Europace Advance Access originally published online on October 6, 2007
Europace 2007 9(11):1091-1092; doi:10.1093/europace/eum197
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ELECTROCARDIOLOGY
A memorable experience
Division of Cardiovascular Medicine, Vanderbilt University Medical Center, 383 Preston Research Building/2220 Pierce Avenue, Nashville TN 37232, USA
Manuscript submitted 6 July 2007. Accepted after revision 17 August 2007.
* Corresponding author. Tel: +1 615 936 1713; +1 615 936 1872. E-mail address: ken.monahan{at}vanderbilt.edu
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The electrocardiographic phenomenon of cardiac memory results from aberrant ventricular activation and causes transient ECG features that can mimic ischaemia. We present the case of a patient with ischaemic cardiomyopathy who exhibited evidence of T-wave memory in the setting of multiple episodes of non-sustained ventricular tachycardia that were triggered by an insect bite.
Key Words: Ventricular tachycardia, Implantable cardioverter-defibrillator
A 60-year-old man with ischaemic heart disease and a history of cardiac arrest presented following ICD discharge.
On the afternoon prior to admission, he was stung by a wasp, but had no immediate symptoms except for pain at the site of the sting. Early the following morning, he received an ICD shock without prodrome. Interrogation of the device revealed no use of pacing for bradycardia and no detected episodes in the previous 9 months, but showed 88 episodes of non-sustained ventricular tachycardia (NSVT) at rates of 140–150 bpm., starting within minutes of the reported time of the insect sting. Electrograms showed the VT to be monomorphic with similar morphology for all episodes. Anti-tachycardia pacing terminated seven events, 80 terminated spontaneously, and a shock was required for the last episode, which occurred 
12 h after the initial occurrence of NSVT. There were no further episodes following ICD discharge.
The admission ECG, obtained 10 h after the ICD shock, showed sinus rhythm with deep symmetric anterolateral T-wave inversions, which were new since previous tracings (Figure 1A). There had been no recent changes to the patient's medical regimen, which included ACE inhibitor, beta-blocker, and mexiletine. Serial cardiac enzymes were normal. Adenosine myocardial perfusion testing showed severely depressed LVEF (20%), and no reversible perfusion or wall motion abnormalities. The patient felt well throughout his hospital course and had no further tachyarrhythmias. An ECG 10 days later was unchanged, whereas 8 weeks after presentation, the T-wave changes had reverted to the previous baseline (Figure 1B). A subsequent ECG showed a wide-complex tachycardia with evidence of a prior inferior infarction, right bundle branch block, right superior axis, and a late-reversal R-wave pattern suggestive of VT with an inferobasal LV origin (Figure 1C). At electrophysiology study, the VT mapped to this region, but was unable to be ablated.
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The striking T-wave changes seen on the presenting ECG are not explained by a major ischaemic event, and represent the transient sequelae of aberrant ventricular activation, the phenomenon of cardiac memory. The predominantly negative QRS complexes in the lateral leads during VT are consistent with the repolarization abnormalities seen in the presenting ECG (Figure 1A). Well-recognized causes of cardiac memory include intermittent left bundle branch block, pre-excitation, or tachyarrhythmias. Although usually reported after prolonged periods of arrhythmia, cardiac memory has been observed following even shorter periods of abnormal ventricular activation than were present in our patient. In this case, an insect bite triggered the frequent NSVT that created this ‘memorable’ ECG.
Conflict of interest: none declared.
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