Laboratory of Experimental Cardiology, Cardiology Research Institute, Tomsk National Research Medical Center of the RAS, Tomsk, Russian Federation.
Department of Pathology, University of Kentucky College of Medicine, Lexington, KY 40506, United States.
Curr Cardiol Rev. 2021;17(2):188-203. doi: 10.2174/1573403X16666200129114330.
The purpose of the review is the analysis of clinical and experimental data on the etiology and pathogenesis of takotsubo syndrome (TS). TS is characterized by contractile dysfunction, which usually affects the apical region of the heart without obstruction of coronary artery, moderate increase in myocardial necrosis markers, prolonged QTc interval (in 50% of patients), sometimes elevation of ST segment (in 19% of patients), increase N-Terminal Pro-B-Type Natriuretic Peptide level, microvascular dysfunction, sometimes spasm of the epicardial coronary arteries (in 10% of patients), myocardial edema, and life-threatening ventricular arrhythmias (in 11% of patients). Stress cardiomyopathy is a rare disease, it is observed in 0.6 - 2.5% of patients with acute coronary syndrome. The occurrence of takotsubo syndrome is 9 times higher in women, who are aged 60-70 years old, than in men. The hospital mortality among patients with TS corresponds to 3.5% - 12%. Physical or emotional stress do not precede disease in all patients with TS. Most of patients with TS have neurological or mental illnesses. The level of catecholamines is increased in patients with TS, therefore, the occurrence of TS is associated with excessive activation of the adrenergic system. The negative inotropic effect of catecholamines is associated with the activation of β2 adrenergic receptors. An important role of the adrenergic system in the pathogenesis of TS is confirmed by studies which were performed using 125I-metaiodobenzylguanidine (125I -MIBG). TS causes edema and inflammation of the myocardium. The inflammatory response in TS is systemic. TS causes impaired coronary microcirculation and reduces coronary reserve. There is a reason to believe that an increase in blood viscosity may play an important role in the pathogenesis of microcirculatory dysfunction in patients with TS. Epicardial coronary artery spasm is not obligatory for the occurrence of TS. Cortisol, endothelin-1 and microRNAs are challengers for the role of TS triggers. A decrease in estrogen levels is a factor contributing to the onset of TS. The central nervous system appears to play an important role in the pathogenesis of TS.
本综述的目的是分析 Takotsubo 综合征（TS）的病因和发病机制的临床和实验数据。TS 的特征是收缩功能障碍，通常影响心脏的心尖区域，而没有冠状动脉阻塞，心肌坏死标志物中度增加，QTc 间期延长（在 50%的患者中），有时 ST 段抬高（在 19%的患者中），N 端脑利钠肽前体水平升高，微血管功能障碍，有时心外膜冠状动脉痉挛（在 10%的患者中），心肌水肿和危及生命的室性心律失常（在 11%的患者中）。应激性心肌病是一种罕见的疾病，在急性冠状动脉综合征患者中观察到 0.6-2.5%。TS 在女性中的发生率高于男性，年龄在 60-70 岁之间，是男性的 9 倍。TS 患者的住院死亡率为 3.5%-12%。并非所有 TS 患者在发病前都有身体或情绪上的压力。大多数 TS 患者患有神经或精神疾病。TS 患者的儿茶酚胺水平升高，因此，TS 的发生与肾上腺素能系统的过度激活有关。儿茶酚胺的负性肌力作用与β2 肾上腺素能受体的激活有关。使用 125I-间位碘苄胍（125I-MIBG）进行的研究证实了肾上腺素能系统在 TS 发病机制中的重要作用。TS 引起心肌水肿和炎症。TS 的炎症反应是全身性的。TS 导致冠状动脉微循环受损并降低冠状动脉储备。有理由相信，血液粘度的增加可能在 TS 患者的微循环功能障碍发病机制中起重要作用。心外膜冠状动脉痉挛不是 TS 发生的必然条件。皮质醇、内皮素-1 和 microRNAs 是 TS 触发因素的挑战。雌激素水平降低是 TS 发病的一个因素。中枢神经系统似乎在 TS 的发病机制中起着重要作用。
