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The use of intracoronary stents has revolutionised percutaneous myocardial revascularisation by reducing the need for urgent surgical intervention and decreasing long term restenosis rates to approximately 15%.1-4 The early use of these devices was complicated by high rates of acute and subacute thrombosis requiring intensive anticoagulation regimens, which were only partially effective at reducing their incidence.5 The importance of the platelet, rather than the coagulation cascade, in the pathogenesis of these complications was confirmed when Schömig et al reported an 82% reduction in myocardial infarctions with a combination of aspirin and ticlopidine compared to heparin, phenprocoumon, and aspirin in patients receiving coronary artery stents.6 Since that time aspirin and ticlopidine have been widely used following stent insertion for four weeks to six months, with reported composite end points of death, myocardial infarction, and revascularisation, of 0–1.9% in the first 30 days.6-8
Ticlopidine
The rationale for combining aspirin and ticlopidine is derived from their different mechanisms of action, which may potentiate one another. Aspirin produces permanent inhibition of the cyclo-oxygenase pathway thus reducing production of thromboxane A2, prostaglandin E2, …