Prevention of ventricular fibrillation by dextrorotatory sotalol in a conscious canine model of sudden coronary death.

The antiarrhythmic and antifibrillatory actions of the dextrorotatory isomer of sotalol, administered in a multiple-dose regimen, were evaluated in conscious dogs 3 to 5 days after anterior myocardial infarction. The intravenous administration of d-sotalol, four 8 mg/kg doses over a 24-hour treatment period, suppressed the induction of ventricular tachycardia by programmed electrical stimulation in six of nine dogs tested, slowed the rate of the induced tachyarrhythmia in two of the remaining three dogs, and provided significant protection (5 of 8 d-sotalol vs 0 of 8 vehicle control) against the development of ventricular fibrillation in response to ischemia at a site distant to a previous myocardial infarction. Increases in ventricular myocardial refractoriness and in QTc and paced QT intervals suggest that class III electrophysiologic actions contribute to the antiarrhythmic properties of dextrorotatory sotalol in this animal model. The degree of beta-adrenergic receptor blockade produced by d-sotalol in this dose regimen was negligible. These findings suggest the potential utility of d-sotalol in the prevention of ventricular tachycardia and ventricular fibrillation in the setting of myocardial infarction, particularly when beta-adrenergic receptor blockade is undesirable or contraindicated.