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 | |
| State | Published - Jul 2005 |
| Externally published | Yes |
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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 journal › Review article
}
TY - JOUR
T1 - Sodium Current and Arrhythmogenesis in Heart Failure
AU - Santana, Luis Fernando
AU - Núñez-Durán, Harol
AU - Dilly, Keith W.
AU - Lederer, W. Jonathan
PY - 2005/7
Y1 - 2005/7
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.
UR - http://www.scopus.com/inward/record.url?scp=33751159419&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=33751159419&partnerID=8YFLogxK
U2 - 10.1016/j.hfc.2005.06.003
DO - 10.1016/j.hfc.2005.06.003
M3 - Review article
C2 - 17386846
AN - SCOPUS:33751159419
VL - 1
SP - 193
EP - 205
JO - Heart Failure Clinics
JF - Heart Failure Clinics
SN - 1551-7136
IS - 2
ER -