Abstract
Takotsubo cardiomyopathy (TTC) is characterized by sudden onset of chest pain and dyspnoea, electrocardiographic changes resembling acute myocardial infarction, slight elevation of cardiac enzymes and transient wall-motion abnormalities of the apex or midventricular myocardium, with or without antecedent stressful events, in the absence of significant coronary narrowing [1–3]. Today, it is widely believed that TTC results from an excessive release of catecholamines resulting in overstimulation of adrenergic receptors on the surface of the cardiomyocytes with consecutive non-responsiveness of the tissue to further adrenergic stimuli.
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