There is an AV sequential pacemaker present. In Figure 1A, sinus P waves are tracked by the ventricular pacer with a long AV delay. Long AV delays are programmed to allow occasional natural AV conduction to take place. In the bottom tracing the PR is shorter and normal (narrow) conducted QRS complexes are present. In this ECG, the large negative T waves in the anterior and inferior leads are the result of “cardiac memory” or “T-wave memory.” Cardiac memory refers to T-wave abnormalities that manifest on resumption of normal ventricular activation after a period of abnormal activation.1,2 Cardiac memory is seen in patients with intermittent wide complex rhythms such as intermittent left bundle branch block, intermittent ventricular preexcitation including following catheter ablation, and with return of normal sinus rhythm after a prolonged episode of ventricular tachycardia.1,2 The most common cause of cardiac memory, however, is intermittent ventricular pacing. Right ventricular pacing causes dyssynchronous left ventricular activation. When normal activation resumes, the T-wave vector tracks the vector of the previously altered QRS complex.3 The longer the duration of ventricular pacing, the longer the memory T waves can persist. Note in our case that during the nonpaced sinus rhythm (Figure 1B), not only were negative T waves seen in the exact same leads that exhibited negative QRS complexes during pacing, but the deepest negative T waves were seen in those leads that exhibited the deepest negative QRS complexes during pacing (Figure 1A). Negative T waves in the chest leads but upright T waves in leads I and aVL and a maximal precordial T-wave inversion that is deeper than the T-wave inversion in lead III, as in our case, are further strong indicators of cardiac memory rather than ischemia.4
Large T-Wave Inversion in a Patient With a Pacemaker—Discussion. Arch Intern Med. 2011;171(15):1315–1316. doi:10.1001/archinternmed.2011.359
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