Antiarrhythmic efficacy and electrophysiologic actions of amiodarone in patients with life-threatening ventricular arrhythmias: Potent suppression of spontaneously occurring tachyarrhythmias versus inconsistent abolition of induced ventricular tachycardia (original) (raw)
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Control of sudden recurrent arrhythmic deaths: Role of amiodarone
American Heart Journal, 1983
Patients resuscitated after out-of-hospital cardiac arrest have electrical instability of the myocardium, with 30% to 40% propensity for recurrent arrest in the first year. About 85% to 90% of such patients have complex ventricular ectopy and runs of ventricular tachycardia; in 70% to 80%, ventricular tachycardia or fibrillation are inducible by programmed electrical stimulation. The attempt to control recurrent cardiac arrest using these parameters and conventional antiarrhythmic drugs has yielded conflicting or variable results. Amiodarone was therefore studied in 40 consecutive patients (with previous cardiac arrests) in whom conventional antiarrhythmic therapy had proved ineffective or was not tolerated. The mean ejection fraction of the group was 0.29 +/- 0.12. At a mean follow-up of 16 months (range 5 to 40 months) six patients had died, three from heart failure, one from liver failure (not drug induced), and two from sudden (presumably arrhythmic) death. Late occurrences of arrhythmia were found in two patients (complicated by digitalis intoxication in one). Ambulatory ECG recordings showed that amiodarone had a potent suppressant effect on ventricular ectopy and runs of VT, but electrophysiologic studies demonstrated that it did not inhibit inducible VT/VF in greater than 65% despite an excellent clinical outcome. Limiting adverse reaction was seen in only one patient; other relatively minor side effects occurred in 10% to 15% of patients receiving maintenance therapy. Our data provide further evidence for the effectiveness of amiodarone in life-threatening ventricular arrhythmias, with a potential for the prolongation of survival in patients resuscitated after out-of-hospital cardiac arrests.
Efficacy and safety of intravenous amiodarone in acute refractory arrhythmias
Clinical Cardiology, 1988
Few data are available on intravenous amiodarone therapy in refractory arrhythmias. This retrospective study in 50 patients (14 with supraventricular and 36 with ventricular tachyarrhythmias) revealed a favorable effect of intravenous amiodarone in the treatment of life-threatening arrhythmias with an overall success rate of 76%. In the subgroup of patients with ventricular fibdlation and concomitant severe congestive heart failure success rate was low (25%, 2/8), whereas effectiveness in patients with ventricular tachycardias was high (> 90%) and proved to be independent of left ventricular function. If patients with recurrent ventricular fibrillation were excluded from the analysis, successful treatment with intravenous amiodarone was achieved in 90%, even in those patients with severely compromised myocardium.
Suppression of long-standing incessant ventricular tachycardia by amiodarone
Journal of Electrocardiology, 1980
A 25 year old man had experienced virtually incessant ventricular tachycardia since the age of 16 years, and complained of increasing lethargy and shortness of breath over the past 5 years. Despite medical therapy with numerous conventional antiarrhythmic agents, no single drug or combination of drugs had successfully controlled the tachycardia. Isotope and contrast angiography revealed an enlarged left ventricle with poor function. Electrophysiological studies demonstrated earliest endoeardial activation at the left ventricular apex. No electrical procedure terminated tachycardia. Following institution of amiodarone, continuous ECG monitoring revealed periods of sinus rhythm alternating with periods of ventricular bigeminy. Repeat isotope angiography indicated a considerable improvement in L.V. function. There was a corresponding reduction in heart size on the chest radiograph. Clinical improvement was evidenced by disappearance of lethargy and shortness of breath. This report demonstrates that amiodarone, a new antiarrhythmic agent, may suppress long standing incessant ventricular tachycardia resistant to other antiarrhythmic agents. The marked reduction in heart size on amiodarone may suggest that the associated cardiomegaly is secondary to tachycardia.
Europace, 2000
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 signalaveraged 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.