Towards the prevention of vein graft failure
Section snippets
Pathophysiology
Thrombotic occlusion of aorto–coronary vein grafts soon after implantation arises from endothelial and medial injury (both physical and functional) during surgical preparation and implantation, resulting in local release of vasoconstrictors, enhanced platelet aggregation, and accumulation of activated clotting factors [4]. Further risks to early patency are imposed by other surgical factors such as anastomosis of the graft to a small native coronary artery with poor distal run-off. Grafts that
Cellular mechanisms
The cellular mechanisms underlying this process are also well established 5, 6. Briefly, medial proliferation of vascular smooth muscle cells (VSMC) soon after graft implantation is followed by their migration through the internal elastic lamina into the intima, where further proliferation is accompanied by sustained extracellular matrix protein synthesis and deposition. Concomitantly, focal intimal accumulations of biologically active oxidised lipids (in particular low density lipoproteins)
Early graft failure
Efforts to reduce early graft failure have focused on the preservation of structural and functional integrity during harvesting and implantation, combined with the subsequent use of antiplatelet or anticoagulant agents. Whereas the efficacy of the latter pharmacological approach has been clearly demonstrated 34, 35, the benefits of measures directed at minimising graft wall injury, such as a `no-touch' technique for graft mobilisation, minimising distension pressure, and selection of storage
Conclusions
Saphenous vein remains an important conduit for coronary revascularisation, and thus efforts to improve understanding of the processes underlying vein graft failure must be maintained. Modifications in vein graft preparation technique and use of antiplatelet therapy have already improved early patency. Greater insight into VSMC proliferation and the influence of atherosclerotic risk factors has offered new avenues of intervention in late graft failure. Pharmacological approaches have been
Discussion
J Wallwork (UK). Professor Angelini, do you think when you were supporting veins with stents, you were inducing the same mechanism that we see naturally in the heart where as soon as an artery becomes intramyocardial it generally becomes less atherosclerotic. Do you think that there is a mechanism which prevents native disease in coronary arteries that you are mimicking in your support system for the veins?
GD Angelini. This is quite possible. Initially, we thought that it was mostly related to
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The influence of hemodynamics on graft patency prediction model based on support vector machine
2020, Journal of BiomechanicsPlatelet function one and three months after coronary bypass surgery in relation to once or twice daily dosing of acetylsalicylic acid
2017, Thrombosis ResearchCitation Excerpt :In successful coronary artery bypass grafting (CABG), the inserted grafts remain patent after the operation. A number of factors may contribute to early thrombotic occlusion of autologous saphenous vein grafts including faulty surgical technique, small caliber target vessels with poor run-off to fibrotic myocardium, inappropriate size and quality of grafts, and perioperative damage to the endothelium of the vein wall which causes platelet activation and interaction of platelets and leukocytes [1,2]. Platelet inhibition with acetylsalicylic acid (ASA) has been used with daily doses ranging from 100 mg to 1500 mg to reduce thrombotic vein graft occlusion after CABG since the early1980s, leading to reductions in the frequency of vein graft occlusion by half [3–7].
Pathology of Saphenous Vein Grafts
2013, Interventional Cardiology ClinicsThe research and preparation of a novel nano biodegradable polymer external reinforcement
2011, Applied Surface ScienceCitation Excerpt :However, after vein grafting, the intimal hyperplasia and luminal stenosis rate is 30–50% [1]. Although patients can be given anticoagulant drugs to improve short-term patency rates postoperatively, the long-term occlusion rate remains greater than 50% [2]. External vascular stents inhibit vein graft restenosis, but still have many shortcomings.