“…The authors have done a good job in pointing out the noxious effects of anesthesia and or surgical stress imparting a host of circulatory and metabolic derangements, the rise of catecholamines, associated with the perianesthetic and perioperative period, and further listing all the commonly employed plausible speculations about the still evasive pathophysiology of TTS. I have some questions and remarks for the kind consideration by the authors: (1) The patient received postoperatively small amounts of norepinephrine (NE) to manage his mild hypotension, with larger doses of this drug given later when the patient's hypotension worsen; it is conceivable that TTS was triggered by the NE infusion, and thus details about the amount given, the rate of infusion, and duration for NE and all the other drugs the patient received perioperatively will be useful. (2) The authors were surprised by the early maintenance of a good left ventricular ejection fraction (LVEF) while there were already regional wall motion abnormalities present, and before the sudden drop of the LVEF, but this is probably due to the rare opportunity the authors had, to see TTS newly emerging under their eyes, a rare occurrence.…”