Towards the prevention of vein graft failure

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Abstract

Improved outcome after coronary bypass surgery over the last decade has been attributed largely to the increasing use of arterial conduits and their superior patency rates over that of saphenous vein grafts [1]. In spite of this trend, autologous saphenous vein has remained an important and convenient conduit for a variety of operative scenarios, and is still used for more than 70% of grafts. As a result, vein graft failure continues to represent a significant clinical and economic burden upon the health care service. Between 15 to 30% of saphenous vein grafts occlude within the first year of surgery, increasing to over 50% after 10 years. By this time, more than 10% of patients will require further intervention to alleviate symptoms arising from occluded grafts and progression of native disease [2]. Graft occlusion arises either from early thrombosis or the later onset of `vein graft disease' and subsequent atherosclerotic changes [3].

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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