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心肌顿抑综合征的分子机制。

Molecular Mechanisms of Takotsubo Syndrome.

机构信息

Department of Cardiovascular Medicine, University of Oxford, Oxford OX1 2JD, UK.

Institute of Molecular and Translational Therapeutic Strategies, Hannover Medical School, 30625 Hannover, Germany.

出版信息

Int J Mol Sci. 2022 Oct 14;23(20):12262. doi: 10.3390/ijms232012262.

Abstract

Takotsubo syndrome (TTS) is a severe but reversible acute heart failure syndrome that occurs following high catecholaminergic stress. TTS patients are similar to those with acute coronary syndrome, with chest pain, dyspnoea and ST segment changes on electrocardiogram, but are characterised by apical akinesia of the left ventricle, with basal hyperkinesia in the absence of culprit coronary artery stenosis. The pathophysiology of TTS is not completely understood and there is a paucity of evidence to guide treatment. The mechanisms of TTS are thought to involve catecholaminergic myocardial stunning, microvascular dysfunction, increased inflammation and changes in cardiomyocyte metabolism. Here, we summarise the available literature to focus on the molecular basis for the pathophysiology of TTS to advance the understanding of the condition.

摘要

心尖球形综合征(TTS)是一种严重但可逆转的急性心力衰竭综合征,发生在高儿茶酚胺应激之后。TTS 患者与急性冠状动脉综合征患者相似,表现为胸痛、呼吸困难和心电图 ST 段改变,但特征为左心室心尖部无运动,基底段运动亢进,不存在罪犯冠状动脉狭窄。TTS 的病理生理学尚不完全清楚,缺乏治疗的证据。TTS 的机制被认为涉及儿茶酚胺性心肌顿抑、微血管功能障碍、炎症增加和心肌细胞代谢改变。在这里,我们总结了现有的文献,重点关注 TTS 病理生理学的分子基础,以促进对该疾病的认识。

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Molecular Mechanisms of Takotsubo Syndrome.心肌顿抑综合征的分子机制。
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