Effects of intravenous amiodarone on ventricular refractoriness, intraventricular conduction, and ventricular tachycardia induction

Abstract

Aims Intravenous amiodarone has recently emerged as an important drug for the acute treatment of ventricular tachyarrhythmias. However, electrophysiological actions and the efficacy of the drug in the suppression of ventricular tachycardia inducibility have not yet been fully established. The present study was designed to address these issues. Methods and Results The study group consisted of 18 patients (all males, mean age 75±14 years), who underwent electrophysiological study due to a history of sustained ventricular tachyarrhythmia or syncope with non-sustained ventricular tachycardia detected on ambulatory ECG monitoring. The effects of 5mg.kg-1or 10mg.kg-1of intravenous amiodarone on (1) ventricular refractoriness (QTc interval, right ventricular effective refractory period and monophasic action potential duration), (2) intraventricular conduction (paced-QRS and signal-averaged QRS duration), and (3) ventricular tachycardia inducibility, were examined. The drug had no significant effect on ventricular refractoriness. However, a relatively small but significant slowing of intraventricular conduction was seen (paced-QRS duration: 182±27ms vs 191±28ms, P< 0·0007; 183±32ms vs 195±33ms, P< 0·0007; and 177±21ms vs 192±24ms, P< 0·003, at the cycle lengths of 600, 500 and 400ms, respectively). This effect was more evident during extrasystolic beats than during stable pacing (for example, at the cycle length of 600ms, the magnitude of amiodarone-induced lengthening of QRS duration was 23·9±17·6ms vs 9·7±7·2ms, P< 0·009, respectively). Intravenous amiodarone did not prevent induction of sustained ventricular tachycardia in any of five patients inducible at baseline. Of six patients with non-sustained ventricular tachycardia, five had sustained ventricular tachycardia or fibrillation induced after amiodarone infusion. Conclusion Intravenous amiodarone does not prolong ventricular refractoriness, slows intraventricular conduction and may facilitate inducibility of sustained ventricular arrhythmias. © 2000 The European Society of Cardiology.