Scorpion envenomation cardiomyopathy: a promising model for takotsubo syndrome

To the Editor:

I enjoyed reading the article by Abroug et al.¹ published in the April, 2015 issue of the Journal, about scorpion cardiomyopathy (SC) and its similarity with takotsubo syndrome (TTS), based on the vast clinical world experience on both, and the SC animal models. Indeed all workers in the field of TTS should study this comprehensive review for possible insights about the human TTS. The authors very convincingly expound on the parallels of SC and TTS, describing an early “vascular phase” after scorpion envenomation “which is related to a profound catecholamine-related vasoconstriction leading to a sharp increase in left ventricular (LV) afterload, thereby impeding LV emptying, and increasing LV filling pressure,” and a subsequent “myocardial phase” occurs, “characterized by a striking alteration in LV contractility (myocardial stunning), low cardiac output, and hypotensive state.”¹ These two phases of SC are reminiscent of the description provided about TTS, where “early events tend to be dominated by sympathetic effects, whereas late events tend to be dominated by parasympathetic effects,”² leading to hypertension and tachycardia early in the clinical course, and bradycardia and hypotension later on. Perhaps with increasing awareness about TTS and earlier evaluations of the afflicted patients we will witness an increased prevalence of tachycardia and/or hypertension in patients with TTS, as compared with the currently appreciated prevalence.³ This author favors the notion that this early heightened afterload phase is instrumental in the subsequently detected apical/midventricular LV “ballooning” seen in patients with TTS.⁴ The authors detected parallel involvement of the right ventricle (RV) to that of LV in patients with SC,¹ as is the case in the increasing reporting of both LV and RV involvement in patients with TTS.³ In reference to therapy of SC, particularly of the “myocardial phase,” and its pathophysiological consequences, the authors recommend employment, among other modalities, of dobutamine infusion, which should probably be avoided in patients with TTS, since it has led to TTS in some patients when administered either for diagnostic or therapeutic purposes.³ Finally, the authors refer to many sophisticated studies, carried out by themselves or others, employing animal (murine and canine) models of SC (Refs. # 36, 37, 51–53,55–58,63, of their article),¹ and such previous experience should be reviewed thoroughly in an effort to detect similarities and differences in the animal phenotypes of SC and TTS, so that advancement can be realized in unraveling the pathophysiological mechanism(s) of human TTS,^4–6 by designing promising animal models of TTS.

Declaration of interest

The author reports no declarations of interest. The author alone is responsible for the content and writing of the paper.