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The management of acute myocardial infarction (AMI) was altered dramatically with the introduction of intracoronary thrombolytic therapy in the late l970s by Rentrop and others.1 The visualization of coronary artery occlusion by angiography performed during the first few hours of AMI and the removal of some of these thrombi at the time of emergent coronary artery bypass surgery convinced the medical community that AMI was, as was thought years earlier, due to “coronary thrombosis.” After the publication of a number of randomized clinical trials (RCTs) of intracoronary and intravenous lytic therapy, reperfusion of acutely occluded coronary artery beds with thrombolytic therapy became a standard treatment of AMI by the mid-1980s.2 While thrombolytic therapy was gaining early acceptance as a means to achieve reperfusion, a parallel pathway for achieving reperfusion was developing with catheter-based techniques. Reports of PTCA for the management of AMI appeared in 1983.3 Soon a vigorous competition developed between pharmacological and mechanical methods of reperfusion. Important differences between these 2 competing approaches were apparent. Thrombolytic therapy could be initiated rapidly once the diagnosis was made, with treatment instituted in the emergency department or even before hospitalization,4 and it did not require the technical skills of a proceduralist for its implementation. However, because reperfusion did not occur until 60 to 90 minutes after the onset of treatment, the occurrence of successful reperfusion (or its failure) could not be ascertained with certainty by use of clinical markers, and there was an obligatory risk of intracranial hemorrhage (ICH) of 0.5% to 1.0%, with higher rates experienced in elderly patients.5 With PTCA, on the other hand, there was an obligatory delay between diagnosis and initiation of the procedure, and highly skilled procedural cardiologists and technical staff were required to be available 24 hours a day. Because a …

Combined Thrombolytic and Platelet Glycoprotein IIb/IIIa Inhibitor Therapy for Acute Myocardial Infarction