LAUSR

To the Editor: I read with great interest the paper by Li et al,1 about the 80yearold woman whose electrocardiogram (ECG), in the setting of takotsubo syndrome (TTS), revealed “fragmentation of the QRS complexes across precordial leads V46, lead aVR, and a positive deflection embedded within the QRS complex in lead V1.” The comprehensive analysis of the authors about the pathogenesis of arrhythmias in patients with TTS, in connection with the vagal influences, and underlying myocardial edema and microfibrosis, are highly appreciated. I have some comments and questions for the authors: (1) In reference to the statement that these ECG changes were resolved in 3 months, it will be of interest to the readers to know whether other ECGs in this patient were recorded between the admission and the 3month time point, and if such ECGs revealed QRS fragmentation or its earlier resolution. (2) Reversible attenuation of the QRS amplitude has been previously described in various combinations of the ECG leads, and lead aVR, in connection with TTS, and attributed to myocardial edema2,3; careful inspection of Figure 1 of the present paper reveals attenuation of the QRS amplitude in leads I, II, III, aVR, aVL, aVF, V1, and V3– V6. (3) Did the patient have any ECGs prior to her admission with TTS, to compare it with the ECG obtained on admission?