Abstract
(1) Ventricular preexcitation causes both secondary and primary T wave changes. The secondary changes disappear immediately after cessation of preexcitation (ablation of accessory pathways) and unmask the primary T wave changes that regress within days, weeks, or months. (2) The pattern of primary T wave change produced by ventricular preexcitation depends on the location of the accessory pathway connections. The septal and posterior connections are associated with more prominent anteriorly directed T wave deflections and deviation of the T wave vector superiorly. The left lateral connections are associated with rightward deviation of the T wave vector in the frontal plane. (3) The primary T wave abnormalities are believed to be caused by local lengthening of repolarization, but the site of the postulated abnormalities needs to be established. (4) The persistence and slow dissipation of the primary T wave change induced by ventricular pacing, left bundle branch block, and presumably ventricular preexcitation have been attributed to the memory of past events. The nature of these events is not known. Several in vitro models demonstrated phenomena of gradual adjustment of ventricular action potential duration to change in cycle length, or to altered pattern of stimulation, but none of such models has mimicked the long-lasting regression of T wave abnormalities. (5) The terms T wave memory and pseudoprimary repolarization changes lack specificity and are unnecessary additions to the electrocardiographic vocabulary.
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