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新冠病毒病(COVID-19)致有心血管病史老年患者心血管系统损伤机制

Mechanisms of Cardiovascular System Injury Induced by COVID-19 in Elderly Patients With Cardiovascular History.

作者信息

Yang Yaliu, Yan Mengwen

机构信息

Department of Cardiology, China-Japan Friendship Hospital, Beijing, China.

出版信息

Front Cardiovasc Med. 2022 May 4;9:859505. doi: 10.3389/fcvm.2022.859505. eCollection 2022.

DOI:10.3389/fcvm.2022.859505
PMID:35600485
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9116509/
Abstract

The coronavirus disease-2019 (COVID-19) pandemic, caused by severe acute respiratory syndrome coronavirus (SARS-CoV-2), represents a great threat to healthcare and socioeconomics worldwide. In addition to respiratory manifestations, COVID-19 promotes cardiac injuries, particularly in elderly patients with cardiovascular history, leading to a higher risk of progression to critical conditions. The SARS-CoV-2 infection is initiated as virus binding to angiotensin-converting enzyme 2 (ACE2), which is highly expressed in the heart, resulting in direct infection and dysregulation of the renin-angiotensin system (RAS). Meanwhile, immune response and hyper-inflammation, as well as endothelial dysfunction and thrombosis implicate in COVID-19 infection. Herein, we provide an overview of the proposed mechanisms of cardiovascular injuries in COVID-19, particularly in elderly patients with pre-existing cardiovascular diseases, aiming to set appropriate management and improve their clinical outcomes.

摘要

由严重急性呼吸综合征冠状病毒2(SARS-CoV-2)引起的2019冠状病毒病(COVID-19)大流行对全球医疗保健和社会经济构成了巨大威胁。除了呼吸道表现外,COVID-19还会引发心脏损伤,尤其是在有心血管病史的老年患者中,导致病情进展至危急状态的风险更高。SARS-CoV-2感染始于病毒与血管紧张素转换酶2(ACE2)结合,ACE2在心脏中高度表达,导致直接感染和肾素-血管紧张素系统(RAS)失调。同时,免疫反应和过度炎症,以及内皮功能障碍和血栓形成也与COVID-19感染有关。在此,我们概述了COVID-19中心血管损伤的潜在机制,特别是在已有心血管疾病的老年患者中,旨在制定适当的管理措施并改善其临床结局。

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本文引用的文献

1
Dyslipidemia Increases the Risk of Severe COVID-19: A Systematic Review, Meta-analysis, and Meta-regression.血脂异常增加重症 COVID-19 的风险:一项系统评价、荟萃分析和元回归分析
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Structural basis for SARS-CoV-2 Delta variant recognition of ACE2 receptor and broadly neutralizing antibodies.SARS-CoV-2 Delta 变体识别 ACE2 受体和广谱中和抗体的结构基础。
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Commentary: Effect of Angiotensin-Converting-Enzyme Inhibitor and Angiotensin II Receptor Antagonist Treatment on ACE2 Expression and SARS-CoV-2 Replication in Primary Airway Epithelial Cells.
评论:血管紧张素转换酶抑制剂和血管紧张素II受体拮抗剂治疗对原代气道上皮细胞中ACE2表达及新型冠状病毒复制的影响
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4
The interacting physiology of COVID-19 and the renin-angiotensin-aldosterone system: Key agents for treatment.新型冠状病毒肺炎与肾素-血管紧张素-醛固酮系统的相互作用生理学:治疗的关键药物。
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Non-severe COVID-19 is associated with endothelial damage and hypercoagulability despite pharmacological thromboprophylaxis.非重症 COVID-19 与内皮损伤和高凝状态有关,尽管进行了药物性血栓预防。
J Thromb Haemost. 2022 Apr;20(4):1008-1014. doi: 10.1111/jth.15660. Epub 2022 Feb 13.
7
Sequelae and Comorbidities of COVID-19 Manifestations on the Cardiac and the Vascular Systems.新冠病毒病在心脏和血管系统表现的后遗症及合并症
Front Physiol. 2022 Jan 14;12:748972. doi: 10.3389/fphys.2021.748972. eCollection 2021.
8
Endothelial Dysfunction in Covid-19 Infection.新型冠状病毒感染中的血管内皮功能障碍。
Am J Med Sci. 2022 Apr;363(4):281-287. doi: 10.1016/j.amjms.2021.12.010. Epub 2022 Jan 31.
9
Post-COVID-19 patients show an increased endothelial progenitor cell production.新冠康复患者的内皮祖细胞生成增加。
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10
Calcium Signaling Pathway Is Involved in the Shedding of ACE2 Catalytic Ectodomain: New Insights for Clinical and Therapeutic Applications of ACE2 for COVID-19.钙信号通路参与 ACE2 催化结构域的脱落:ACE2 在 COVID-19 临床和治疗应用中的新见解。
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