Abstract
Acute ventricular arrhythmias in myocardial infarction are thought to be dependent, at least in part, on the activity of the adrenergic nervous system. When a heart has its catecholamine stores depleted by prior treatment with reserpine or by cardiac denervation, the incidence of early “malignant” arrhythmias decreases(1). Conversely, intravenous injections of catecholamines produce ventricular arrhythmias in animals with pre-existing myocardial ischemia but not in those without(2). The purpose of this paper is to examine the principles relating catecholamine adrenergic activity to the development of ventricular arrhythmias.
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