Cardiac Memory

Abstract

C lassic definition of the term cardiac memory (CM) refers to the persistent T-wave changes on the ECG after a period of wide QRS rhythms that become evident once normal ventricular activation pattern is restored. It is related to the term ventricular electric remodeling sometimes used in basic science literature. Although CM itself is considered as an adaptive reaction to the change in the ventricular activation sequence, its manifestations (usually T-wave inversions, TWIs) are often confused with pathological conditions manifesting with TWI, such as myocardial ischemia or infarction. Although originally CM was described after restoration of the normal ventricular activation (narrow QRS), recently it was described and studied in wide QRS rhythms significantly expanding the clinical relevance of this phenomenon. Although complex molecular mechanisms of CM have been previously reviewed extensively, practical clinical application of this phenomenon received much less attention. In this article, we will focus on the clinically relevant aspects of CM including its diagnostic use in narrow and wide QRS rhythms. We will also examine how the fundamental CM property of being initiated by the changes in the geometry of the ventricular contraction might open new perspectives in wide QRST morphology analysis by establishing parallels between electric and mechanical functions of the heart. History, Properties, and Adaptive Nature of Cardiac MemoryIn 1915, White 1 was the first to observe the phenomenon of transient TWI after single ventricular premature beats. Later in the 1940s, TWIs after conversion to sinus rhythm were described after paroxysmal tachycardias.2 Since then abnormal T waves of various duration have been documented after intermittent ventricular pre-excitation, 3-5 ventricular pacing, 6,7 intermittent left bundle branch block (LBBB), 8,9 ventricular tachycardia, 10 and even QRS widening associated with sodium channel blocker toxicity. 11In 1982, Rosenbaum et al 10 introduced the term heart memory and presented the first unified hypothesis of how abnormal ventricular activation could lead to the development of T-wave abnormalities regardless of the wide QRS cause by a process he referred to as electrotonic modulation. In this seminal article, 3 principles of CM were formulated: (1) the direction of the T waves in sinus rhythm follows (remembers) the direction of the QRS complex during preceding episode of abnormal activation; (2) the amplitude of memory T waves increases the longer abnormal conduction continues, and (3) repeat episodes of abnormal activation after complete normalization of T waves result in more rapid and prominent accumulation of T-wave changes (hence the term memory). The authors hypothesized that CM represents adaptation of myocardial repolarization to the new activation sequence.The adaptive nature of CM was subsequently confirmed in both animal and human studies. Costard-Jäckle et al 12 and later Sosunov et al 13 in an isolated rabbit heart demonstrated the presence of an inverse relatio...

Arrhythmic risk stratification in post-myocardial infarction patients with preserved ejection fraction: the PRESERVE EF study

“…Post-angiographically proven MI patients, at least 40 days after the event (90 days after surgery if they underwent coronary artery bypass grafting), 15 , 16 with LVEF ≥40% (also assessed after 40 or 90 days, respectively from the index event), either revascularized or not—but without any evidence of active ischaemia (following negative myocardial scintigraphy/exercise treadmill test/stress echocardiography in the previous 6 months), on optimal tolerated medical therapy, were enrolled. Exclusion criteria were: (i) presence of a secondary prevention indication for ICD implantation, (ii) presence of a permanent pacemaker, due to potential effects on NIRF acquisition following pacemaker dependency and cardiac memory, 17 (iii) persistent, long-standing persistent and permanent atrial fibrillation, (iv) neurological symptoms (presyncope or syncope) within the last 6 months, (v) patients with systemic illnesses (cancer, liver failure, end-stage renal disease, rheumatic diseases, and thyroid dysfunction), (vi) administration of antiarrhythmic medication other than β-blockers, and (vii) age ≥80 or ≤18 years old.…”

Clinical Dilemma - Cardiac Memory vs Myocardial Ischemia

“…CM is persistence of TWI developed after a period of abnormal ventricular activation once normal ventricular activation is restored [1][2][3]. Abnormal ventricular activation that precedes CM is often due to artificial pacemaker activity but also intrinsic ventricular ectopic focus, like intermittent left bundle branch block, Wolff-Parkinson-White (WPW), ventricular tachycardia [2,[4][5][6][7][8]. It was described that the T-wave axis during the CM has the same direction as QRS axis during the abnormal ventricular activation that caused CM (Figure 3, red arrows) [3].…”

Cardiac Memory: A Rare Cause of Postoperative Deep T Wave Inversions

“…Our patient was known to have structural heart disease and therefore, baseline ST-T changes are expected and thus, the TWIs seen in Figure 1 are likely due to LVH or an old infarct. Existing data in patients with structural heart disease suggest that when TWIs are present in leads I and aVL at baseline, they can remain inverted even with the development of CM [5].…”