Abstract |
The possibility that an asynchronous increase in the ventricular monophasic action potential duration is the basis of the quinidine-induced torsade de pointes, has led us to study the electrophysiological effects of increasing doses of intravenous quinidine. We measured the monophasic action potential duration and the ventricular effective refractory period at several right ventricular myocardial sites in the anaesthetized dog. Our results showed that quinidine induces a dose-dependent prolongation in ventricular effective refractory period and in ventricular monophasic action potential duration. These increases were uniform throughout the right ventricle. No variations in repolarization or in refractoriness were observed between the four ventricular sites studied. The results suggest that quinidine does not have a direct effect on dispersion of repolarization, and that mechanisms other than its direct electrophysiological action are involved in the development of torsade de pointes.
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Authors | J Brugada, A Sassine, D Escande, C Masse, P Puech |
Journal | European heart journal
(Eur Heart J)
Vol. 8
Issue 12
Pg. 1340-5
(Dec 1987)
ISSN: 0195-668X [Print] England |
PMID | 3436332
(Publication Type: Journal Article)
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Chemical References |
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Topics |
- Animals
- Dogs
- Dose-Response Relationship, Drug
- Electrocardiography
- Heart Conduction System
(drug effects)
- Heart Rate
(drug effects)
- Heart Ventricles
(drug effects)
- Quinidine
(pharmacology)
- Tachycardia
(chemically induced)
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