Evidence for a pivotal role of platelets in vascular reocclusion and restenosis

Reocclusion and restenosis continue to be the major clinical complications following emergency and elective coronary interventions. Reocclusion ultimately occurs in more than 25% of patients after successful thrombolysis for acute myocardial infarction [l] and may have major adverse consequences, ranging from mortality to compromised cardiac function. After percutaneous transluminal coronary angioplasty (PTCA), the risk associated with acute occlusion leading to myocardial infarction, emergency repeat PTCA, or coronary bypass surgery, may occur in up to 8% of patients [2]. Even more frequent and to date resistant to therapy is the possibility of restenosis, which occurs in 30-40% of patients after PTCA and requires an additional percutaneous intervention or bypass operation within the following year. Substantial evidence directly implicates platelets in reocclusion and restenosis. In fact, current clinical data suggest that platelets represent the most beneficial therapeutic target to reduce the risk of reocclusion and restenosis. In line with this “controversy series” thrombin is being considered the alternative to platelets in the pathogenesis of vascular reocclusion and restenosis. By virtue of its capacity to mediate fibrin formation, platelet activation and cellular migration and proliferation, thrombin undoubtedly is an important player in reocclusion and restenosis. Nevertheless, thrombin inhibitors have yet to match the dramatic effects of platelet antagonists in patients.