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Updated: Jun 22, 2026
08:28
Methods for ECG Evaluation of Indicators of Cardiac Risk, and Susceptibility to Aconitine-induced Arrhythmias in Rats Following Status Epilepticus
Published on: April 5, 2011
Effects of quinidine on ventricular repolarization
J Brugada1, A Sassine, D Escande
1Laboratoire de Physiologie I, Institut de Biologie, Montpellier, France.
European Heart Journal
|December 1, 1987
Summary
Quinidine prolongs ventricular effective refractory period and monophasic action potential duration uniformly in dogs. This suggests quinidine
Area of Science:
- Cardiovascular Electrophysiology
- Pharmacology
Background:
- Torsade de pointes (TdP) is a polymorphic ventricular tachycardia associated with drug-induced QT prolongation.
- Quinidine is known to cause TdP, but the precise electrophysiological mechanisms remain debated.
- The role of dispersion of repolarization in quinidine-induced TdP is a key area of investigation.
Purpose of the Study:
- To investigate the electrophysiological effects of increasing intravenous quinidine doses on ventricular repolarization and refractoriness.
- To determine if quinidine causes non-uniform changes in ventricular electrophysiology that could explain TdP.
- To assess the direct impact of quinidine on dispersion of repolarization.
Main Methods:
- Electrophysiological measurements in anesthetized dogs.
- In vivo assessment of monophasic action potential duration (MAPD).
- Measurement of ventricular effective refractory period (VERP) at multiple myocardial sites.
Main Results:
- Quinidine induced a dose-dependent prolongation of both VERP and MAPD.
- These electrophysiological effects were uniform across all studied right ventricular myocardial sites.
- No significant variations in repolarization or refractoriness were observed between different ventricular locations.
Conclusions:
- Quinidine's direct electrophysiological actions do not appear to cause dispersion of repolarization.
- The findings suggest that mechanisms other than direct electrophysiological effects are responsible for quinidine-induced TdP.
- Further research is needed to elucidate the non-electrophysiological factors contributing to TdP.
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