Effects of quinidine on ventricular repolarization

The possibility that an asynchronous increase in the ventricularmonophasic action potential duration is the basis of the quinidine-inducedtorsade de pointes, has led us to study the electrophysiologicaleffects of increasing doses of intravenous quinidine. We measuredthe monophasic action potential duration and the ventriculareffective refractory period at several right ventricular myocardialsites in the anaesthetized dog.Our results showed that quinidineinduces a dose-dependent prolongation in ventricular effectiverefractory period and in ventricular monophasic action potentialduration. These increases were uniform throughout the rightventricle. No variations in repolarization or in refractorinesswere observed between the four ventricular sites studied.Theresults suggest that quinidine does not have a direct effecton dispersion of repolarization, and that mechanisms other thanits direct electrophysiological action are involved in the developmentof torsade de pointes.