STEPHEN E. EPSTEIN, M.D.; ROBERT E. GOLDSTEIN, M.D.; DAVID R. REDWOOD, M.D.; KENNETH M. KENT, M.D.; ELDON R. SMITH, M.D.
Most deaths from acute myocardial infarction occur before arrival of medical aid: the terminal mechanism appears to be ventricular fibrillation. Circumstantial evidence suggests that sinus bradycardia, commonly observed during the prehospital phase of acute myocardial infarction, predisposes to ventricular fibrillation and thereby contributes importantly to early death. It was found, however, that moderately severe bradycardia accompanying experimental acute myocardial infarction did not predispose to serious ventricular arrhythmias. Moreover, the frequency of serious arrhythmia increased when either spontaneous or postatropine heart rate was above 80. Explanations for these findings are that decreasing heart rate during acute myocardial infarction reduces ischemic injury and increases electrical stability of the myocardium and that vagal stimulation per se increases electrical stability. On the other hand, nitroglycerin exerted marked beneficial effects on ischemic injury and electrical stability. The clinical implications of these findings on pharmacologic therapy of acute myocardial infarction are presented.
EPSTEIN SE, GOLDSTEIN RE, REDWOOD DR, et al. The Early Phase of Acute Myocardial Infarction: Pharmacologic Aspects of Therapy. Ann Intern Med. 1973;78:918–936. doi: https://doi.org/10.7326/0003-4819-78-6-918
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Published: Ann Intern Med. 1973;78(6):918-936.
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