Effects of disopyramide phosphate on ventricular arrhythmias in experimental myocardial infarction.

A myocardial infarction model in which infarction is the result of an occluding thrombus was used to evaluate the effectiveness of disopyramide phosphate (DP) in abolishing postinfarction ventricular arrhythmis. Two types of ventricular arrhythmias were observed, rapid multifocal arrhythmias. and slow unifocal rhythms. DP, in doses of 5 mg/kg, were effective against slow ventricular tachycardia. The time course of action varied with the type of rhythm present. Conversion of the slow ventricular tachycardia usually occurred within a minute whereas abolition of the rapid ventricular tachycardia took 5 to 10 minutes. Effective arrhythmia control could be maintained by a bolus dose (3 mg/kg) followed by a constant infusion at a rate of 0.2 mg/kg/min. DP had minimal effects on arterial blood pressure at antiarrhythmic doses. The drug had significant hypotensive effects if infused at rates greater than 2 mg/kg/min. However, the hypotensive effect was always transient at doses of 5 mg/kg or less. DP produced significant changes in the lead II electrocardiogram. At doses of 5 mg/kg, the drug significantly increased the P-R and Q-Tc intervals and increased the QRS duration. The drug slowed conduction through all parts of the conducting system to approximately the same degree with perhaps a slightly greater slowing through the atrioventricular node. However, the changes observed were never more than 20%