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  • Title: Frequency-dependent electrophysiologic effects of d,l-sotalol and quinidine and modulation by beta-adrenergic stimulation.
    Author: Sager PT, Behboodikhah M.
    Journal: J Cardiovasc Electrophysiol; 1996 Feb; 7(2):102-12. PubMed ID: 8853020.
    Abstract:
    INTRODUCTION: Frequency-dependent electrophysiologic actions of oral quinidine and oral sotalol may be clinically important, but these properties and their modulation by beta-adrenergic sympathetic stimulation have not been determined. METHODS AND RESULTS: The frequency-dependent effects of oral quinidine (n = 17) and oral d,l-sotalol (n = 17) were determined at: (1) drug-free baseline; (2) during steady-state drug dosing; and (3) during isoproterenol infusion to patients receiving quinidine or d,l-sotalol. The monophasic APD90 and RVERP were prolonged 12% to 17% (P < 0.001) during pharmacologic therapy, and frequency-dependent effects were only observed for the RVERP during sotalol. In both drug groups, isoproterenol significantly reduced the sinus cycle length and reduced the RVERP to a greater extent at longer than at shorter paced cycle lengths. While isoproterenol fully reversed quinidine's effects on the APD90 and RVERP, sotalol-induced APD90 prolongation was reduced by only 2% to 4%, and the RVERP was unaffected. Isoproterenol attenuated the frequency-dependent effects of quinidine on QRS duration by a relatively fixed amount of 7% to 10%. Isoproterenol fully reversed quinidine-induced, but did not affect sotalol-induced prolongation in the sustained VT cycle length. CONCLUSIONS: (1) Over the range of examined cycle lengths, oral quinidine and d,l-sotalol did not exert frequency-dependent effects on ventricular repolarization. (2) Isoproterenol fully reversed quinidine's effects on refractoriness, repolarization, and prolongation of VT cycle length, whereas d,l-sotalol's effects were largely preserved, despite significant reductions in sinus cycle length. (3) These results suggest that beta-blockade is important in preventing reversal of antiarrhythmic drug effects by augmented sympathetic nervous system tone.
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