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Frequency‐Dependent Electrophysiologic Effects of d,1‐Sotalol and Quinidine and Modulation by Beta‐Adrenergic Stimulation
Author(s) -
SAGER PHILIP T.,
BEHBOODIKHAH MAHNAZ
Publication year - 1996
Publication title -
journal of cardiovascular electrophysiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.193
H-Index - 138
eISSN - 1540-8167
pISSN - 1045-3873
DOI - 10.1111/j.1540-8167.1996.tb00505.x
Subject(s) - sotalol , quinidine , medicine , repolarization , stimulation , effective refractory period , antiarrhythmic agent , refractory period , cardiology , endocrinology , anesthesia , electrophysiology , heart disease , atrial fibrillation
Frequency‐Dependent Effects of Sotalol and Quinidine. 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,I‐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,I‐sotalol. The monophasic APD 90 and RVKRP 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 APD 90 and RVERP, sotalol‐induced APD 90 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,I‐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,I‐sotalol 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.