Journal
INTERNATIONAL JOURNAL OF CARDIOLOGY
Volume 326, Issue -, Pages 243-247Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.ijcard.2020.11.016
Keywords
2019 coronavirus; Renin-angiotensin system; Thromboinflammatoty microangiopathy; Complement; von Willebrand factor
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This study concisely reviews the clinical, autopsy, experimental, and molecular data of COVID-19, and highlights the disruption of ACE2 and thromboinflammatory microangiopathy as distinctive features. The entry of the virus into microvessels may trigger significant inflammatory reactions, including thrombosis and organ damage.
We concisely review clinical, autopsy, experimental and molecular data of 2019 coronavirus disease (COVID-19). Angiotensin-converting enzyme 2 disruption and thromboinflammatory microangiopathy emerge as distinctive features. Briefly, entry of the virus into microvessels can profoundly disrupt the local renin-angiotensin system, cause endothelial injury, activate the complement cascade and induce powerful thromboinflammatory reactions, involving, in particular, von Willebrand factor, that, if widespread, may lead to microvascular plugging, ischemia and, ultimately, organ failure. We believe the current COVID-19 data consolidate a widely unrecognised paradigm of potentially fatal thromboinflammatory microvascular disease. (C) 2020 Elsevier B.V. All rights reserved.
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