high at 15%, and 10-year patency is only 60%. SVG failure is associated with a significant increase in major adverse cardiovascular events (MACE), including death, myocardial infarction (MI), and the need for repeat revascularization. Predictors of vein graft occlusion include tobacco use, hypertension, dyslipidemia, and small target vessel diameter (<2 mm). SVG percutaneous coronary intervention (PCI) comprises an important subset of interventions in the cardiac catheterization laboratory. According to the American College of Cardiology National Cardiovascular Data Registry, there were over 90,000 patients (5.7% of all PCIs) who underwent SVG PCI between 2004 and 2009.
SVG disease occurs in 3 phases: early (before hospital discharge); intermediate (1 month to 1 year); and late (beyond 1 year). Early graft failure is due to thrombotic closure, usually at the site of anastomosis, as a result of endothelial injury and the release of inflammatory cytokines during surgery. Technical factors, such as poor distal runoff, graft kinking, and small target vessel diameter, predispose grafts to early occlusion. After the first month, exposure of the vein grafts to arterial pressure results in neointimal hyperplasia. This pathophysiologic process causes intimal damage, fibrosis, platelet aggregation, the release of growth factors, and smooth muscle cell proliferation. After the first year, aggressive atherosclerotic narrowing occurring over the already abnormal endothelium is the main mechanism for graft failure.
Atherosclerotic plaques in SVGs are more diffuse, friable, contain more foam and inflammatory cells, have absent or small fibrous caps, and little or no calcification in comparison to native coronary atherosclerosis. These characteristics predispose SVGs to extensive thrombotic burden and distal embolization during coronary graft interventions, resulting in the no-reflow phenomenon, and hence, more periprocedural MI. Grafts particularly susceptible to these effects are those of an older age with more ectasia and greater plaque burden.
Abstract and Introduction
Abstract
Saphenous vein grafts are prone to degeneration and occlusion. Vein graft disease continues to be a significant problem in maintaining long-term benefits after coronary artery bypass surgery. The neointimal hyperplasia and aggressive atherosclerosis that occur in saphenous vein grafts make interventions particularly challenging due to plaque embolization and the no-reflow phenomenon. This review discusses the pathophysiology of vein graft disease and the various percutaneous strategies that have been applied to manage vein grafts. We review the issues surrounding stent selection and various approaches to embolic protection devices. Finally, we discuss the technical steps that optimize success in treating this challenging patient subset.
Introduction
Degeneration and occlusion of saphenous vein grafts (SVG) continue to be significant problems in maintaining long-term benefit in patients who have undergone coronary artery bypass graft (CABG) surgery. SVG occlusion during the first year is high at 15%, and 10-year patency is only 60%. SVG failure is associated with a significant increase in major adverse cardiovascular events (MACE), including death, myocardial infarction (MI), and the need for repeat revascularization. Predictors of vein graft occlusion include tobacco use, hypertension, dyslipidemia, and small target vessel diameter (<2 mm). SVG percutaneous coronary intervention (PCI) comprises an important subset of interventions in the cardiac catheterization laboratory. According to the American College of Cardiology National Cardiovascular Data Registry, there were over 90,000 patients (5.7% of all PCIs) who underwent SVG PCI between 2004 and 2009.
SVG disease occurs in 3 phases: early (before hospital discharge); intermediate (1 month to 1 year); and late (beyond 1 year). Early graft failure is due to thrombotic closure, usually at the site of anastomosis, as a result of endothelial injury and the release of inflammatory cytokines during surgery. Technical factors, such as poor distal runoff, graft kinking, and small target vessel diameter, predispose grafts to early occlusion. After the first month, exposure of the vein grafts to arterial pressure results in neointimal hyperplasia. This pathophysiologic process causes intimal damage, fibrosis, platelet aggregation, the release of growth factors, and smooth muscle cell proliferation. After the first year, aggressive atherosclerotic narrowing occurring over the already abnormal endothelium is the main mechanism for graft failure.
Atherosclerotic plaques in SVGs are more diffuse, friable, contain more foam and inflammatory cells, have absent or small fibrous caps, and little or no calcification in comparison to native coronary atherosclerosis. These characteristics predispose SVGs to extensive thrombotic burden and distal embolization during coronary graft interventions, resulting in the no-reflow phenomenon, and hence, more periprocedural MI. Grafts particularly susceptible to these effects are those of an older age with more ectasia and greater plaque burden.
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