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Review
. 2023 Jan 28;13(3):478.
doi: 10.3390/diagnostics13030478.

Atherosclerosis, Cardiovascular Disorders and COVID-19: Comorbid Pathogenesis

Yulia A Makarova  1 , Varvara A Ryabkova  1   2 , Vladimir V Salukhov  3 , Boris V Sagun  3 , Aleksandr E Korovin  1   3 , Leonid P Churilov  1   4
Affiliations
Review

Atherosclerosis, Cardiovascular Disorders and COVID-19: Comorbid Pathogenesis

Yulia A Makarova et al. Diagnostics (Basel). .

Abstract

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.

Keywords: COVID-19; atheroma; atherosclerosis; autoimmunity; cardiovascular system; cytokines; endothelium; inflammation; lipoproteins; renin-angiotensin system; vasa vasorum.

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Conflict of interest statement

The authors declare no conflict of interest. The funders had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript; or in the decision to publish the results.

Figures

Figure 1
Figure 1
The relationship between potential mechanisms of acute cardiac injury in COVID-19 with the focus on pro-inflammatory autacoids.
Figure 2
Figure 2
Mutual potentiation of the main pathophysiological mechanisms triggered by SARS-CoV-2 in case of damage to the cardiovascular system.
See this image and copyright information in PMC

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