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International Journal of Arrhythmia 2012;13(3): 24-27.
ECG & EP CASES
T Wave Memory Caused by
Sustained Idiopathic Left
Ventricular Tachycardia

Sung-Hwan Kim, MD
Division of Cardiology, Department of Internal Medicine, Seoul St. Mary's Hospital, College of Medicine, The Catholic University of Korea, Seoul, Korea




Introduction

   The duration of ventricular activation, or QRS interval, is normally 60-100 ms. A widening of the QRS interval indicates prolonged ventricular activation that did not go through the normal conduction system. Prolonged activation can be classified according to 3 groups with different root causes: (1) abnormal conduction system (i.e., right or left bundle branch block), (2) ventricular origin (i.e., VT/fibrillation), (3) and ventricular preexcitation.
   Most tachycardias are characterized by a wide QRS interval and are ventricular in origin, especially in patients with structural heart disease. In cases of patients with an abnormal conduction system, including aberrancy or preexcitation, it is not easy to differentiate VT from supraventricular tachycardia. However, differential diagnosis is very important because the treatments and prognoses differ substantially.
   In cases of VT, ventricular activation originates in the ventricle itself and atrial activation originates in the sinus node. Therefore, evidence of atrioventricular dissociation is a strong indicator of VT. If, however, either the typical morphology of a bundle branch block or preexcitation is observed in the ECG, it would suggest supraventricular tachycardia.

Case

   A 41-year-old man with a 3-hour history of palpitations visited a local clinic and was referred to a general hospital. His blood pressure was 100/70 mmHg and his heart rate was 190 bpm. His ECG suggested VT; therefore, the patient was administered amiodarone infusion (300 mg loading dose and 900 mg/day continuous infusion). The tachycardia persisted and electrical cardioversion was attempted (biphasic 100 J, 200 J) but was unsuccessful. Verapamil injection also failed to terminate the tachycardia. Therefore, the patient was referred to our hospital. In the emergency room, his heart rate decreased but the patient was still tachycardic (Figure 1). An electrophysiological study was performed that immediately confirmed the diagnosis of VT. A circuit was mapped in the area of the posterior fascicle (Figure 2) and successfully terminated with ablation. After the procedure, surface ECGs showed T wave inversion with the same vector as the QRS complex during VT (Figure 3). Serial cardiac biomarker tests and echocardiograms showed no evidence of myocardial infarction or ischemia. The occurrence of T wave memory caused by prolonged VT was hypothesized. One month later, the T wave inversion had disappeared (Figure 4). The patient was followed for 6 months. Antiarrhythmic medication was not prescribed and there was no recurrence during this time.





Discussion

   Of the 3 waveforms in the ECG: the P wave reflects atrial activation, the QRS complex is associated with ventricular activation, and the T wave indicates ventricular repolarization. Cardiac memory is most clearly seen in the T wave. T wave changes occur in various circumstances and are referred to as primary or secondary.1 Primary T wave changes are derived entirely from the ion channel and electrical determinants of repolarization, and are independent of the QRS complex;2 for instance, the changes occurring in patients with hyperkalemia or hypokalemia. Secondary T wave changes, on the other hand, arise from an altered sequence of activation and are dependent on the QRS complex. Such T waves can be observed during ventricular pacing or ventricular arrhythmia, and may occur in normal or diseased hearts. After a period of abnormal activation (i.e., ventricular pacing, sustained ventricular arrhythmia, or preexcitation), a change in the T wave can persist even after sinus rhythm and normal activation are returned. In these cases, the T wave retains the vector of the previously abnormal QRS complex.3 Long periods of abnormal activation can increase the magnitude of these T wave changes; this is referred to as accumulation. The duration of T wave memory can extend far beyond the termination of the inciting stimulus, persisting even after normal rhythm and activation return.


References

  1. Katz AM. T wave “memory”: possible causal relationship to stressinduced changes in cardiac ion channels? J Cardiovasc Electrophysiol. 1992;3:150-159.
  2. Rosen MR. The heart remembers: clinical implications. Lancet. 2001;357:468-471.
  3. Shvilkin A, Danilo P Jr, Wang J, Burkhoff D, Anyukhovsky EP, Sosunov EA, Hara M, Rosen MR. Evolution and resolution of long-term cardiac memory. Circulation. 1998;97:1810-1817.
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