Key result
A bidirectional relationship exists between atherosclerosis and COVID-19, where cardiovascular disease increases viral susceptibility and SARS-CoV-2 exacerbates atherogenesis and plaque instability.
Why the study?
The bidirectional pathophysiological interactions between atherosclerosis and COVID-19 at the vascular, cellular, and molecular levels required comprehensive description.
COVID-19 and atherosclerosis share a comorbid pathogenesis with bidirectional influences, where SARS-CoV-2 infection can exacerbate atherogenesis and trigger plaque instability.
May guide risk stratification in comorbid patients; leaves open causal mechanisms and need for prospective validation.
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.
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Makarova et al. (2023) conducted a review in Atherosclerosis and COVID-19. COVID-19 and Atherosclerosis was evaluated. A bidirectional relationship exists between atherosclerosis and COVID-19, where cardiovascular disease increases viral susceptibility and SARS-CoV-2 exacerbates atherogenesis and plaque instability.
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