I read with interest the abstract by Sta. Cruz and Codolosa1 published recently in CHEST (March 2014), about a diabetic patient with recurrent isolated right ventricular Takotsubo syndrome in the setting of diabetic ketoacidosis and pulmonary aspiration. The authors ascribe the recurrent Takotsubo syndrome in their patient to dysautonomia, as inferred from the bradycardia and the “elevated pressures of the upper and lower esophageal sphincters suggestive of increased vagal tone.”1 Do the authors imply that there was diminished autonomic sympathetic activity and a resultant increased influence of the parasympathetic autonomic nervous system? If this is the position of the authors, why was there an enhanced “hypercontractility of the basal segments” of the right ventricle, a response that customarily should be attributed to the contractility-enhancing sympathetic component of the autonomic nervous system? Alternatively, one could hypothesize that the different parts of the right ventricle were under the influence of the two different components of the autonomic nervous system.