Supported by Grant Za 210/1-1 from the Deutsche Forschungsge-meinschaft, Bonn, Germany.
Electrophysiologic Features of Torsades de Pointes:
Insights from a New Isolated Rabbit Heart Model
Article first published online: 20 APR 2007
Journal of Cardiovascular Electrophysiology
Volume 8, Issue 10, pages 1148–1158, October 1997
How to Cite
ZABEL, M., HOHNLOSER, S. H., BEHRENS, S., LI, Y.-G., WOOSLEY, R. L. and FRANZ, M. R. (1997), Electrophysiologic Features of Torsades de Pointes:. Journal of Cardiovascular Electrophysiology, 8: 1148–1158. doi: 10.1111/j.1540-8167.1997.tb01001.x
Part of the results were reported in abstract form at the 69th Scientific Sessions of the American Heart Association, New Orleans, Louisiana, November 10–13, 1996.
- Issue published online: 20 APR 2007
- Article first published online: 20 APR 2007
- Manuscript received 27 March 1997; Accepted for publication 16 July 1997
- ventricular action potential;
- torsades de pointes;
- dispersion of repolarization
Torsades de Pointes in the Isolated Rabbit Heart. Introduction: The exact electrophysiologic mechanism of torsades de pointes (TdP) is under intense investigation. No isolated animal heart model of this particular arrhythmia exists.
Methods and Results: In isolated rabbit hearts, TdP was induced by means of bradyeardia in the presence of a high concentration of d-sotalol (10−4 M) and shortly after lowering the concentration of potassium and magnesium in the perfusate. Multiple simultaneous epicardial and endocardial monophasic action potentials (MAPs) and volume-conducted 12-lead ECGs were recorded. d-Sotalol prolonged repolarization and increased dispersion of ventricular repolarization compared to baseline recordings. With the onset of low potassium and magnesium concentrations, repolarization was further prolonged and dispersion of repolarization was further increased followed by the occurrence of early afterdepolariZations (EADs) in the majority of MAP recordings, i.e., at both endocardial and epicardial locations of both ventricles, upon increase of EAD amplitude, triggered arrhythmias with TdP of up to 42 heats ensued in 10 of 11 hearts studied. MAP duration at 90% repolarization (APD90), dispersion of APD90, and the incidence of EADs as well as dispersion of the QT interval and T wave area were significantly higher in heats triggering higemini, couplets, or runs of TdP.
Conclusion: TdP observed in this new isolated heart model was associated with markedly increased dispersion of ventricular repolarization and the occurrence of EADs in multiple locations of the heart. TdP is initiated when the amplitude of an EAD reaches threshold for initiation of the first beat of an episode.