Department of Physiology, AIIMS Bhubaneswar, Odisha, 751019, India.
Vasc Health Risk Manag. 2022 Mar 5;18:105-112. doi: 10.2147/VHRM.S355410. eCollection 2022.
The coronavirus disease 2019 (COVID-19) pandemic caused by severe acute respiratory coronavirus 2 (SARS-CoV2) has brought out changes in our daily life and has caused severe morbidity and mortality across the globe. Especially, post covid complications may remain a threat to the patient's life. It may also increase the burden on existing health infrastructure and the country's economy. This disease affects the respiratory system and other organ systems of the body, such as the cardiovascular system. The aim of the present narrative review is to understand how COVID-19 infection deranges vascular homeostasis, leading to endothelial dysfunction and arterial stiffness in the acute phase and following infection. To this effect, definite keywords were employed to obtain relevant information using PubMed database and Google Scholar search engines. It was documented that preexisting cardiovascular disease enhances morbidity in COVID-19 patients. Moreover, an elevated risk of development of new onset cardiovascular events has also been reported. Even a small amount of myocardial injury was significantly associated with death. The presence of virus in myocardial cells has also been documented. Furthermore, endothelial dysfunction and arterial stiffness were documented in the acute phase and 3-4 weeks to 4 months after COVID infection. The virus enters endothelial cells by binding with ACE2 "receptor" on its surface and deranges cellular machinery. It results in reduced conversion of Ang II to Ang (1-7). Accumulated Ang II then activates PI3K-Akt signaling pathway and regulates endothelial activation and production of IL-6 and reactive oxygen species (ROS). An imbalance between renin angiotensin aldosterone system (RAAS) and kallikrein kinin system (KKS) also occurs, which may cause endothelial dysfunction. It is understandable that the underlying pathophysiology of this altered arterial stiffness is multifactorial, involving various cellular and immunological biomolecules.
新型冠状病毒病 2019(COVID-19)大流行是由严重急性呼吸综合征冠状病毒 2(SARS-CoV2)引起的,它改变了我们的日常生活方式,并在全球范围内造成了严重的发病率和死亡率。特别是,新冠病毒感染后并发症可能仍然对患者的生命构成威胁。它还可能增加现有卫生基础设施和国家经济的负担。这种疾病会影响呼吸系统和身体的其他器官系统,如心血管系统。本叙述性综述的目的是了解 COVID-19 感染如何扰乱血管内稳态,导致急性感染和感染后内皮功能障碍和动脉僵硬。为此,使用 PubMed 数据库和 Google Scholar 搜索引擎使用明确的关键字来获取相关信息。有文献记载,心血管疾病会增加 COVID-19 患者的发病率。此外,还报道了新发心血管事件风险增加。即使心肌损伤很小,也与死亡显著相关。心肌细胞中存在病毒也有记录。此外,在 COVID 感染后急性阶段和 3-4 周到 4 个月,也记录到内皮功能障碍和动脉僵硬。病毒通过与 ACE2 表面上的“受体”结合进入内皮细胞,扰乱细胞机制。这导致 Ang II 向 Ang(1-7)的转化减少。然后,积累的 Ang II 激活 PI3K-Akt 信号通路,并调节内皮细胞激活和白细胞介素 6 和活性氧物质(ROS)的产生。肾素血管紧张素醛固酮系统(RAAS)和激肽释放酶激肽系统(KKS)之间的平衡也会发生变化,这可能导致内皮功能障碍。可以理解的是,这种改变的动脉僵硬的潜在病理生理学是多因素的,涉及各种细胞和免疫生物分子。