**1. Introduction**

The *Takotsubo* syndrome (TTS), first described in 1990 by Sato et al., is a transient cardiac dysfunction characterised by a variety of ventricular wall-motion abnormalities [1, 2]. Its name is derived from the resemblance of the left ventricle at end-systole to the octopus-pots of Japanese fishermen in the Hiroshima fish markets [3]; however, alternative nomenclatures such as stress or stress-induced cardiomyopathy, apical ballooning syndrome and 'broken heart syndrome' have also been used to label this usually reversible form of acute heart failure [4–7]. This clinical entity essentially mimics an acute coronary syndrome, wherein patients

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present with acute chest pain, and demonstrates the typical biomarker profile (release of cardiac troponin and creatine kinase) and/or electrocardiographic abnormalities suggesting significant coronary stenosis. Interestingly, the distinguishing factor in Takotsubo syndrome is the absence of an occlusive coronary vascular disease, which correlates with these changes [8]. Although, the pathophysiology of this disorder remains unclear, recent hypotheses have suggested a form of acute catecholaminergic myocardial stunning to explain the pattern of temporary LV dysfunction and regional wall-motion abnormality commonly seen at the time of presentation [9].
