Further validation of the epinephrine pathophysiology rat model of Takotsubo syndrome.

Abstract

The pathophysiology of Takotsubo syndrome (TTS), the reversible cardiomyopathy affecting mainly the left ventricle, with primarily apical and midventricular "ballooning" and basal hypercontractility, continues to be elusive. Many etiological hypotheses have been advanced with a pivotal recent one, which has attributed the TTS to a switch of the function of the beta-2 adrenergic receptors from the canonical cardiostimulatory to cardiodepressant mode, engendered by large doses of epinephrine administration. This worthy animal model has not been explored to its fullest, and thus the author of this viewpoint proposes a series of essential experimental enhancements, in order for the model to provide additional indirect insights, pertaining to the pathophysiology of TTS in humans.