Key result
Intravenous amiodarone slowed intraventricular conduction and did not prevent induction of sustained ventricular tachycardia.
Why the study?
Does intravenous amiodarone improve ventricular refractoriness and prevent ventricular tachycardia induction in patients with a history of ventricular tachyarrhythmias?
Does intravenous amiodarone improve ventricular refractoriness and prevent ventricular tachycardia induction in patients with a history of ventricular tachyarrhythmias?
Intravenous amiodarone slows intraventricular conduction without prolonging ventricular refractoriness and may paradoxically facilitate the induction of sustained ventricular arrhythmias during electrophysiological testing.
Answers are grounded in this paper and cite their sources.
IV amiodarone may slow conduction without preventing VT induction; hypothesis-generating and should not yet change practice.
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 5 mg.kg(-1) or 10 mg.kg(-1) of 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 +/- 27 ms vs 191 +/- 28 ms, P<0.0007; 183 +/- 32 ms vs 195 +/- 33 ms, P<0.0007; and 177 +/- 21 ms vs 192 +/- 24 ms, P<0.003, at the cycle lengths of 600, 500 and 400 ms, respectively). This effect was more evident during extrasystolic beats than during stable pacing (for example, at the cycle length of 600 ms, the magnitude of amiodarone-induced lengthening of QRS duration was 23.9 +/- 17.6 ms vs 9.7 +/- 7.2 ms, 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.
No takes yet. Share an insight, caveat, or question.
Piotr Kułakowski (2000) studied sustained ventricular tachyarrhythmia or syncope with non-sustained ventricular tachycardia (n=18). Intravenous amiodarone vs. baseline was evaluated on ventricular refractoriness, intraventricular conduction, and ventricular tachycardia inducibility (p=<0.0007). Intravenous amiodarone slowed intraventricular conduction and did not prevent induction of sustained ventricular tachycardia.
Synapse has enriched 10 related papers. Consider them for comparative context: