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)