To the Editor The cardiotoxicity of antitumor agents, including complications such as pump failure and arrhythmias, has been a growing concern. Although rare, these events can be fatal and irreversible, warranting careful monitoring and follow-up. The authors reported a patient who developed Takotsubo-like cardiac dysfunction and ventricular tachycardia (VT) following the administration of afatinib, a second-generation epidermal growth factor receptor tyrosine kinase inhibitor, for the treatment of non-small-cell lung cancer (1). Although this case is intriguing, several concerns should be raised.
It is uncertain whether the arrhythmia described was indeed VT. The authors noted that the arrhythmia was refractory to electrical cardioversion (1). Typically, VT can be terminated transiently by cardioversion. Furthermore, a pulse rate of 116 bpm during arrhythmia may not be sufficient to cause severe hemodynamic compromise. In addition, the electrocardiogram during arrhythmia appears to show 1:1 atrioventricular conduction in lead V1, suggesting the possibility of supraventricular tachycardia rather than VT.
The interpretation of repolarisation abnormalities may warrant further consideration. After resuscitation, the T-wave inversion in leads V5-V6 is not clearly evident (1), raising the possibility that QT prolongation induced by amiodarone, rather than Takotsubo-like dysfunction, accounted for these findings (2).
While the authors emphasized a Takotsubo-like mechanism, coronary ischemia cannot be entirely excluded. Coronary computed tomography images showing a large left anterior descending artery surrounding the apex. Moreover, the electrocardiogram during arrhythmia appears to show ST-segment elevation in leads II, III, aVF, and aVL, suggesting ischemic involvement in the territory of the left anterior descending artery. Previous reports have documented coronary artery spasms associated with tyrosine kinase inhibitor therapy (3), and the observed T-wave inversion after resuscitation may represent a post-ischemic change rather than stress-induced cardiomyopathy.
The authors state that they have no Conflict of Interest (COI).
References
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