2022
DOI: 10.1016/j.cpcardiol.2021.100992
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COVID-19 and Peripheral Artery Thrombosis: A Mini Review

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Cited by 6 publications
(6 citation statements)
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“…Thrombolytic drugs are a potential treatment for COVID-19 thrombotic complications ( 80 , 81 ) and ARDS ( 82 ). In China, drugs commonly used for thrombolytic therapy include urokinase, streptokinase, and rt-PA, which promote fibrinolysis by activating plasminogen ( Table 2 , row 13-15).…”
Section: Discussionmentioning
confidence: 99%
“…Thrombolytic drugs are a potential treatment for COVID-19 thrombotic complications ( 80 , 81 ) and ARDS ( 82 ). In China, drugs commonly used for thrombolytic therapy include urokinase, streptokinase, and rt-PA, which promote fibrinolysis by activating plasminogen ( Table 2 , row 13-15).…”
Section: Discussionmentioning
confidence: 99%
“…Similar to other coronaviruses, a significant association has been found between COVID-19 and the risk of thrombosis. A meta-analysis found that arterial thrombosis occurs in 4.4% of cases ( 14 ). The pathophysiology of thromboembolism in COVID-19 involves several aspects.…”
Section: Discussionmentioning
confidence: 99%
“…Given the complexity and multifactor dependence of the mechanism, the aetiology of hypercoagulopathy in Covid‐19 is not precisely explained. Downregulation of ACE2 by SARS‐CoV‐2 and subsequent Ang II accumulation, 167 pneumonia‐induced hypoxia, 168 and release of neutrophil extracellular traps (NETs) 169 are among proposed mechanisms for the condition. However, endotheliopathy and massive inflammatory response have been indicated as two main features of prothrombotic presentations associated with Covid‐19.…”
Section: The Indirect Effects On the Nervous Systemmentioning
confidence: 99%
“…166 Given the complexity and multifactor dependence of the mechanism, the aetiology of hypercoagulopathy in Covid-19 is not precisely explained. Downregulation of ACE2 by SARS-CoV-2 and subsequent Ang II accumulation, 167 pneumonia-induced hypoxia, 168 and release of neutrophil extracellular traps (NETs) 169 stimulates neutrophils to release excessive NETs, all resulting in a higher coagulable condition. 175 Taken together, infection-triggered complement hyperactivation induces a maladaptive inflammatory and coagulatory response, which in turn, feeds back and amplifies complement activation and clot formation.…”
Section: Hypercoagulable Statementioning
confidence: 99%