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血浆肾上腺素水平及其与应激性心肌病的因果关系再探讨:得出不同结论的批判性综述

Plasma Epinephrine Level and its Causal Link to Takotsubo Syndrome Revisited: Critical Review with a Diverse Conclusion.

作者信息

Y-Hassan Shams

机构信息

Coronary Artery Disease Area, Heart and Vascular Theme, Karolinska Institute and Karolinska University Hospital, Stockholm, Sweden.

出版信息

Cardiovasc Revasc Med. 2019 Oct;20(10):907-914. doi: 10.1016/j.carrev.2018.10.026. Epub 2018 Nov 7.

DOI:10.1016/j.carrev.2018.10.026
PMID:30446399
Abstract

Takotsubo syndrome (TS) is a recognized acute cardiac syndrome with a clinical presentation resembling that of an acute coronary syndrome (ACS). The defining feature of TS is the reversible left ventricular wall motion abnormality (LVWMA), which has a unique circumferential pattern resulting in a conspicuous ballooning of the left ventricle during systole, and extending beyond the coronary artery supply territory. The pathogenesis of TS is still elusive and several pathophysiological mechanisms have been proposed. A common portrayal of the syndrome in the literature is that the disease is characterized by massive surge of plasma catecholamines including epinephrine. Based on the assumption of massive plasma epinephrine elevation, some investigators hypothesized that the circulatory plasma epinephrine plays a pivotal role in the pathogenesis of TS. One typical such hypothesis is epinephrine induced switch in signal trafficking causing apical or mid-apical ballooning in TS. In-depth analysis of the literature reveals that no study with certainty has shown "massive" plasma epinephrine elevations in TS. Furthermore, the literature evidences challenging the epinephrine-induced switch in signal trafficking are substantial. In this review, sufficient data, indicating that the plasma epinephrine in TS is either normal or moderately elevated in all studies, are provided. Noteworthy, epinephrine may act as a trigger factor for TS-induction but there is no evidence for a direct causal link between epinephrine and TS.

摘要

应激性心肌病(TS)是一种公认的急性心脏综合征,其临床表现类似于急性冠状动脉综合征(ACS)。TS的定义特征是可逆性左心室壁运动异常(LVWMA),其具有独特的圆周模式,导致左心室在收缩期明显膨出,并超出冠状动脉供血区域。TS的发病机制仍不明确,已经提出了几种病理生理机制。文献中对该综合征的常见描述是,该疾病的特征是包括肾上腺素在内的血浆儿茶胺大量激增。基于血浆肾上腺素大量升高的假设,一些研究人员推测循环血浆肾上腺素在TS的发病机制中起关键作用。一个典型的此类假设是,肾上腺素诱导信号转导转换,导致TS患者心尖或心尖中部膨出。对文献的深入分析表明,没有一项研究能确定地显示TS患者血浆肾上腺素“大量”升高。此外,有大量文献证据对肾上腺素诱导的信号转导转换提出质疑。在这篇综述中,提供了充分的数据,表明在所有研究中,TS患者的血浆肾上腺素要么正常,要么中度升高。值得注意的是,肾上腺素可能是诱发TS的触发因素,但没有证据表明肾上腺素与TS之间存在直接因果关系。

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