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Mechanoelectrical Feedback Has a Role in the Development of Cardiac Memory
Cardiac memory is characterized by an altered T wave during sinus rhythm that is induced by a period of ventricular pac-ing or arrhythmia. Returning to sinus rhythm (normal activation) after an interval of abnormal ventricular depolarization (ventricular pacing or arrhythmia) may result in a change in the T wave vector that persists for a time period of minutes to weeks. Cardiac memory, expressed as a specific pattern of T-wave change on an ECG, is associated with reduced tran-sient outward potassium current (Ito), reduced epicardial mRNA levels of Kv4.3 (one of the molecular correlates of Ito) and altered L-type calcium channel kinetics. The molecular and genetic changes associated with cardiac memory have been studied but the triggers responsible for inducing memory remain unknown. We hypothesize that mechanoelectrical feedback contributes to the initiation of cardiac memory. Two lines of evidence support this hypothesis. First, cardiac an-giotensin II synthesis and release as a consequence of altered stretch imposed by ventricular pacing is accompanied by a reduction in Ito density and an increased ICa,L. Second, alterations in ventricular activation by pacing are associated with regional changes in myocardial strain, and myocardial strain strongly influences the repolarization properties of myo-cytes. Confirmation of this hypothesis will elucidate the electrophysiological trigger responsible for inducing cardiac memory.
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