Literature DB >> 26949436

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

John E Madias1.   

Abstract

Entities:  

Year:  2015        PMID: 26949436      PMCID: PMC4759119          DOI: 10.1016/j.joa.2015.09.005

Source DB:  PubMed          Journal:  J Arrhythm        ISSN: 1880-4276


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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.

Conflict of interest

The author declares no conflict of interest related to this article.
  4 in total

1.  Hypokalemia from beta 2-receptor stimulation by circulating epinephrine.

Authors:  M J Brown
Journal:  Am J Cardiol       Date:  1985-08-30       Impact factor: 2.778

2.  Prominent J-wave and T-wave alternans associated with mechanical alternans in a patient with takotsubo cardiomyopathy.

Authors:  Rintaro Hojo; Seiji Fukamizu; Takeshi Kitamura; Kota Komiyama; Yasuhiro Tanabe; Tamotsu Tejima; Mitsuhiro Nishizaki; Harumizu Sakurada; Masayasu Hiraoka
Journal:  J Arrhythm       Date:  2014-05-09

Review 3.  Stress (Takotsubo) cardiomyopathy--a novel pathophysiological hypothesis to explain catecholamine-induced acute myocardial stunning.

Authors:  Alexander R Lyon; Paul S C Rees; Sanjay Prasad; Philip A Poole-Wilson; Sian E Harding
Journal:  Nat Clin Pract Cardiovasc Med       Date:  2008-01

4.  Hypokalemia from beta2-receptor stimulation by circulating epinephrine.

Authors:  M J Brown; D C Brown; M B Murphy
Journal:  N Engl J Med       Date:  1983-12-08       Impact factor: 91.245

  4 in total

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