Abstract
Takotsubo syndrome (TTS) typically manifests as acute chest pain and/or dyspnea triggered by intense psychological or physiological stress that mimics an acute myocardial infarction [1]. The current understanding of the pathogenesis of TTS suggests that sympathetic nervous system (SNS) activation plays a central role. Specifically, stress can activate the SNS and lead to the over-release of catecholamine, which have toxic effects on myocardial tissue when present at excessive levels. However, the brain changes associated with TTS and the connection between the brain and the heart in patients with this disease remain unclear [2].
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