Combining a class I antiarrhythmic agent with amiodarone prevented the induction of sustained ventricular tachycardia in only 3% of patients, but rendered the tachycardia hemodynamically stable in 34%.
Cohort (n=31)
Does the combination of amiodarone and class I antiarrhythmic agents prevent the induction of sustained ventricular tachycardia or improve hemodynamic stability in patients with inducible, sustained ventricular tachycardia?
Combining amiodarone with class I antiarrhythmic agents rarely suppresses inducible ventricular tachycardia but often prolongs the tachycardia cycle length, potentially improving hemodynamic stability.
BACKGROUND: Clinical experience suggests that combinations of antiarrhythmic agents provide more effective control of ventricular tachyarrhythmias than does therapy with single agents. METHODS AND RESULTS: Antiarrhythmic and electrophysiological effects of three class I antiarrhythmic agents, one from each subclass A, B, and C, were assessed in single use and in combination with amiodarone in patients with inducible, sustained ventricular tachycardia that was not suppressed by monotherapy with these agents. Thirty-one patients underwent an electrophysiology test on four occasions: at baseline; after 2-4 days of treatment with quinidine, mexiletine, or encainide; after 2 weeks of treatment with 1,200 mg/day amiodarone; and last, after 2-4 days of treatment with both amiodarone and the previously tested class I agent. The combination of a class I agent and amiodarone prevented the induction of sustained ventricular tachycardia in only one of 31 (3%) patients. Ventricular tachycardia became hemodynamically stable in 11 of 31 (34%) patients because of a marked prolongation in the tachycardia cycle length. It increased from 323 +/- 39 to 423 +/- 84 msec (n = 11, p less than 0.01) by adding encainide to amiodarone therapy, and it showed a tendency to lengthen when quinidine was added to amiodarone (from 373 +/- 77 to 425 +/- 58 msec; n = 10, NS). Each class I agent increased amiodarone-induced depression in myocardial conduction, but the extent of the additional depression seemed to differ among the three subclasses. Ventricular refractoriness was increased by all class I agents when used in combination with amiodarone, although not by mexiletine or encainide when used alone. CONCLUSIONS: Class I antiarrhythmic agents slow ventricular conduction and increase ventricular refractoriness when used in combination with amiodarone. When amiodarone and class I drugs by themselves do not suppress the induction of ventricular tachycardia, the combination of amiodarone and a class I agent seldom results in noninducibility; however, it often lengthens the ventricular tachycardia cycle length and may render the ventricular tachycardia hemodynamically stable.
Toivonen et al. (Mon,) conducted a cohort in Inducible, sustained ventricular tachycardia (n=31). Combination of class I antiarrhythmic agents (quinidine, mexiletine, or encainide) and amiodarone vs. Baseline, class I agent alone, and amiodarone alone was evaluated on Prevention of induction of sustained ventricular tachycardia. Combining a class I antiarrhythmic agent with amiodarone prevented the induction of sustained ventricular tachycardia in only 3% of patients, but rendered the tachycardia hemodynamically stable in 34%.