Antithrombotic therapy with intracoronary stenting.

Following the first report of successful intracoronary stenting in humans, there was early enthusiasm for the potential of this technology to prevent occlusion or restenosis following angioplasty. Such enthusiasm however was quickly tempered by concerns regarding early thrombotic stent occlusion and its associated high risk of myocardial infarction or death, following the report of a 24% incidence of stent thrombosis in the first 105 patients receiving the Wallstent.' An almost simultaneous report of the first 226 patients receiving a PalmazSchatz stent showed an 18% rate of stent thrombosis in patients treated with aspirin and dipyridamole, with a dramatic improvement to only 0-6% following the addition of warfarin. As management of thrombotic stent occlusion proved to be consistently associated with a poor outcome, a concerted effort was directed towards its prevention through more aggressive antithrombotic regimens. Despite experimentation with a wide variety of regimens, which included combinations of heparin, urokinase, dextran, warfarin, aspirin, dipyridamole, and sulphinpyrazone, stent thrombosis continued to occur in roughly 4% of patients. Also, these intense antithrombotic protocols contributed to a 10-30% incidence of vascular complications as well as a substantial prolongation of hospital stays. It was not until after successful stent placement was reported using only antiplatelet therapy in conjunction with intravascular ultrasound guidance to assure optimal stent deployment that the trend towards increasing anticoagulation began to reverse.3 Further refinements have now brought us to the point where combined antiplatelet therapy along with high pressure balloon inflations are the standard of care, having produced results that are the basis for the majority of patients receiving stents in many interventional laboratories today.