Wang Xiaopu, Pei Junyu, Hu Xinqun
Department of Cardiovascular Medicine, The Second Xiangya Hospital, Central South University, Changsha, 139 Middle Renmin Road, Hu'nan 410011, China.
Cardiol Res Pract. 2020 Mar 9;2020:4150291. doi: 10.1155/2020/4150291. eCollection 2020.
Takotsubo syndrome (TTS), also known as stress cardiomyopathy, is a type of acute heart failure syndrome triggered by intense psychological or physiological stress. TTS typically manifests as acute chest pain, dyspnea or syncope that mimics an acute myocardial infarction but does not involve coronary artery obstruction. 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. In recent years, several published reports have revealed the role of this brain-heart connection in the pathogenesis of TTS. This review summarizes recent studies regarding SNS activation, catecholamine overload, and the brain-heart connection in patients with TTS from both pathophysiological and mechanistic aspects.
应激性心肌病(TTS),又称应激性心肌病,是一种由强烈心理或生理应激引发的急性心力衰竭综合征。TTS通常表现为急性胸痛、呼吸困难或晕厥,类似于急性心肌梗死,但不涉及冠状动脉阻塞。目前对应激性心肌病发病机制的认识表明,交感神经系统(SNS)激活起着核心作用。具体而言,应激可激活SNS并导致儿茶酚胺过度释放,当儿茶酚胺水平过高时,会对心肌组织产生毒性作用。然而,与应激性心肌病相关的大脑变化以及该疾病患者大脑与心脏之间的联系仍不清楚。近年来,几篇已发表的报告揭示了这种脑心联系在应激性心肌病发病机制中的作用。本综述从病理生理和机制两个方面总结了关于应激性心肌病患者交感神经系统激活、儿茶酚胺过载以及脑心联系的最新研究。