Takotsubo syndrome and polymorphic ventricular tachycardia: The chicken or the egg

Abstract

To the Editor, I read with great interest the study by Hojo et al. [1], published in the Journal, about a 74-year-old woman with bouts of polymorphic ventricular tachycardia (PVT) in the setting of Takotsubo syndrome (TTS) who was found to be hypokalemic and had prominent T-wave and J-wave electrical alternans, and mechanical alternans. The following are some thoughts and questions for the authors’ kind consideration: (1) It is conceivable that TTS came first, as the authors propose, followed by J-wave and T-wave alternans, and QTc interval prolongation, which led to PVT, with perhaps some further facilitation caused by the underlying hypokalemia. However, it is also possible that the patient had bouts of PVT precipitated by the underlying hypokalemia (although later hypokalemia was not associated with electrocardiographic repolarization changes), J-wave and T-wave alternans, and QTc interval prolongation, which in turn led to the physical stress that triggered the TTS. (2) Why did the patient’s hypokalemia take 56 h to control? Was there any reason that larger potassium infusions, of course under close potassium blood level monitoring, were not implemented? (3) The mechanical alternans could have been a phenomenon previously encountered in association with T-wave alternans and in the absence of heart failure, or could have been an epiphenomenon of the precipitated left ventricular failure due to TTS. (4) Although this patient’s hypokalemia was attributed to the hydrocortisone “she had taken for pituitary adrenal insufficiency after surgery for a pituitary tumor” [1], it is conceivable that hypokalemia was also further aggravated by the underlying circulating catecholamines (particularly epinephrine), and thus poorly responded to the potassium infusion. Both, TTS [2] and hypokalemia [3], [4] have been shown to be mediated by specific β2-adrenoreceptor stimulation.