Sodium Current and Arrhythmogenesis in Heart Failure

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.