Key result
The pathogenesis of Takotsubo syndrome is multifactorial, with catecholamine excess playing a central role in mediating toxic effects on the myocardium and vasculature.
This review highlights the central role of catecholamine excess and its toxic effects on the myocardium in the pathogenesis of Takotsubo syndrome.
Supports mechanistic research on catecholamine effects in Takotsubo; leaves open whether targeting improves outcomes.
Takotsubo syndrome (TTS) is an enigmatic disease with a multifactorial and still unresolved pathogenesis. Postulated mechanisms include catecholamine excess, coronary artery spasm, and microvascular dysfunction, however catecholamines seem to play a central role in the pathophysiology of TTS. In facts catecholamines have relevant effects on the vasculature and myocardium. Toxic direct effects of catecholamine on myocardium are mediated by multiple pathway including functional hypoxia, metabolic changes and changes in membrane permeability leading to various electrolytic imbalances. Recently report of familial cases has suggested a genetic component. Further research is required to help clarify the proposed hypotheses and to increase our understanding of the cardiovascular responses to acute stress and the pathophysiology underpinning TTS.
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Masarone et al. (2017) conducted a review in Takotsubo syndrome. The pathogenesis of Takotsubo syndrome is multifactorial, with catecholamine excess playing a central role in mediating toxic effects on the myocardium and vasculature.
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