2020
DOI: 10.1590/1806-9282.66.3.366
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Viral infections and atherothrombosis: Another caution in the wake of COVID-19?

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Cited by 8 publications
(5 citation statements)
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“…The neurological involvement in this case was not discovered until Day 26 postinfection, which highlights the importance of clinical values, such as NLR, lymphocyte-to-CRP ratio (LCRPR), and lymphocyte-to-platelet ratio (LPR), as prognostic indicators of severe inflammation and possible neurological complications. Other studies have shown that COVID-19-induced severe inflammation and inflammatory infiltrates consisting of T cells, macrophages, and neutrophils contribute to the rupture of atheromatous plaques in patients with pre-existing atheromatous disease due to the production of proteolytic enzymes and endothelial cell disruption [99][100][101]. Although the use of protease inhibitors in these patients may be beneficial, they should be carefully used as they may promote SARS-CoV-2-induced hypercoagulation.…”
Section: Cerebrovascular Diseasesmentioning
confidence: 99%
“…The neurological involvement in this case was not discovered until Day 26 postinfection, which highlights the importance of clinical values, such as NLR, lymphocyte-to-CRP ratio (LCRPR), and lymphocyte-to-platelet ratio (LPR), as prognostic indicators of severe inflammation and possible neurological complications. Other studies have shown that COVID-19-induced severe inflammation and inflammatory infiltrates consisting of T cells, macrophages, and neutrophils contribute to the rupture of atheromatous plaques in patients with pre-existing atheromatous disease due to the production of proteolytic enzymes and endothelial cell disruption [99][100][101]. Although the use of protease inhibitors in these patients may be beneficial, they should be carefully used as they may promote SARS-CoV-2-induced hypercoagulation.…”
Section: Cerebrovascular Diseasesmentioning
confidence: 99%
“…COVID-19 inflammation induces a prothrombotic milieu among patients who are at risk of vascular events and those with the pre-existing atheromatous disease. Among patients with coronary disease, evidence suggests that virally induced inflammatory infiltrates such as T cells, macrophages, and neutrophils populate the atheromatous plaque leading to a cascade of events including vascular permeability, endothelial disruption, and exposure of prothrombotic elements such as collagen, tissue factor, and platelet adhesion molecules, which all play a role in thrombogenesis (68). Furthermore, it is known that carotid artery plaques with features of a thin fibrous cap, large core lipid, intraplaque bleeding, and the abundance of monocyte-derived macrophages and activated smooth muscle cells cause instability and vulnerability to plaque rupture (69).…”
Section: Inflammation-induced Plaque Progression and Vulnerabilitymentioning
confidence: 99%
“…The COVID-19-induced severe inflammation and inflammatory infiltrate consisting of T cells, macrophages and neutrophils contribute to the rupture of atheromatous plaques in patients with pre-existing atheromatous disease due to the production of proteolytic enzymes and endothelial cell disruption [60].…”
Section: авторmentioning
confidence: 99%