I enjoyed reading the very important report by Schwarz et al ., published online ahead of print on June 6, 2017, in JASE , about the persistence of systolic and diastolic mechanotemporal deformation and detection of fibrosis at 4-month follow-up evaluation of 52 patients with takotsubo syndrome (TTS), contrasted with a cohort of 44 healthy control subjects of the same age, gender, and comorbidity distribution. I have some remarks for the kind consideration of the authors.

First, Table 1 in the article reveals that the patients with TTS had a prevalence of diabetes mellitus of 9%, similar to the prevalence among comorbidity-matched control subjects of 8% and lower than what one would expect for a cohort of mainly women of the general population of a mean age of 66 years, in keeping with recent literature.

Second, I applaud the decision of the authors to use a homogeneous cohort of patients with severe TTS of apical and midcavitary distribution, and I hope that the opportunity will not be lost to evaluate further at least a few of these patients with repeat cardiac magnetic resonance imaging and echocardiography at 1-year follow-up, or at any time between 4 months and 1 year (as the authors allude to), to evaluate their course of recovery and the possible presence or absence of restoration to normalcy.

Third, a “chronic TTS condition” (i.e., persisting symptoms both at rest and with exercise) has been suspected, and the authors provide us with the diagnostic blueprint for the objective evaluation of such patients with TTS at follow-up.

Fourth, was there any correlation between the acute and 4-month echocardiographic or cardiac magnetic resonance imaging metrics and the peak levels of troponin I, C-reactive protein, and brain natriuretic peptide?

Fifth, the intriguing finding of persistently increased extracellular matrix volume at 4-month follow-up on cardiac magnetic resonance imaging testing, attributed to microscopic fibrosis, by the time myocardial edema has probably subsided, and affecting the heart globally (i.e., both the acutely abnormally and normally or supernormally contracting myocardial regions), may have pathophysiologic connotations. Probably there are acute cardiomyocyte injurious influences (no matter the mechanism of TTS) also affecting normally and supernormally (i.e., base of the heart) functioning cardiac territories.