Saphenous Vein Graft Disease

Abstract

Saphenous vein graft (SVG) disease after coronary artery bypass grafting (CABG) occurs in three phases: thrombosis, intimal hyperplasia, and atherosclerosis. Within the first month, thrombosis plays a major role. From month 1 to month 12, intimal hyperplasia occurs. Beyond 12 months, atherosclerosis becomes the primary cause for late graft failure. Endothelial damage has been shown to be the major underlying pathophysiology of SVG disease. Many factors contribute to endothelial damage from the moment the vein is harvested to when the vein is grafted into an arterial environment. To address this disease process, various therapeutic modalities, from surgical methods to medical treatment, have been evaluated. Surgically, the technical method of harvesting the vein has been shown to affect SVG patency. From a pharmacologic perspective, only two guideline class I recommended medications, aspirin and statins, have been shown to improve short- and long-term SVG patency after CABG. Despite these surgical and medical advances, SVG disease remains a significant problem with 1-year patency rates of 89% dropping to 61% after 10 years. This review discusses the pathogenesis of SVG disease, predictors of SVG failure, and current surgical and pharmacologic therapies to address SVG disease, including possible future treatment.

Physiology of in-situ arterial revascularization in coronary artery bypass grafting: Preoperative, intraoperative and postoperative factors and influences

“…The “competitive flow” from moderately stenosed native TVECA has been posited as a major cause for late in situ IMA graft failure. This is in contradistinction to causes for vein graft failures[53]. Additional causes of late arterial graft failure include factors typically attributed to other conduit failures, such as poor run-off of the distal native coronary circulation, thrombogenic factors, and size mis-match might be factors as well[50].…”

“…Since the Achilles’ heel of CABG has been the late development of atherosclerotic disease in vein graft conduits (in patients operated upon 15-50 years ago)[53], the full effect of this postoperative statin intervention still remains to be evaluated. Importantly, the benefits of statin therapy in non-surgical patients with SIHD are incontrovertible[92].…”

Intimal hyperplasia induced by vascular intervention causes lipoprotein retention and accelerated atherosclerosis

“…Interestingly, high prevalence of atherosclerosis is also seen following insertion of coronary artery bypass grafts (CABG), especially when using saphenous vein‐grafts (Motwani and Topol 1998; Kim et al. 2013; Yahagi et al. 2016).…”

“…The atherosclerotic lesions appear already within 1 year after implantation, and between 2 and 5 years after intervention complex lesions with necrotic cores are seen (Motwani and Topol 1998; Kim et al. 2013). Since the grafted veins do not have atherosclerosis at the time of surgery, these are new atherosclerotic lesions developed after the intervention.…”

The Anticoagulant Effect of PGI2S and tPA in Transgenic Umbilical Vein Endothelial Cells Is Linked to Up-Regulation of PKA and PKC

“…Endothelial cell disorders can result in blood clots, as the vascular endothelium forms a barrier between the blood and the vascular wall that isolates antigens from the host immune system, and the coagulation system from the coagulation cascade promoter. Vascular endothelial cells can also generate anticoagulation components [6]. In 1979, Herring et al [7,8] implanted endothelial cells into artificial blood vessels, and then transferred these vessels into the arterial system of dogs.…”