Propranolol-induced reduction of signs of ischemic injury during acute myocardial infarction.

The effect of intravenous administration of propranolol (3 to 10 mg) was studied in 12 patients with acute anterior transmural myocardial infarction within the first 8 hours from the onset of pain. Criteria for inclusion in the study were persistence of ischemic pain, S-T segment elevation of 0.3 or more mg in at least two standard precordial leads, heart rate of 80 or more beats/min, mean arterial pressure of 75 or more mm Hg and cardiac index of 2.5 or more liters/min per m2. Within 30 minutes of administration of propranolol, the sum of S-T segment elevations from leads V1 through V6 (sigmaST6) and the average S-T segment elevation over the left precordium recorded from multiple unipolar leads (ST) decreased significantly by 40 and 39%, respectively. At the same time, there was a significant reduction in heart rate (from 100+/-3 [standard error of the mean] to 79+/-4 beats/min), mean arterial pressure (from 112+/-6 to 95+/-5 mm Hg) and cardiac output (from 6.1+/-0.3 to 4.1+/-0.3 liters/min). Pulmonary capillary wedge pressure remained unaltered. Four hours later the hemodynamic variables had returned to control level, but the beneficial effect on myocardial injury persisted. These electrocardiographic changes were accompanied by resolution of ischemic pain and cessation of ventricular arrhythmias. The effects of propranolol were more pronounced in patients with angiographically demonstrable flow to the affected area of myocardium. Thus, administration of propranolol in the early hours of myocardial infarction can significantly reduce the signs of myocardial ischemic injury without excessively depressing myocardial function.