title: Antagonism of quinidine's electrophysiologic effects by epinephrine in patients with ventricular tachycardia.
abstract: The purpose of this study was to determine whether pharmacologically induced elevations in the plasma epinephrine concentration within reported physiologic limits alter the response to quinidine during electropharmacologic testing. Twenty-one patients with coronary artery disease and a history of unimorphic ventricular tachycardia were found to have inducible sustained unimorphic ventricular tachycardia that was suppressed by treatment with oral quinidine gluconate. Epinephrine was then infused at a rate of either 25 or 50 ng/kg per min and testing was repeated. These infusion rates of epinephrine were previously demonstrated to result in elevations of the plasma epinephrine concentration in the range of concentrations that occur during a variety of stresses. Quinidine significantly lengthened the ventricular refractory periods and the QRS duration at a ventricular pacing cycle length of 350 ms, which was used as an index of intraventricular conduction. Epinephrine partially or completely reversed the effects of quinidine on ventricular refractory periods, but had no effect on QRS duration. During electropharmacologic testing of quinidine, no ventricular tachycardia was inducible in 12 patients, and only nonsustained ventricular tachycardia, 8 to 48 beats in duration, was inducible in 9 patients. Retesting during infusion of epinephrine demonstrated inducible sustained unimorphic ventricular tachycardia in 2 of the 12 patients in whom quinidine had completely suppressed the induction of ventricular tachycardia and in 8 of the 9 patients in whom only nonsustained ventricular tachycardia had been inducible during testing of quinidine. In conclusion, physiologic elevations in the plasma epinephrine concentration may reverse quinidine-induced prolongation of ventricular refractoriness but not intraventricular conduction.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor.
authors.forename: F
authors.initials: F
authors.lastname: Morady
authors.forename: W H
authors.initials: WH
authors.lastname: Kou
authors.forename: A H
authors.initials: AH
authors.lastname: Kadish
authors.forename: S D
authors.initials: SD
authors.lastname: Nelson
authors.forename: L K
authors.initials: LK
authors.lastname: Toivonen
authors.forename: J A
authors.initials: JA
authors.lastname: Kushner
authors.forename: S
authors.initials: S
authors.lastname: Schmaltz
authors.forename: M
authors.initials: M
authors.lastname: de Buitleir
mesh_terms: D000368:Aged; D001794:Blood Pressure / Q000187:drug effects; D002304:Cardiac Pacing, Artificial; D004562:Electrocardiography; D004837:Epinephrine / Q000008:administration & dosage / Q000097:blood / Q000494:pharmacology*; D005260:Female; D006339:Heart Rate / Q000187:drug effects; D006352:Heart Ventricles; D006801:Humans; D008297:Male; D008875:Middle Aged; D011802:Quinidine / Q000008:administration & dosage / Q000037:antagonists & inhibitors* / Q000097:blood / Q000494:pharmacology; D013610:Tachycardia / Q000097:blood / Q000188:drug therapy / Q000503:physiopathology*
chemical_list: D011802:Quinidine; D004837:Epinephrine