Sodium Current and Arrhythmogenesis in Heart Failure

Luis Fernando Santana; Harol Núñez-Durán; Keith W. Dilly; W. Jonathan Lederer

doi:10.1016/j.hfc.2005.06.003

Sodium Current and Arrhythmogenesis in Heart Failure

Luis Fernando Santana, Harol Núñez-Durán, Keith W. Dilly, W. Jonathan Lederer

Research output: Contribution to journal › Review article

9 Scopus citations

Abstract

The low sodium arrhythmic mechanism hypothesis is demonstrated in normal cells with unmodified sodium (Na⁺) and calcium (Ca²⁺) channels, in long QT syndrome models, and in heart failure model systems. The authors propose that the changes in Ca²⁺ influx during the early part of the action potential and during the plateau and repolarization phases of the action potential sum to influence contractility and arrhythmogenesis. The importance of both of these changes is supported by their present work, which suggests that antiarrhythmic agents should be examined for their actions on low sodium arrhythmic mechanism and action potential duration.

Original language	English (US)
Pages (from-to)	193-205
Number of pages	13
Journal	Heart Failure Clinics
Volume	1
Issue number	2
DOIs	https://doi.org/10.1016/j.hfc.2005.06.003
State	Published - Jul 2005
Externally published	Yes

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ASJC Scopus subject areas

Cardiology and Cardiovascular Medicine

Cite this

Santana, L. F., Núñez-Durán, H., Dilly, K. W., & Lederer, W. J. (2005). Sodium Current and Arrhythmogenesis in Heart Failure. Heart Failure Clinics, 1(2), 193-205. https://doi.org/10.1016/j.hfc.2005.06.003

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AU - Núñez-Durán, Harol

AU - Dilly, Keith W.

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N2 - The low sodium arrhythmic mechanism hypothesis is demonstrated in normal cells with unmodified sodium (Na+) and calcium (Ca2+) channels, in long QT syndrome models, and in heart failure model systems. The authors propose that the changes in Ca2+ influx during the early part of the action potential and during the plateau and repolarization phases of the action potential sum to influence contractility and arrhythmogenesis. The importance of both of these changes is supported by their present work, which suggests that antiarrhythmic agents should be examined for their actions on low sodium arrhythmic mechanism and action potential duration.

AB - The low sodium arrhythmic mechanism hypothesis is demonstrated in normal cells with unmodified sodium (Na+) and calcium (Ca2+) channels, in long QT syndrome models, and in heart failure model systems. The authors propose that the changes in Ca2+ influx during the early part of the action potential and during the plateau and repolarization phases of the action potential sum to influence contractility and arrhythmogenesis. The importance of both of these changes is supported by their present work, which suggests that antiarrhythmic agents should be examined for their actions on low sodium arrhythmic mechanism and action potential duration.

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Access to Document

10.1016/j.hfc.2005.06.003