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The Myocardial Infarction Triage and Intervention Trial of prehospital versus hospital administration of thrombolytic therapy markedly reduced hospital treatment times, but the 2 groups had similar outcomes. However, patients treated < 70 minutes from symptom onset had better short-term outcomes. The purpose of this study was to determine the long-term influence of very early thrombolytic treatment for acute myocardial infarction. A total of 360 patients were followed for vital status and cardiac-related hospital admissions over a period of 34 +/- 16 months. Patients enrolled in the trial had symptoms for < or = 6 hours, ST-segment elevation on the prehospital electrocardiogram, and no risk factors for serious bleeding. They received aspirin and recombinant tissue plasminogen activator either before or after hospital arrival. Primary end points in this study included long-term survival and survival free of death or readmission to the hospital for angina, myocardial infarction, congestive heart failure, or revascularization. Two-year survival was 89% for prehospital- and 91% for hospital-treated patients (p = 0.46). Event-free survival at 2 years was 56% and 64% for prehospital- and hospital-treated patients, respectively (p = 0.42). In patients treated < 70 minutes from symptom onset, 2-year survival was 98%, and it was 88% for those treated later (p = 0.12). Two-year event-free survival was 65% for patients treated early and 59% for patients treated later (p = 0.80). In this trial, poorer long-term survival was associated with advanced age, history of congestive heart failure, and coronary artery bypass surgery performed before the index hospitalization, but not with time to treatment. [ABSTRACT FROM AUTHOR]

Maximal benefits of coronary reperfusion after acute myocardial infarction (AMI) with ST-segment elevation may be attenuated by neutrophil-mediated reperfusion injury. Inflammatory mediators released from potentially viable myocytes cause activation of neutrophils, which traverse the endothelium and enter the myocardium. This process involves interaction between the neutrophil-expressed CD11/CD18 and endothelial-expressed intercellular adhesion molecule-1 (ICAM-1). Preclinical studies have shown that monoclonal antibodies (MAb) to CD18 can limit infarct size and preserve left ventricular function. We sought to determine the initial clinical safety and tolerability of Hu23F2G (LeukArrest), a humanized MAb to CD11/CD18, in patients with AMI who underwent percutaneous transluminal coronary angioplasty (PTCA). Sixty patients with AMI were randomized to low- (0.3 mg/kg) or high-dose (1.0 mg/kg) Hu23F2G or to placebo immediately before PTCA. We found no clinically significant differences in vital signs, physical examination, laboratory evaluation, or need for subsequent cardiac interventions. In Hu23F2G treatment groups, serum concentration of Hu23F2G increased rapidly to 3,234 +/- 1,298 microg/L (low-dose group) and 15,558 +/- 4409 microg/L (high-dose group) between 5 and 60 minutes, then declined over 72 hours to near-baseline values. Myocardial single-photon emission computed tomographic imaging 120 to 260 hours after PTCA showed no statistically significant differences in final left ventricular defect size. Hu23F2G was well tolerated, with no increase in adverse events, including infections. Thus, Hu23F2G appears safe and well tolerated in patients undergoing PTCA for AMI. [ABSTRACT FROM AUTHOR]