Cardiac Memory - from Theory to Clinical Practice

Abstract

Cardiac memory (CM) is defined as changes in T wave polarity and vector that appear after cessation of a period of abnormal ventricular depolarization of various causes. The mechanisms responsible for CM development are initiation by local stretch, requiring myocardial contraction, followed by a cascade of intracellular signals that lead to a reduction in repolarization currents, especially Ito. In practice, CM is a frequently encountered ECG phenomenon, especially in patients with intermittent ventricular pacing, and knowledge of the ECG pattern of CM may help quick differential diagnosis from ischemia. While CM is most often a benign finding, in rare cases, association between CM and severe bradycardia or other factors for QT prolongation may be pro-arrhythmic and requires emergency care.

FIGURE 1.

ECG example (paper speed 25 mm/s, scale 10 mm/mV) of post-pacing cardiac memory in a patient with DDD pacemaker and septal position of the right ventricular lead. Panel A: baseline ECG, panel B: ventricular pacing with short atrio-ventricular interval, panel C: post-pacing cardiac memory, seen as negative T waves in the leads where the paced QRS complex was negative and positive T waves in the leads where the paced QRS complex was positive.

FIGURE 2.

ECG example (paper speed 25 mm/s, scale 10 mm/mV) of cardiac memory in a patient with ventricular pre-excitation. Panel A: initial ECG, showing ventricular pre-excitation over a postero-septal accessory pathway, with negative delta waves in the inferior leads. Panel B: ECG after radiofrequency ablation of accessory pathway, showing ventricular activation entirely over the His-Purkinje system (normal PR interval, narrow QRS, disappearance of delta waves) and cardiac memory, seen as negative T waves in the leads where the delta wave was negative, and tall positive T waves in the leads where the delta wave was positive.

FIGURE 3.

ECG example (paper speed 25 mm/s, scale 10 mm/mV) of possible implication of cardiac memory in arrhythmogenesis. Panel A shows an idioventricular rhythm at 55/min in a patient with single-chamber VVI(R) pacemaker, programmed with hysteresis at 40/min. Panel B shows paced rhythm in the same patient at VVI 75/min after 24 hours. Note that the idioventricular rhythm has a QRS vector markedly different from that of the paced QRS, and that the pattern of negative T waves in this rhythm respects the “rules” of post-pacing cardiac memory. The QTc interval is very prolonged (663 ms) during ventricular rhythm, and cardiac memory may contribute to these potentially arrhythmogenic changes.