Pathomechanisms of SARS-CoV-2 infection and development of atherosclerosis in patients with COVID-19: A review

Abstract

The pandemic of coronavirus disease 2019 (COVID-19) has posed a major health challenge for over 2 years. The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) that causes it belongs to single-stranded ribonucleic acid viruses and causes acute respiratory distress syndrome. The initial outbreak was discovered in December 2019 in Wuhan province, where SARS-CoV-2 quickly spread to other countries. In addition to respiratory disorders, it has been shown that during and after COVID-19 infection, cardiovascular diseases are often developed or exacerbated, such as: arterial hypertension, coronary artery disease, arrhythmias, heart failure and thromboembolic complications. In view of the higher prevalence of atherosclerosis in patients with COVID-19, we described the pathomechanisms of the development of this infection and the possible correlations between SARS-CoV-2 infection and thromboembolic complications. We focused on the role of the inflammatory response, renin-angiotensin system and endothelial dysfunction in the development of atherosclerosis in patients with COVID-19. A thorough understanding of the hemodynamic mechanisms and the impact of the infection on the cardiovascular system will allow for the proper selection of appropriate therapy in patients after SARS-CoV-2 infection.Abbreviations: ACE2 = angiotensin-converting enzyme 2, ACS = acute coronary syndromes, ARDS = acute respiratory distress syndrome, COVID-19 = coronavirus disease 2019, EC = endothelial cells, IL-10 = interleukin 10, IL-1β = interleukin 1 β, IL-6 = interleukin 6, NO = nitric oxide, SARS-CoV-2 = severe acute respiratory syndrome coronavirus 2, TNFα = tumor necrosis factor α.

COVID-19 and metabolic syndrome

“…Variety of pathogenic mechanisms by which COVID-19 could accelerate atherosclerosis has been proposed [38] . Endothelial dysfunction and atherosclerotic plaque instability can lead to plaque rupture and atherothrombosis [27] .…”

Molecular Linkage between Immune System Disorders and Atherosclerosis

“…During COVID-19 infection, on the basis of excessive activity of the RAA system, vasoconstriction, as well as the expansion of the inflammatory process and remodeling of the vessel wall occur, which, combined with the emerging hypertension, provide us with a whole range of risk factors for atherosclerosis. On top of this, other abnormalities may arise, such as hypernatremia, hypokalemia, accelerated tissue fibrosis, tissue inflammation, and tissue proliferation [84,85].…”

“…The cytokine storm initiated by SARS-CoV-2 leads to the exposure of the deeper layers of the vasculature, and the adhesion factors located in there combine with immune cells and platelets to form clots. The result of the cytokine storm is the formation of disseminated intravascular coagulation (DIC) syndrome, which further stimulates interleukin production that amplifies the cytokine storm therefore forming a vicious circle [84][85][86].…”

Evidence of Autoinflammation as the Principal Mechanism of Myocardial Injury in SARS-CoV-2 PCR-Positive Autopsy Hearts

“…The mechanism of cardiac injury in patients dying of SARS-CoV-2 after severe respiratory illness followed by cardiovascular complications is controversial. Direct viral infection as well as various indirect causes have been postulated (2)(3)(4)(5)(6)(7). A recent study comparing 153,760 US SARS-C0V-2 infected veterans to a large cohort of normal controls showed the risk of cardiovascular outcomes hazard ratio for any prespeci ed cardiovascular outcomes regardless of acute presentation was 1.63 ± 0.09 (2).…”

“…Many patients infected with this virus develop cardiovascular (CV) complications including myocardial infarctions, stroke, arrhythmia, heart failure, and sudden cardiac death. Speci cally, patients with SARS-CoV-2 have a high prevalence of severe myocardial injury (20-28%) (2)(3)(4). The mechanism of cardiac injury in patients dying of SARS-CoV-2 after severe respiratory illness followed by cardiovascular complications is controversial.…”