Literature DB >> 19084812

Role of late sodium current in modulating the proarrhythmic and antiarrhythmic effects of quinidine.

Lin Wu1, Donglin Guo, Hong Li, James Hackett, Gan-Xin Yan, Zhen Jiao, Charles Antzelevitch, John C Shryock, Luiz Belardinelli.   

Abstract

BACKGROUND: Quinidine is used to treat atrial fibrillation and ventricular arrhythmias. However, at low concentrations, it can induce torsade de pointes (TdP).
OBJECTIVE: The purpose of this study was to examine the role of late sodium current (I(Na)) as a modulator of the arrhythmogenicity of quinidine in female rabbit isolated hearts and cardiomyocytes.
METHODS: Epicardial and endocardial monophasic action potentials (MAPs), ECG signals, and ion channel currents were measured. The sea anemone toxin ATX-II was used to increase late I(Na).
RESULTS: Quinidine had concentration-dependent and often biphasic effects on measures of arrhythmogenicity. Quinidine increased the duration of epicardial MAP (MAPD(90)), QT interval, transmural dispersion of repolarization (TDR), and ventricular effective refractory period. Beat-to-beat variability of MAPD(90) (BVR), the interval from peak to end of the T wave (Tpeak-Tend) and index of Tpeak-Tend/QT interval were greater at 0.1 to 3 micromol/L than at 10-30 micromol/L quinidine. In the presence of 1 nmol/L ATX-II, quinidine caused significantly greater concentration-dependent and biphasic changes of Tpeak-Tend, TDR, BVR, and index of Tpeak-Tend/QT interval. Quinidine (1 micromol/L) induced TdP in 2 and 13 of 14 hearts in the absence and presence of ATX-II, respectively. Increases of BVR, index of Tpeak-Tend/QT interval, and Tpeak-Tend were associated with quinidine-induced TdP. Quinidine inhibited I(Kr), peak I(Na), and late I(Na) with IC(50)s of 4.5 +/- 0.3 micromol/L, 11.0 +/- 0.7 micromol/L, and 12.0 +/- 0.7 micromol/L.
CONCLUSION: Quinidine had biphasic proarrhythmic effects in the presence of ATX-II, suggesting that late I(Na) is a modulator of the arrhythmogenicity of quinidine. Enhancement of late I(Na) increased proarrhythmia caused by low but not high concentrations of quinidine.

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Year:  2008        PMID: 19084812      PMCID: PMC2669543          DOI: 10.1016/j.hrthm.2008.09.008

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


  29 in total

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Authors:  W M Jackman; K J Friday; J L Anderson; E M Aliot; M Clark; R Lazzara
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2.  Effects of quinidine on action potentials and ionic currents in isolated canine ventricular myocytes.

Authors:  J J Salata; J A Wasserstrom
Journal:  Circ Res       Date:  1988-02       Impact factor: 17.367

Review 3.  Electrophysiologic mechanisms of the long QT interval syndromes and torsade de pointes.

Authors:  H L Tan; C J Hou; M R Lauer; R J Sung
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Authors:  R Lazzara
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5.  Torsade de pointes due to quinidine: observations in 31 patients.

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6.  Hydroquinidine therapy in Brugada syndrome.

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10.  Incidence and clinical features of the quinidine-associated long QT syndrome: implications for patient care.

Authors:  D M Roden; R L Woosley; R K Primm
Journal:  Am Heart J       Date:  1986-06       Impact factor: 4.749

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2.  In silico assessment of drug safety in human heart applied to late sodium current blockers.

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Review 4.  Late sodium current associated cardiac electrophysiological and mechanical dysfunction.

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Review 6.  Minimizing repolarization-related proarrhythmic risk in drug development and clinical practice.

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Review 7.  The role of late I Na in development of cardiac arrhythmias.

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Review 9.  Arrhythmic risk biomarkers for the assessment of drug cardiotoxicity: from experiments to computer simulations.

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10.  Simulation and mechanistic investigation of the arrhythmogenic role of the late sodium current in human heart failure.

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