Glycoprotein IIb/IIIa Receptor Blockade in Acute Myocardial Infarction

Abstract

Pharmacologic reperfusion with fibrinolytic therapy remains the principal method of infarct-artery recanalization for patients with acute myocardial infarction (AMI). Its universal availability, ease of administration, and effectiveness have been demonstrated in an impressive array of clinical trials in the last two decades (1–3). Nevertheless, significant limitations and unfulfilled expectations continue to render this therapy less than perfect. Three generations of fibrinolytic agents have not been able to solve three vexing problems: restoration of normal flow [Thrombolysis in Myocardial Infarction (TIMI) grade 3] in the infarct artery is achieved in fewer than half the patients at 60 min from drug administration: one-fourth of those with epicardial reperfusion have impaired microvascular perfusion (4,5); and finally, major bleeding [particularly intracranial hemorrhage (ICH)] remains high and has a major impact on outcome. Three recent megatrials (6–8) comparing the parent tissue plasminogen activator (t-PA) molecule with novel compounds, specifically designed to address some of t-PA’s deficiencies, have failed to demonstrate, in general, superior efficacy (mortality reduction) or safety (ICH reduction). Some progress has been made with respect to major, nonintracranial, hemorrhage (9) and treatment of patients presenting beyond 4 h from symptom onset (8).