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应激性心肌病患者室性心律失常的发病机制及其对长期预后的影响

Pathogenesis of Ventricular Arrhythmias and Its Effect on Long-Term Prognosis in Patients With Takotsubo Cardiomyopathy.

作者信息

Pena Escobar Julio A, Aung Myat, Amin Saba, Gulraiz Azouba, Gandhi Fenil R, Malik Bilal Haider

机构信息

Internal Medicine, California Institute of Behavioral Neurosciences & Psychology, Fairfield, USA.

Medicine, California Institute of Behavioral Neurosciences & Psychology, Fairfield, USA.

出版信息

Cureus. 2020 Oct 26;12(10):e11171. doi: 10.7759/cureus.11171.

Abstract

Takotsubo cardiomyopathy (TTC), also known as broken heart syndrome, stress cardiomyopathy (SCM), or apical ballooning syndrome, is a non-ischemic cardiac disease with an initial clinical presentation that is very similar to acute coronary syndrome (ACS). Ventricular arrhythmias (VAs) contribute significantly to an increase in the rates of death in patients with TTC, especially during the acute phase, in which patients with TTC are more susceptible to develop life-threatening arrhythmias (LTA) such as ventricular tachycardia (VT), ventricular fibrillation (VF), torsades de pointes (TdP), and sudden cardiac death (SCD). However, the pathophysiology of TTC and how VA occurs are still a mystery. We aim to review previous literature and discuss the possible mechanisms of VA in TTC patients. VA usually complicates the acute phase of the disease and worsens the long-term prognosis. Alterations of repolarization (negative T wave, prolonged QTc) indicate a high risk of arrhythmic events (TdP, VT, VF, and SCD). Catecholamine effect on myocardial cells and myocardial edema can create a substrate for the development of VA. Some of the most commonly proposed mechanisms for the development of VA in patients with TTC are coronary vasospasm, myocardial stunning due to catecholamines, re-entry, and triggered activity. Further prospective studies, including a more significant number of patients, are required to understand the disease's pathophysiology better and improve LTA management in patients with TTC.

摘要

应激性心肌病(TTC),也被称为心碎综合征、应激性心肌病(SCM)或心尖球囊样综合征,是一种非缺血性心脏病,其初始临床表现与急性冠状动脉综合征(ACS)非常相似。室性心律失常(VA)显著导致TTC患者死亡率增加,尤其是在急性期,在此期间TTC患者更容易发生危及生命的心律失常(LTA),如室性心动过速(VT)、心室颤动(VF)、尖端扭转型室性心动过速(TdP)和心源性猝死(SCD)。然而,TTC的病理生理学以及VA如何发生仍是个谜。我们旨在回顾既往文献并讨论TTC患者发生VA的可能机制。VA通常使疾病急性期复杂化并恶化长期预后。复极改变(负向T波、QTc延长)表明心律失常事件(TdP、VT、VF和SCD)风险高。儿茶酚胺对心肌细胞的作用和心肌水肿可形成VA发生的基础。TTC患者发生VA最常被提出的一些机制是冠状动脉痉挛、儿茶酚胺导致的心肌顿抑、折返和触发活动。需要进一步的前瞻性研究,包括纳入更多患者,以更好地理解该疾病的病理生理学并改善TTC患者的LTA管理。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dd0b/7689872/0c981be5c04f/cureus-0012-00000011171-i01.jpg

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