Literature DB >> 17467634

Cellular basis for the electrocardiographic and arrhythmic manifestations of Timothy syndrome: effects of ranolazine.

Serge Sicouri1, Katherine W Timothy, Andrew C Zygmunt, Aaron Glass, Robert J Goodrow, Luiz Belardinelli, Charles Antzelevitch.   

Abstract

BACKGROUND: Timothy syndrome is a multisystem disorder associated with QT interval prolongation and ventricular cardiac arrhythmias. The syndrome has been linked to mutations in Ca(V)1.2 resulting in gain of function of the L-type calcium current (I(Ca,L)). Ranolazine is an antianginal agent shown to exert an antiarrhythmic effect in experimental models of long QT syndrome.
OBJECTIVE: The purpose of this study was to develop and characterize an experimental model of Timothy syndrome by using BayK8644 to mimic the gain of function of I(Ca,L) and to examine the effects of ranolazine.
METHODS: Action potentials from epicardial and M regions and a pseudo-electrocardiogram (ECG) were simultaneously recorded from coronary-perfused left ventricular wedge preparations, before and after addition of BayK8644 (1 microM).
RESULTS: BayK8644 preferentially prolonged action potential duration of the M cell, leading to prolongation of the QT interval and an increase in transmural dispersion of repolarization (from 44.3 +/- 7 ms to 86.5 +/- 25 ms). Stimulation at cycle lengths of 250-500 ms led to ST-T wave alternans due to alternation of the plateau voltage of the M cell action potential as well as development of delayed afterdepolarizations in epicardial and M cell action potentials. Ventricular extrasystoles and tachycardia (monomorphic, bidirectional, or torsades de pointes) developed spontaneously or after rapid pacing. Peak and late I(Na) were unaffected by BayK8644. Clinically relevant concentrations of ranolazine (10 microM) suppressed all actions of BayK8644.
CONCLUSION: A left ventricular wedge model of long QT syndrome created by augmentation of I(Ca,L) recapitulates the ECG and arrhythmic manifestations of Timothy syndrome, which can be suppressed by ranolazine.

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Year:  2007        PMID: 17467634      PMCID: PMC1951535          DOI: 10.1016/j.hrthm.2006.12.046

Source DB:  PubMed          Journal:  Heart Rhythm        ISSN: 1547-5271            Impact factor:   6.343


  36 in total

1.  A subpopulation of cells with unique electrophysiological properties in the deep subepicardium of the canine ventricle. The M cell.

Authors:  S Sicouri; C Antzelevitch
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2.  Effects of dihydropyridine calcium channel modulators on cardiac sodium channels.

Authors:  A Yatani; D L Kunze; A M Brown
Journal:  Am J Physiol       Date:  1988-01

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4.  Antagonism by ranolazine of the pro-arrhythmic effects of increasing late INa in guinea pig ventricular myocytes.

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5.  Ca(V)1.2 calcium channel dysfunction causes a multisystem disorder including arrhythmia and autism.

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Review 7.  Electrophysiologic properties and antiarrhythmic actions of a novel antianginal agent.

Authors:  Charles Antzelevitch; Luiz Belardinelli; Lin Wu; Heather Fraser; Andrew C Zygmunt; Alexander Burashnikov; José M Di Diego; Jeffrey M Fish; Jonathan M Cordeiro; Robert J Goodrow; Fabiana Scornik; Guillermo Perez
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8.  Anti-ischemic effects and long-term survival during ranolazine monotherapy in patients with chronic severe angina.

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9.  Efficacy of permanent pacing in the management of high-risk patients with long QT syndrome.

Authors:  A J Moss; J E Liu; S Gottlieb; E H Locati; P J Schwartz; J L Robinson
Journal:  Circulation       Date:  1991-10       Impact factor: 29.690

10.  Electrophysiological effects of ranolazine, a novel antianginal agent with antiarrhythmic properties.

Authors:  Charles Antzelevitch; Luiz Belardinelli; Andrew C Zygmunt; Alexander Burashnikov; José M Di Diego; Jeffrey M Fish; Jonathan M Cordeiro; George Thomas
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  36 in total

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5.  Dysfunctional Cav1.2 channel in Timothy syndrome, from cell to bedside.

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6.  The Timothy syndrome mutation of cardiac CaV1.2 (L-type) channels: multiple altered gating mechanisms and pharmacological restoration of inactivation.

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7.  Transseptal dispersion of repolarization and its role in the development of Torsade de Pointes arrhythmias.

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Journal:  J Cardiovasc Electrophysiol       Date:  2009-11-10

8.  Synergistic electrophysiologic and antiarrhythmic effects of the combination of ranolazine and chronic amiodarone in canine atria.

Authors:  Serge Sicouri; Alexander Burashnikov; Luiz Belardinelli; Charles Antzelevitch
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9.  Antiarrhythmic effects of the highly selective late sodium channel current blocker GS-458967.

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10.  Molecular endpoints of Ca2+/calmodulin- and voltage-dependent inactivation of Ca(v)1.3 channels.

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