I read the report by Norcliffe-Kaufmann et al published in the January 15, 2015, issue of the Journal, about the autonomic nervous system (ANS) evaluation of 10 women with a history of confirmed Takotsubo syndrome (TTS), which they had suffered more than a mean of 3 years previously, with comparisons with 10 normal control subjects. The authors’ ANS comprehensive assessment at rest and during physical, emotional, and cognitive stimulation was further amplified with measurements of brachial artery flow-mediated vasodilation, ambulatory blood pressure monitoring, and plasma catecholamine levels. They found that the hyperadrenergic state of the patients with TTS continues to be present long after the index TTS episode, with associated reduced parasympathetic modulation, whereas the plasma catecholamine levels did not differ between TTS women and controls, prompting the authors to conclude that this “impaired baroreflex control may, therefore, play a role in TTS.” The pathophysiology of TTS is still elusive, but the speculations of the authors are plausible. I have some comments for the authors’ assessment: (1) It is surprising that there was evidence for a continuing hyperadrenrgic state, which was not translated to elevated plasma catecholamine levels in the patients with a history of TTS, which suggests that excessive autonomic sympathetic arousal (if not overwhelming like at the time of the TTS inception) can be associating with normal plasma catecholamine overspill. There is previous work documenting elevation of plasma catecholamines in patients with a history of TTS, unlike what was observed in the present study, with the authors of the latter attributing the variation to the difference in the “elapsed time between the TTS event and testing”. (2) Although the authors detected a heightened sympathetic ANS state in their patients with TTS, this may reflect a post-traumatic stress disorder response to their previous illness, which it is possible that there was not present before the index TTS occurrence and could be different qualitatively and quantitatively from the one triggering the TTS. (3) The authors state that “comparatively little is known about parasympathetic function in patients with TTS” ; although it is true that TTS is characterized by excessive adrenergic ANS stimulation with a profuse noradrenaline overspill, the parasympathetic ANS is not always an inactive bystander, usually overcome by an underlying overwhelming sympathetic seethe; indeed, a parasympathetic predominance is often manifest in the acute phase of the TTS illness, after a period of sympathetic ANS dominance. This is exemplified by the persistent bradycardia and/or hypotension (sometimes relative in degree) in patients with TTS and heart failure (including cardiogenic shock), presenting to the hospital late after the inception of the illness, or many hours after admission to the hospital, in patients presenting early in the course of their illness, or the ones suffering TTS, after being admitted to the hospital for other reasons.