Abstract
One of the hallmarks of the SARS-CoV-2 infection has been the inflammatory process that played a role in its pathogenesis, resulting in mortality within susceptible individuals. This uncontrolled inflammatory process leads to severe systemic symptoms via multiple pathways; however, the role of endothelial dysfunction and thrombosis have not been truly explored. This review aims to highlight the pathogenic mechanisms of these inflammatory triggers leading to thrombogenic complications. There are direct and indirect pathogenic pathways of the infection that are examined in detail. We also describe the case of carotid artery thrombosis in a patient following SARS-CoV-2 infection while reviewing the literature on the role of ACE2, the endothelium, and the different mechanisms by which SARS-CoV-2 may manifest both acutely and chronically. We also highlight differences from the other coronaviruses that have made this infection a pandemic with similarities to the influenza virus.
Highlights
The clinical therapeutics that have been suggested in the course of SARS-CoV-2 infection have immediately noted the uncontrolled inflammatory process as an important hurdle to overcome
This evidence strongly suggested that SARS-CoV-2 infection, involving epithelial cells in the lungs and airways of patients with COVID-19 who progressed toward respiratory failure, could be identified during the acute stage of lung injury and was absent in the organizing stage [101]
The studies reporting autopsy findings were scarce in number, the vascular features identified were consistent with the presence of distinctive cardiac, pulmonary vascular, and endothelial pathobiological features in these cases of COVID-19 [28,100–104]
Summary
The clinical therapeutics that have been suggested in the course of SARS-CoV-2 infection have immediately noted the uncontrolled inflammatory process as an important hurdle to overcome. We describe the case of a carotid artery thrombosis that occurred in a patient with COVID-19 to highlight endothelial dysfunction during. We believe that the data presented in this overview could provide a basis for understanding the role of endothelial dysfunction and assist virologists and health providers (family doctors, internists, cardiologists, and intensivists) in the physician–patient discussion about the risks and expectations after the involvement of the endothelium in SARS-CoV-2 infection. Computed tomography (CT) and magnetic resonance imaging (MRI) revealed an ischemic stroke at the junction of the perfusion territories of the left anterior cerebral artery (ACA) and the left middle cerebral artery (MCA). (D): MRI brain diffusion-weighted imaging showing punctiform lesions in hypersignal diffusion visible in left fronto-parietal FLAIR at the level of the left ACA-MCA territory, with decreased apparent diffusion coefficient. Abbreviation: ACA, anterior cerebral artery; CT, computed tomography; MCA, middle cerebral artery; MRI, magnetic resonance
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