2021
DOI: 10.1016/j.jvs.2021.07.131
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Toward a unified pathophysiology in COVID-19 acute aortopathies

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Cited by 4 publications
(3 citation statements)
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“…Moreover, Strazzulla et al [ 12 ] discovered that the total number of neutrophils (OR:1.20; 95% CI:1.04–1.40; p = 0.01) and lymphocytes (OR:0.45; 95% CI:0.23–0.86; p = 0.01) were independently associated with acute pulmonary embolism a cohort of 184 COVID-19 patients. Furthermore, Roncati L. et al explained the influence of an abnormal inflammatory response in severe COVID-19 patients on pro-coagulant status through platelet release [ 56 , 57 , 58 ].…”
Section: Discussionmentioning
confidence: 99%
“…Moreover, Strazzulla et al [ 12 ] discovered that the total number of neutrophils (OR:1.20; 95% CI:1.04–1.40; p = 0.01) and lymphocytes (OR:0.45; 95% CI:0.23–0.86; p = 0.01) were independently associated with acute pulmonary embolism a cohort of 184 COVID-19 patients. Furthermore, Roncati L. et al explained the influence of an abnormal inflammatory response in severe COVID-19 patients on pro-coagulant status through platelet release [ 56 , 57 , 58 ].…”
Section: Discussionmentioning
confidence: 99%
“…In fact, it has been estimated that over 30% of patients admitted to intensive care with COVID-19 suffer from systemic thromboembolism, including from aortic thrombi ( Klok et al, 2020 , Buikema et al, 2021 ). In addition, the infection often leads to thrombosis in non-atherosclerotic vessels ( de Roquetaillade et al, 2021 ): this occurrence is likely mediated by the viral-induced apoptosis of vascular endothelial cells and subsequent mononuclear infiltration with development of a severe leukocytoclastic vasculitis; newly formed antiphospholipid antibodies along with COVID-19-coagulopathy then promote local vascular thromboses ( Roncati et al, 2021 ). Nevertheless, aortic thrombosis could also be an innocent bystander in the case of acute ischemic stroke, even in COVID-19 patients ( Kashi et al, 2020 ).…”
Section: Discussionmentioning
confidence: 99%
“…Aneurysms can increase in size owing to activated metalloproteinases, and typically in the aorta, can result in vasa vasorum thrombosis, increasing the risk of rupture. 6 Similarly, in cardiomyocytes, COVID-19 virions will accelerate their apoptosis, followed by myocardial invasion of inflammatory cells, typically lymphocytes. The consequent myocarditis favors the occurrence of dysrhythmia, decreases the ventricles’ ejection fraction, and can lead to a secondary myocardial fibrosis.…”
mentioning
confidence: 99%