Intravenous Beta Blocker Therapy for Acute Myocardial Infarction
It has been known since 1959 (1) that blood levels of epinephrine and norepinephrine are raised after myocardial infarction and that the extent of the rise parallels the severity of infarction. Although it is likely that large infarcts cause high catecholamine levels rather than high catecholamine levels causing large infarcts, most cardiologists have thought that stimulation of the heart by epinephrine and norepinephrine must be harmful by increasing myocardial oxygen uptake or by causing life-threatening arrhythmias. When beta blockade with propranolol became available in the early 1960s and was shown to be effective for the treatment of angina pectoris, a number of trials were done comparing propranolol given orally in a dose of 10–20 mg 4 times daily with conventional treatment for acute myocardial infarction. Although initial results were conflicting, evidence suggested that hospital mortality and morbidity from infarction were not affected by oral administration of the beta blocker. By today’s standards, however, these trials were too small to avoid the Type 2 error, treatment was started too late for any beneficial effects on infarct size, and the first pass effect of hepatic metabolism (which prevents a therapeutic blood level being achieved after a first oral dose), was ignored. At this time, it was considered that intravenous administration of a beta blocker during developing infarction was potentially dangerous by causing excessive cardiac depression, so no trials using intravenous administration were attempted.
KeywordsPlacebo Catheter Ischemia Norepinephrine Epinephrine
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