title: Reversal of antiarrhythmic drug effects by epinephrine: quinidine versus amiodarone.
abstract: Although previous studies have demonstrated that the electrophysiologic effects of many antiarrhythmic agents can be reversed by catecholamines, the susceptibility of amiodarone to such reversal is unknown. The objective of this study was to compare the relative degree of reversal of the electrophysiologic effects of quinidine and amiodarone by epinephrine infusions that result in plasma epinephrine levels similar to those achieved during various physiologic stresses. Twenty-nine patients who had inducible sustained monomorphic ventricular tachycardia and underwent electropharmacologic testing with quinidine and amiodarone were enrolled in the study. The variables measured before and during an epinephrine infusion (25 or 50 ng/kg per min) included the sinus cycle length, mean arterial pressure, QT interval and effective refractory period at drive train cycle lengths of 600 and 400 ms. The effective refractory period measured at a drive train cycle length of 600 ms shortened less during amiodarone therapy (2 +/- 2%) than during quinidine therapy (6 +/- 4%) or than in the baseline state (6 +/- 4%; p less than 0.01). Similar results were obtained during evaluation of the effective refractory period at a cycle length of 400 ms. Epinephrine infusion, at both 25 and 50 ng/kg per min, completely reversed the effects of quinidine and partially reversed the effects of amiodarone on the effective refractory period. The effects of epinephrine on the sinus cycle length and QT interval were similar in the baseline state and in conjunction with quinidine and amiodarone. Twenty-four patients underwent programmed ventricular stimulation during amiodarone therapy alone and in conjunction with either a 25- or a 50-ng/kg per min infusion of epinephrine.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: University of Michigan Medical Center, Department of Internal Medicine, Ann Arbor, Michigan 48109-0022.
authors.forename: H
authors.initials: H
authors.lastname: Calkins
authors.forename: J
authors.initials: J
authors.lastname: Sousa
authors.forename: R
authors.initials: R
authors.lastname: el-Atassi
authors.forename: S
authors.initials: S
authors.lastname: Schmaltz
authors.forename: A
authors.initials: A
authors.lastname: Kadish
authors.forename: F
authors.initials: F
authors.lastname: Morady
mesh_terms: D000638:Amiodarone / Q000037:antagonists & inhibitors* / Q000627:therapeutic use; D002304:Cardiac Pacing, Artificial; D004562:Electrocardiography; D004594:Electrophysiology; D004837:Epinephrine / Q000494:pharmacology*; D005260:Female; D006329:Heart Conduction System / Q000187:drug effects / Q000503:physiopathology; D006801:Humans; D008297:Male; D008875:Middle Aged; D011802:Quinidine / Q000037:antagonists & inhibitors* / Q000627:therapeutic use; D013610:Tachycardia / Q000175:diagnosis / Q000188:drug therapy* / Q000503:physiopathology
chemical_list: D011802:Quinidine; D000638:Amiodarone; D004837:Epinephrine