JRSM >
Volume 96, Number 3 >
Pp. 131-132
Department of Internal Medicine, University Hospital, Bern,
Switzerland
1 Division of Cardiology, Department of Internal Medicine, Triemli Hospital,
Zürich, Switzerland
Correspondence to: Barbara Naegeli, Division of Cardiology, Department of Internal Medicine, Triemli Hospital, 8063 Zürich, Switzerland E-mail: barbara.naegeli{at}triemli.stzh.ch
Cardiac memory describes the phenomenon whereby the T-wave abnormalities that result from a change in the direction of cardiac activation, as during ventricular pacing, persist for a while after the end of pacing.
CASE HISTORY
A woman of 85 was admitted after a syncope. For the past three months she had been experiencing dizziness and dyspnoea on exercise. Her heart rate was 60/min, blood pressure was 105/60 mmHg and there was a mitral systolic murmur. There was moderate cardiomegaly on the chest radiograph and echocardiography revealed biatrial dilatation and severe mitral valve insufficiency. A 12-lead electrocardiogram (ECG) showed atrial flutter with non-specific lateral repolarization abnormalities, and on a 24-hour recording the ventricular rate ranged from 37 to 170/min. During the hospital stay she converted spontaneously to bradycardic sinus rhythm, heart rate 40/min (Figure 1, A). The diagnosis was consistent with sick sinus syndrome; a dual chamber pacemaker was implanted and was seen to function (Figure 1, B). The next day, the patient reported acute chest pain and a 12-lead ECG showed new T-wave inversions with an intrinsic ventricular rhythm (Figure 1, C). The pain resolved rapidly and the T-wave abnormalities returned to baseline within 24 hours (Figure 1, D). The initial differential diagnosis in this episode included: acute myocardial ischaemia due to plaque rupture, or coronary embolism arising from the large left atrium; the mitral valve disease and the intermittent atrial arrhythmia; drug effects; penetration of the ventricular lead (which had passive fixation); and cardiac memory phenomenon with simultaneous non-cardiac pain. Acute myocardial necrosis was excluded by repeated analysis of heart enzymes, which never exceeded the normal range. Drugs that cause repolarization abnormalities, e.g. digitalis, were not being given at that time. Ventricular lead penetration was excluded by the absence of a pericardial effusion on repeat echocardiography. Therefore, we considered these transient repolarization abnormalities consistent with cardiac memory phenomenon.
|
COMMENT
Although the existence of cardiac memory has been known for many years, there is still limited information regarding its physiological significance and clinical implications. Clinicians do, however, need to be aware that this electrical curiosity, also termed Chatterjee phenomenon1, can imitate acute myocardial ischaemia. Cardiac memory is characterized by persistent but reversible T-wave changes on the surface ECG induced by an abnormal electrical activation pattern: the reported stimuli include ventricular pacing2, intermittent left bundle branch block3, periods of pre-excitation observed in Wolff—Parkinson—White syndrome4, and episodes of tachycardia5. The extent and the direction of T-wave deviation depend on the duration and the direction of the abnormal electrical activation; the phenomenon can persist for several weeks. The underlying cellular mechanisms are unclear, but existing data point to modification of specific potassium channels and changes in the phosphorylation status of the cAMP responsive element binding protein (CREB)6.
REFERENCES
CiteULike 
Complore 
Connotea 
Del.icio.us 
Digg 
Reddit 
Technorati What's this?
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
