Mechanisms of ventricular arrhythmias associated with myocardial infarction

Abstract

Ventricular ectopic beats may be generated during acute myocardial infarction as the result of enhanced automaticity in the His-Purkinje system, focal reexcitation due to the flow of current between myocardial fibers which are repolarized at disparate times, or reentry of the impulse induced by local impairment of excitability and conductivity in the ventricular tissues. The ectopic beats occur more frequently when the basic ventricular rate is slow, and the danger of fatal episodes of ventricular fibrillation is also increased at slow ventricular rates. Fibrillation is more likely to be induced by early ectopic beats in the ventricle during myocardial infarction, because the development of sustained ectopic activity and turbulent impulse propagation is facilitated by increased inhomogeneity of the ventricular tissues with respect to excitability and conductivity. The aggressive prevention and treatment of ventricular ectopic beats and bradyarrhythmia was emphasized as one of the most effective means of preventing life-threatening ventricular fibrillation and lowering mortality rates from acute myocardial infarction. The mechanisms of action of various drugs and the efficacy of increased ventricular rates in suppressing ectopic activity were discussed. It was concluded that the artificial pacing of the heart at relatively rapid rates is a valuable adjunct to the measures used in the management of ventricular arrhythmias associated with acute myocardial infarction.