The pharmacology of cardiac memory.

Cardiac memory is an altered T wave during sinus rhythm that is induced by a period of ventricular pacing or arrhythmia. The T wave is characterized by a vector that tracks that of the previously paced or arrhythmic QRS complex. Although initially considered a clinical oddity, cardiac memory is of interest both as an example of the general biological property of memory - as studied most extensively in neural tissues - and because of its implications regarding the control of cardiac rhythm. Signal transduction of cardiac memory appears to involve an angiotensin II-regulated pathway initiated by altered stress/strain patterns in the myocardium. The end result is altered density and kinetics of the transient outward current and perhaps other ion currents as well, and an altered transmural gradient for repolarization. The altered repolarization pattern is accompanied by altered responses to specific antiarrhythmic drugs that may be anti- or proarrhythmic.