Introduction

Evidence for the occurrence of coronary thrombosis early after percutaneous coronary interventions in humans was provided by serial angioscopic studies that demonstrated the development of varying degrees of thrombosis in over 90% of cases within 60 min after successful coronary balloon angioplasty. Furthermore, studies on the effectiveness of acute PTCA during unstable angina have indicated not only an increased number of periprocedural complications but a relatively high incidence of restenosis. Based on experimental and clinical evidence, it has been suggested that arterial thrombosis promotes the fibroproliferative response during later restenosis and progression of atherosclerosis. The platelet IIb/IIIa and αv/β3 integrin receptor blocker, abciximab (ReoPro), reduced the need for recurrent clinical revascularization only in the EPIC trial, which enrolled patients with unstable angina (due, in general, to coronary thrombosis). In contrast, the later EPILOG trial in patients without acute coronary thrombosis failed to show a reduction in the need for recurrent revascularization, consistent with a role of early acute thrombosis in the pathogenesis of clinical restenosis. The incidence of periprocedural complications and ‘clinically apparent’ thrombosis after PTCA and stenting is sharply decreased by the administration of antiplatelet regimens, including the platelet IIb/IIIa receptor blockers and aspirin/ticlopidine or plavix. The efficacy of such interventions for the long-term prevention of ‘subclinical’ thrombosis and platelet deposition is uncertain, especially after these agents are withdrawn.