The Influence of Thromboxane Receptor Blockade on Platelet Uptake in Dacron Grafts in Man

Human prosthetic vascular grafts do not sustain a growth of endothelium on the luminal surface and remain thrombogenic indefinitely1. Whilst large diameter aortic grafts develop a thin layer of platelet thrombus as pseudointima, smaller prostheses such as those in the femoro-popliteal position have a thrombosis and occlusion rate approaching 60% at 1 year after implantation2. Platelet inhibitory therapy is established in the prevention of thrombosis but the combination of aspirin plus dipyridamole produces frequent gastro-intestinal side effects. This has been shown in the recent Persantin Aspirin Re-infarction Study3 where 25% of patients had to discontinue aspirin therapy. Thromboxane A2 (TXA2) which is a product of aracidonic acid metabolism, is a powerful stimulator of platelet aggregation4. It is produced by enzymes including cyclo-oxygenase and thromboxane synthetase in platelets and the natural biological opponent of TXA2 is prostocyclin (PGI2).