Abstract
The saphenous vein remains the most frequently used conduit for coronary artery bypass grafting, despite reported unsatisfactory long-term patency rates. Understanding the pathophysiology of vein graft failure and attempting to improve its longevity has been a significant area of research for more than three decades. This article aims to review the current understanding of the pathophysiology and potential new intervention strategies. A search of three databases: MEDLINE, Web of Science, and Cochrane Library, was undertaken for the terms "pathophysiology," "prevention," and "treatment" plus the term "vein graft failure." Saphenous graft failure is commonly the consequence of four different pathophysiological mechanisms, early acute thrombosis, vascular inflammation, intimal hyperplasia, and late accelerated atherosclerosis. Different methods have been proposed to inhibit or attenuate these pathological processes including modified surgical technique, topical pretreatment, external graft support, and postoperative pharmacological interventions. Once graft failure occurs, the available treatments are either surgical reintervention, angioplasty, or conservative medical management reserved for patients not eligible for either procedure. Despite the extensive amount of research performed, the pathophysiology of saphenous vein graft is still not completely understood. Surgical and pharmacological interventions have improved early patency and different strategies for prevention seem to offer some hope in improving long-term patency.
Highlights
The saphenous vein remains the most frequently used conduit for coronary artery bypass grafting, despite reported unsatisfactory long‐term patency rates
There has been increased interest in understanding the pathophysiology involved in the development of vein grafts disease as many therapeutics have been suggested, none has been successful enough to make them widely adopted. This is in part related to our limited understanding of the complex pathological processes involved in the development of the disease starting from vascular inflammation (VA) to superimposed atherosclerosis, the cross‐talk between the different cells forming the long saphenous vein (LSV) and the influence of the circulating cells and other molecules
Some studies have found that poorly controlled Diabetes mellitus (DM) is associated with worse survival after Coronary artery bypass grafting (CABG), while others found no significant difference in the rate of LSV graft occlusion.[30,33]
Summary
Conduits for CABG are the left internal thoracic artery (LITA) and the long saphenous vein (LSV). More than one graft and can be harvested at the same time as the LITA For these reasons, the LSV remains one of the most commonly used conduits for CABG.[3] Other conduits not extensively used are the radial artery and the right internal thoracic artery.[1]. There has been increased interest in understanding the pathophysiology involved in the development of vein grafts disease as many therapeutics have been suggested, none has been successful enough to make them widely adopted This is in part related to our limited understanding of the complex pathological processes involved in the development of the disease starting from vascular inflammation (VA) to superimposed atherosclerosis, the cross‐talk between the different cells forming the LSV and the influence of the circulating cells and other molecules. The overall process is thought to be marked by complex interactions between several factors owned to either the patient or the technique which will impact the pathophysiology of the disease, making its study challenging
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