Journal Article

P.3. Basic Science, Sudden Death Risk Stratification and Ventricular Arrhythmias

H.R. Lu, E. Vlaminckx and D.J. Gallacher

in EP Europace

Published on behalf of European Heart Rhythm Association of the European Society of Cardiology (ESC)

Volume 7, issue s3, pages S46-S46
Published in print October 2005 | ISSN: 1099-5129
Published online October 2005 | e-ISSN: 1532-2092 | DOI:
P.3. Basic Science, Sudden Death Risk Stratification and Ventricular Arrhythmias

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Early afterdepolarizations (eads) has been proposed as mechanism responsible for torsades te pointes in drug-induced long QT. Eads may be facilitated by Ca2+/calmodulin-dependent protein kinase II (cam kinase).

Methods and Results

In the present study, we investigated possible suppression of sparfloxacin-induced eads in isolated rabbit Purkinje fibers with a calmodulin antagonist W-7. In sparfloaxcin-perfused preparations at 1 x 10−4 M, eads were inducible in 8 out of the 10 preparations at 0.2 Hz. The induction of eads by sparfloaxcin was associated with large prolongation of the duration of the action potential (APD) and increase in the triangulation of the action potential. Cam kinase blockade with the calmodulin antagonist W-7 inhibited sprafloxacin-induced eads in a concentration-dependent manner (3 of 10, 1of 10 and 0 of 8 inducible at 0.5 μmol, 5 μmol and 50 μmol, respectively; p < 0.05). W-7 inhibited eads at without 0.5 μ Mol or 5 μmol shortening APD and reduction of Vmax.


The present findings support the hypothesis that cam kinase is a proarrhythmic signaling molecule and demonstrates that eads are facilitated by cam kinase in drug-induced long QT in rabbit in vitro.

Journal Article.  0 words. 

Subjects: Cardiovascular Medicine

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