Cardiac memory (CM) refers to persistent T-wave changes on resumption of normal conduction after a period of abnormal ventricular activation. Traditionally, to observe CM, normal ventricular activation had to be restored, limiting the exploration of this phenomenon in clinical practice.

This study sought to prove that CM can be detected during continuous aberrant activation and to establish factors affecting its magnitude using a vectorcardiographic technique.

Sixteen nonpacemaker-dependent patients (11 male, age 72 ± 8 years, mean ± SD) undergoing pacemaker/internal cardioverter-defibrillator implantation were paced in DDD mode with a short atrioventricular (AV) delay for 7 days to induce CM. Electrocardiograms were acquired during AAI and DDD pacing at a constant rate before and after CM induction. Dower transform–derived vectorcardiograms were reconstructed and analyzed.

T vector during AAI pacing changed in both magnitude (baseline, 0.26 ± 0.10 mV; Day 7, 0.39 ± 0.13 mV, P < .01) and direction aligning with the paced QRS vector (baseline DDD QRS − AAI T angle 125° ± 36°; Day 7, 39° ± 21°, P < .01). During DDD pacing, there was no change in T-vector direction, but T amplitude decreased (baseline, 1.06 ± 0.32 mV; Day 7, 0.71 ± 0.26 mV, P < .01). CM measured as T-vector peak displacement (TPD) was identical in AAI and DDD mode (TPD 0.46 ± .0.17 mV and 0.46 ± 0.17 mV, respectively). Individual CM magnitude correlated with QRS/T-vector amplitude ratio during DDD pacing at baseline (r = 0.90).

CM can be reliably shown during continuous ventricular pacing, expanding its application to situations in which abnormal ventricular activation persists. Its magnitude is determined by the QRS/T-amplitude ratio of the ventricular paced beat.