Antithrombotic Therapy in Peripheral Arterial Occlusive Disease: Vein Grafts and Arterial Prostheses
There are similarities and differences in the pathophysiology of thrombotic occlusion of vein grafts and arterial prostheses. Both are subject to early occlusion from technical problems that reduce or disturb blood flow. Antithrombotic therapy might prevent or delay some of these occlusions. Both are also vulnerable to intermediate and late occlusions from neointimal hyperplasia (smooth muscle cell proliferative lesions). However, the sites of neointimal hyperplasia differ for vein grafts and for vascular prostheses. In vein grafts the process can be either diffuse, leading to progressive luminal reduction of the entire graft, or focal, causing isolated stenoses at anastomoses or valve sites. Vascular prostheses, in contrast, are subject to the development of neointimal hyperplasia at anastomoses where the process stems from the adjacent artery. Patency of vein grafts and vascular prostheses is also adversely affected by progressive inflow and outflow atherosclerosis that reduces flow through the conduit.
Despite some studies in experimental animals suggesting that antiplatelet therapy reduces neointimal hyperplasia, there are conflicting reports that show no effect. Furthermore, it is doubtful that antiplatelet therapy prevents neointimal hyperplasia in humans. The progressive narrowing of saphenous vein aortocoronary bypass grafts seen on follow-up angiograms is due to neointimal hyperplasia and is not mitigated by treatment with aspirin and dipyridamole.
The principal difference between thrombotic occlusion of vein bypasses and that of prosthetic bypasses has to do with surface thrombogenicity. Because they are lined with endothelium, vein grafts are inherently less thrombogenic than vascular prostheses that never develop a complete endothelial lining Source buying antibiotics online. Vein grafts may lose variable amounts of their endothelial lining during harvesting and implantation, which may contribute to early occlusion. This suggests the rationale for early antithrombotic therapy that could be discontinued after healing at anastomotic sites and repavement of the graft with endothelium. Arterial prostheses, on the other hand, are highly thrombogenic at the time of implantation and remain so.
Studies with indium-Ill-labeled platelets in humans demonstrate marked uptake of labeled platelets on femoral-popliteal bypass prostheses of Dacron or PTFE, but little or no uptake on vein bypasses in the same position. Treatment with aspirin plus dipyridamole significantly reduces labeled platelet uptake on femoral-popliteal bypass prostheses but has no effect on vein bypasses because of the low baseline level of platelet accumulation. In similar studies, aspirin plus dipyridamole decreased uptake of labeled platelets on aortofem-oral bypass prostheses, but other antiplatelet agents had no effect. Other studies in patients with Dacron aortofemoral bypass prostheses show continued uptake of labeled platelets on these prostheses when studied years after implantation. This points out the difference in healing responses between man and experimental animals that develop an endothelialized neointima that completely covers the luminal surface of large aortic and iliac prostheses within months to years after implantation.