Pathophysiological insights from dobutamine-induced Takotsubo syndrome

I enjoyed immensely the case report by Hajsadeghi et al. (1) regarding the 74-year-old woman with Takotsubo syndrome (TTS) in the setting of dobutamine stress echocardiography (DSE) and the associated comprehensive meta-analysis of 22 similar patients from the international literature. The particulars of DSE-induced TTS are well presented and should act as a spring board for contemplating about the pathophysiology of TTS, which remains elusive, using data as the ones presented herein (1). I would like to engage the authors with some inquiries for their kind consideration: 1) Why do the authors refer to “catecholamine surge and alteration of responses to different types of receptors on the endocardium leading to microvascular dysfunction” (1), as opposed to receptors on cardiomyocytes throughout the ventricular wall thickness? 2) When we perform DSE, a baseline echocardiogram is obtained, followed by an echocardiogram at the peak pharmacological effect of dobutamine; one wonders about a stage of hypercontractility preceding the stage of regional wall motion abnormalities of TTS. Did the authors’ review of the literature disclose any such information? 3) The authors documented that imaging in younger patients with TTS, undergoing DSE, revealed the reverse and mid-ventricular variants, rather than the apical variety of TTS (1); consequently do the authors have any thoughts about the effect of dobutamine, in particular, and the topographic distribution of the various types of β-adrenergic receptors in the ventricular myocardium, as a function of age?