Abstract
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.
Highlights
TTS syndrome is classified as both a primary and an acquired cardiomyopathy by the American Heart Association (AHA),[3] and as an
In the meantime, according to recent position paper of Heart Failure Association (HFA),[6] this entity should be clinically labeled as an acute, reversible, heart failure syndrome
Postulated mechanisms include catecholamine excess, coronary artery m spasm, and microvascular dysfunction, howevm er catecholamines seem to play a central role in the pathophysiology of TTS
Summary
William Shakespeare The role of catecholamines seems to be cen- administered catecholamines,[22] pheochromotral to the pathophysiology of TTS, and leads to cytoma[23] and acute brain injury[24] cause similar. During the past two decades, a novel cardiac multiple potentially relevant direct and indi- reversible myocardial dysfunction. Syndrome with transient left ventricular sys- rect effects on the systemic vasculature, coro- In addition, myocardial biopsies of patients tolic dysfunction has been reported.[1,2] nary vasculature, and myocardium.[18] with TTS demonstrate typical features of cate-. The overstimulation of catecholamine receptors enhances cardiac contractility and heart rate, with secondary increase in myocardial oxygen demand that may outweigh oxygen delivery, creating areas of functional hypoxia which can be exacerbated by vasoconstriction in the coronary macro- and micro-circulation and which reduce the supply of high energy phosphates.[31]. Changes in membrane permeability leading to various electrolytic imbalances, disturb multiple cellular homeostatic processes fostering additional myocardial toxicity.[33]. Martin and coll. showed decreased reactive hyperemia in response to mental stress in patients with prior TTS;[34] these finding suggest that vasomotor dysfunction is involved in the pathogenesis of this unique syndrome
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