ABSTRACT

Cardiac memory refers to T-wave inversions (TWI) on electrocardiograms (ECGs) after an episode of abnormal ventricular activation or wide electrical activity of ventricular muscles (QRS complex). We present the case of a 62-year-old woman with symptomatic bradycardia due to sinus pause. She immediately underwent temporary transvenous ventricular pacing. In the following days, intrinsic normal sinus rhythm was resumed at 69 bpm and a narrow QRS was observed (97 ms). Additionally, deep TWI was observed in leads II, III, aVF, and V3-V6. The distribution of TWI, normal echocardiogram and laboratory results, non-significant coronary angiogram, and recent right ventricular pacing correspond to possible cardiac T-wave memory. Follow-up 12-lead ECG four weeks later showed that T-wave morphology returned to normal baseline. This further confirmed the final diagnosis of cardiac memory-induced TWI. Recognizing cardiac memory-induced TWI is important for physicians to facilitate proper evaluation and management of TWI and prevent unnecessary further cardiac diagnostic tests.

INTRODUCTION

The typical definition of cardiac memory refers to the T-wave changes [usually T-wave inversions (TWI)] on the electrocardiogram (ECG) after an episode of abnormal ventricular activation or wide QRS complex that appears after the pattern of normal ventricular activation returns (1, 2). TWI as cardiac memory manifestations often mimic other pathological conditions that may manifest as TWI, such as myocardial infarct or ischemia, myopericarditis, takotsubo cardiomyopathy, and cerebrovascular accident (1, 2). Here we report a case of cardiac memory manifesting as new-onset TWI after ventricular pacing in a patient with symptomatic bradycardia due to sinus pause.

CASE REPORT

A 62-year-old female presented to the emergency room with intermittent chest pain and dizziness. She had a history of uncontrolled hypertension for one year. On arrival, blood pressure was 144/76 mmHg, heart rate was 20-30 beats per minute (bpm), respiratory rate was 22 breaths per minute, and oxygen saturation was 97% on free air. Other physical examinations were within normal limits. A 12-lead ECG showed periodic sinus pause at a rate of 30 bpm (Figure 1). Bedside echocardiography revealed normal left ventricle systolic function (ejection fraction sof 68% by teicholz) and no abnormal wall motion. Serial troponin levels were negative. Electrolytes (sodium, potassium, chloride, calcium, and magnesium) and thyroid function tests were within the normal range. She was diagnosed with symptomatic bradycardia due to sinus pause, and temporary transvenous ventricular pacing was immediately performed. A12-lead ECG was obtained after temporary pacing insertion, which showed a right ventricular paced rhythm (QRS width 150 ms) at 75 bpm (Figure 2). The patient was then scheduled for permanent pacemaker (PPM) implantation because of symptomatic bradycardia (sinus pause) with no potential causes.

On the following days, intrinsic normal sinus rhythm was resumed at a rate of 69 bpm and narrow QRS (97 ms) was observed on ECG (Figure 3). Additionally, deep TWI was observed in leads II, III, aVF, and V3-V6 (Figure 3). She was asymptomatic at this time. However, suspicion of myocardial ischemia or infarction is raised. Repeat echocardiography revealed no wall motion abnormality. Troponin and electrolytes were within the normal range. Coronary angiography was then performed before PPM implantation. There was no significant stenosis found on angiography (Figure 4). Finally, due to the T-wave direction in sinus rhythm following (remembering) the QRS complex direction during the previous episode of wide QRS or abnormal ventricular activation (ventricular pacing), TWI was concluded to be a manifestation of cardiac memory after ventricular pacing. A dual chamber PPM DDDR was implanted successfully. She was then discharged with no symptoms. Follow-up ECG at the outpatient clinic four weeks later showed that T-wave morphology had returned to normal baseline (Figure 5).

Written informed consent for the publication of this case report and accompanying images was obtained from the patient.

DISCUSSION

Cardiac memory is a common but rarely recognized phenomenon in which T-waves in a sinus or intrinsic rhythm follow or remember the QRS vector from a previous abnormal activation (1, 3). It manifests on ECG or vector cardiogram as TWI during any intrinsic or sinus rhythm with normal ventricular activation that occurs after periods of abnormal myocardial activation (e.g. after ventricular pacing, ventricular tachycardia, left bundle branch block, intermittent ventricular preexcitation, and pre-excitation ablation) (4, 5). Cardiac memory is associated with prolonged repolarization in the initial active area (1). The cellular mechanisms of cardiac memory are currently unclear, but changes in several ion channels, cell coupling, and receptors, including the temporary outward current, Ito, ICa, Na/Ca exchanger, IKr, stretch-activated receptors, AT1 receptors, and redistribution of gap junctions, have been reported (1, 3, 6).During intrinsic sinus rhythm with a normal rate, a new and deeper TWI (Figure 3) in this patient appeared in the lead with a negative QRS complex during the previous ventricular paced rhythm (leads II, III, aVF, and V3 to V6). The distribution of TWI, normal echocardiogram and laboratory results, non-significant coronary angiogram, and recent right ventricular pacing correspond to possible cardiac t-wave memory. TWI on arrival might be caused by bradycardia (Figure 1).

Cardiac memory may persist for several weeks after ventricular conduction returns to normal (1). Attenuation of the TWI in this patient was documented four weeks later on a follow-up 12-lead ECG in which T-wave morphology returned to normal baseline. This further confirmed the final diagnosis of cardiac memory-induced TWI.

Once other causes of TWI are ruled out, cardiac memory-induced TWI does not require specific treatment (5). In patients without pacemakers, cardiac memory may imply intermittent ventricular preexcitation, intermittent left bundle branch block, or paroxysmal ventricular tachycardia, and ambulatory heart rhythm monitoring may be appropriate to determine the potential causes (4, 5). Cardiac memory in this patient was most likely secondary to temporary ventricular pacing; hence, no further workup or treatment was necessary.

Recognizing cardiac memory as a potential cause of TWI is essential to prevent unnecessary hospitalization, further cardiac diagnostic workup, or cardiac catheterization. T-wave morphological analysis can help distinguish ischemia-induced from cardiac memory-induced TWI after right ventricularpacing. A study by Shvilkin et al. (7) demonstrated that the combination of 1) positive T-wave in aVL and isoelectric or positive T-wave in lead I and 2) maximum TWI in the precordial lead greater than that in the inferior lead, as shown in this patient, has a sensitivity of 92% and specificity of 100% for cardiac memory-induced TWI from right ventricular pacing.

Cardiac memory is a pattern of T-wave changes, usually TWI, following the resolution of abnormal ventricular activation or wide QRS rhythm. Recognizing the cardiac memory phenomenon is essential for physicians to facilitate appropriate evaluation and management, which may help avoid unnecessary hospitalization and further cardiac diagnostic tests.