The pathogenesis of takotsubo syndrome (TS) has not been established yet. The literature data dealing with the pathogenesis of TS are abundant but scattered among different medical specialities. Subarachnoid hemorrhage and other acute intracranial diseases and injuries are among the important and currently well-recognized trigger factors for TS. In both induced and spontaneous subarachnoid hemorrhages, signs suggestive of increased cardiac sympathetic overactivity have been documented. Surgical and pharmacological sympathectomy has shown to have protective cardiac effects in both animal and human studies. Increase in local release of norepinephrine from the heart of patients with TS has been measured. Signs of both cardiac sympathetic denervation and myocardial lesions adjacent to the cardiac nerve terminals have been seen. Furthermore, the systematized and typically circumferential pattern of ventricular wall motion abnormality is incongruent with the coronary artery supply region and appears most likely to follow the cardiac sympathetic nerve distribution. In conclusion, compelling literature data support the hypothesis that acute cardiac sympathetic disruption and norepinephrine seethe and spillover is causing TS in predisposed patients. TS is most probably an acute cardiac sympathetic disease entity causing myocardial stunning in which takotsubo is one among other cardiac image study findings. 1. Introduction Takotsubo syndrome (TS), also known as neurogenic stunned myocardium, is characterized by a constellation of certain clinical findings: a clinical presentation mimicking that of acute coronary syndrome, a reversible typically regional ventricular wall motion abnormality with a peculiar circular pattern that does not match with the coronary artery supply region, and a coronary angiography showing no identifiable coronary artery culprit lesion to account for the observed regional ventricular wall motion abnormality [1–7]. The condition may occur in the setting of severe emotional stress, often after the sudden death of a loved one—hence the alternative name “broken heart syndrome” [3, 8]. Countless physical stress factors ranging from the most severe diseases to the most physiological processes may trigger the disease [5, 6, 9–11]. Among the diseases and injuries, which have provided a great contribution to the understanding of the pathogenicity of TS and are currently well-recognized trigger factors for TS, are the induced (animal), spontaneous (human) subarachnoid hemorrhage, brain death, and other intracranial processes [2, 12–22]. In this
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