Makarova Yulia A, Ryabkova Varvara A, Salukhov Vladimir V, Sagun Boris V, Korovin Aleksandr E, Churilov Leonid P
Laboratory of the Microangiopathic Mechanisms of Atherogenesis, Saint Petersburg State University, 199034 Saint-Petersburg, Russia.
M.V. Chernorutsky Department of Internal Medicine (Hospital Course), Pavlov First Saint Petersburg State Medical University, 197022 Saint-Petersburg, Russia.
Diagnostics (Basel). 2023 Jan 28;13(3):478. doi: 10.3390/diagnostics13030478.
The article describes how atherosclerosis and coronavirus disease 19 (COVID-19) may affect each other. The features of this comorbid pathogenesis at various levels (vascular, cellular and molecular) are considered. A bidirectional influence of these conditions is described: the presence of cardiovascular diseases affects different individuals' susceptibility to viral infection. In turn, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) can have a negative effect on the endothelium and cardiomyocytes, causing blood clotting, secretion of pro-inflammatory cytokines, and thus exacerbating the development of atherosclerosis. In addition to the established entry into cells via angiotensin-converting enzyme 2 (ACE2), other mechanisms of SARS-CoV-2 entry are currently under investigation, for example, through CD147. Pathogenesis of comorbidity can be determined by the influence of the virus on various links which are meaningful for atherogenesis: generation of oxidized forms of low-density lipoproteins (LDL), launch of a cytokine storm, damage to the endothelial glycocalyx, and mitochondrial injury. The transformation of a stable plaque into an unstable one plays an important role in the pathogenesis of atherosclerosis complications and can be triggered by COVID-19. The impact of SARS-CoV-2 on large vessels such as the aorta is more complex than previously thought considering its impact on vasa vasorum. Current information on the mutual influence of the medicines used in the treatment of atherosclerosis and acute COVID-19 is briefly summarized.
本文描述了动脉粥样硬化与冠状病毒病19（COVID-19）可能如何相互影响。文中考虑了这种合并发病机制在各个层面（血管、细胞和分子）的特征。描述了这些病症的双向影响：心血管疾病的存在会影响不同个体对病毒感染的易感性。反过来，严重急性呼吸综合征冠状病毒2（SARS-CoV-2）会对内皮细胞和心肌细胞产生负面影响，导致血液凝固、促炎细胞因子的分泌，从而加剧动脉粥样硬化的发展。除了已确定的通过血管紧张素转换酶2（ACE2）进入细胞的途径外，目前正在研究SARS-CoV-2进入细胞的其他机制，例如通过CD147。合并症的发病机制可能由病毒对动脉粥样硬化形成有意义的各个环节的影响所决定：低密度脂蛋白（LDL）氧化形式的产生、细胞因子风暴的引发、内皮糖萼的损伤以及线粒体损伤。稳定斑块向不稳定斑块的转变在动脉粥样硬化并发症的发病机制中起重要作用，并且可能由COVID-19引发。考虑到SARS-CoV-2对滋养血管的影响，其对主动脉等大血管的影响比之前认为的更为复杂。文中简要总结了目前关于用于治疗动脉粥样硬化和急性COVID-19的药物相互影响的信息。
