ABSTRACT
Introduction The first aortocoronary saphenous vein graft (SVG) implantation was performed in May 1967 by Garret and colleagues, with the subsequent pioneering work of Favaloro initiating the era of surgical revascularization of ischemic heart disease. 1,2 This major advance in surgical revascularization provided a significant improvement in angina relief and, in selected patients, improved long-term prognosis. 3,4 However, it has come to be recognized that SVG bypass surgery is of a palliative nature and does have some important limitations, including the fact that an accelerated atherosclerotic process develops within the graft over time, often resulting in untoward clinical sequelae. Several studies have reported up to 15% SVG occlusion during the first postsurgical year, with a further 1-2% closure rate between years 1 and 6. After 6 years, the attrition rate increases to 4-5% per year, as only 60% of the SVGs are patent by 10 years and less than 50% of these patent grafts remain free of significant obstruction. 3-8 Degenerative atherosclerotic SVG disease, as well as the progression of the native coronary vascular disease process, results in approximately 35% of patients requiring either reoperation or percutaneous revascularization 10-12 years after surgery. 9 The increased risk of a second bypass operation is well established, with a 3-5-fold increase in mortality and myocardial infarction. 7,10 With recognition of these limitations, SVG percutaneous intervention in patients with prior coronary bypass surgery (CABG) has been recommended. However, percutaneous treatment has similarly been associated with an increased periprocedural risk, as well as lower long-term patency as compared with interventions performed in native coronary arteries. 11 Coronary atheroembolism from the diseased vein graft appears to be the major cause of the increased risk associated with reoperations and vein graft percutaneous interventions. 7,10
Pathogenesis of saphenous vein graft disease Three pathophysiological processes are involved in the pathogenesis of SVG disease: thrombosis, intimal hyperplasia, and atherosclerosis. While these processes are interrelated, each appears to be temporally distinct, with thrombosis being the main mechanism of SVG occlusion during the first month after surgery, at an incidence of 3-12%. 6,7 This thrombotic occlusion is a consequence of several mechanisms, including vessel wall alterations during the vein harvesting process, changes in blood rheology and flow dynamics, and surgery-related technical factors. Intimal hyperplasia is the major contributor to disease progression between 1 month and 1 year. While this process rarely produces a significant degree of stenosis, it provides the basis for the later development of graft atheroma. Atherosclerosis is the dominant pathological process after the first year. Approximately 75-85% of acute coronary events in patients with prior CABG (unstable angina or acute non-ST-elevation or ST-elevation myocardial infarction (MI)) are caused by the atherosclerotic process developed in the SVG. 12 Although the fundamental process of atheroma development and the predisposition factors are similar in SVG and in native arteries, there are some differences that are considerations when contemplating percutaneous treatment strategies. Vein graft atherosclerosis tends to be diffuse, concentric, and friable. There is often a poorly developed or absent fibrous atheroma cap, with a little evidence of calcification. 13-
17 There is a higher plaque lipid content, resulting from increased lipid uptake and slower lipolysis. 18,19 In addition, the compensatory enlargement (positive remodeling) described in coronary native arteries undergoing atherosclerotic disease progression does not appear to occur in the SVG atheromatous process. 20 Late thrombosis is a frequent event in old SVGs with advanced atherosclerosis.
