EFFECTS OF DISOPYRAMIDE PHOSPHATE ON VENTRICULAR ARRHYTHMIAS IN EXPERIMENTAL MYOCARDIAL-INFARCTION

Abstract

A myocardial infarction model [dog] in which infarction is the result of an occluding thrombus was used to evaluate the effectiveness of disopyramide phosphate (DP) in abolishing postinfarction ventricular arrhythmias. Two types of ventricular arrhythmias were observed, rapid multifocal arrhythmias and slow unifocal rhythms. DP, 5 mg/kg, was effective in abolishing the rapid multifocal rhythms. Lower doses, 1 and 3 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 1 min whereas abolition of the rapid ventricular tachycardia took 5-10 min. 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 per 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 per min. The hypotensive effect was always transient at doses of 5 mg/kg or less. DP produced significant changes in the lead II ECG. 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. The changes observed were never more than 20%.