Sodium Current and Arrhythmogenesis in Heart Failure

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

Research output: Contribution to journalReview article

9 Citations (Scopus)

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 languageEnglish (US)
Pages (from-to)193-205
Number of pages13
JournalHeart Failure Clinics
Volume1
Issue number2
DOIs
StatePublished - Jul 2005
Externally publishedYes

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Action Potentials
Heart Failure
Sodium
Long QT Syndrome
Calcium Channels

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

Sodium Current and Arrhythmogenesis in Heart Failure. / Santana, Luis Fernando; Núñez-Durán, Harol; Dilly, Keith W.; Lederer, W. Jonathan.

In: Heart Failure Clinics, Vol. 1, No. 2, 07.2005, p. 193-205.

Research output: Contribution to journalReview article

Santana, LF, Núñez-Durán, H, Dilly, KW & Lederer, WJ 2005, 'Sodium Current and Arrhythmogenesis in Heart Failure', Heart Failure Clinics, vol. 1, no. 2, pp. 193-205. https://doi.org/10.1016/j.hfc.2005.06.003
Santana, Luis Fernando ; Núñez-Durán, Harol ; Dilly, Keith W. ; Lederer, W. Jonathan. / Sodium Current and Arrhythmogenesis in Heart Failure. In: Heart Failure Clinics. 2005 ; Vol. 1, No. 2. pp. 193-205.
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