The report by Shiomura et al, published online ahead of print on May 21, 2015, in the Journal , about the determinants of rapid (within <10 days, 30 patients) or delayed (≥10 days, 28 patients) recovery of the left ventricular (LV) systolic dysfunction of a consecutive cohort of 58 patients with takotsubo syndrome (TTS) showed in the univariate analyses that male gender, brain natriuretic peptide (BNP) level, body mass index (BMI), nonuse of calcium channel blockers (CCBs), and LV end-diastolic diameter at baseline were associated with delayed recovery; at multiple logistic regression analysis, BNP and nonuse of CCBs were determinants of a delayed recovery, whereas leptosomic (BMI <20 kg/m ² ) build was an independent predictor of rapid recovery. Thus, low BNP and BMI levels and use of CCBs are linked to a speedy recovery of LV systolic function in patients with TTS. I would appreciate the authors’ response on the following issues: (1) a limitation of the database is that using a dichotomous classification of the patients’ LV systolic dysfunction timing of recovery, only a coarse assessment of the determinants is accomplished (i.e., there must be a difference in a patient’s recovery in 11 days compared with 6 months, although such finer discrimination can only be attained with repeated a priori arranged imaging testing over the course of outpatient follow-up); (2) considering that 14% of patients with early recovery had diabetes mellitus (DM), whereas 26% of the patients with delayed recovery had DM, and in the context of a recent report on the low prevalence of DM in TTS, I wonder whether all the patients with DM or the ones with delayed recovery were “overwhelmed” by a serious co-morbidity, surgery, sepsis, decompensated respiratory, or other catastrophic illness, compared with a subgroup presented without provocation or following emotional stress; and (3) it is surprising that the authors speculate that the LV systolic dysfunction recovery, provided by the use of CCBs at baseline, could be mediated singly by the “multivessel epicardial coronary artery spasm and coronary microvascular impairment” alleviation by these drugs (an unlikely possibility), instead of also attributing it to a protective influence from calcium sequestration of the cardiomyocytes, consisting of “contraction bands consistent with cytoplasmic calcium overload,” the reversible end result in the pathophysiological cascade of TTS, which occurs rapidly after the inception of illness (“intense rapid calcification makes it likely that the subcellular mechanisms that underlie the development of coagulative myocytolysis involve calcium entry”).