tetano
Editor, Senior Moderator
Int J Cardiol
. 2020 Nov 9;S0167-5273(20)34090-0.
doi: 10.1016/j.ijcard.2020.11.016. Online ahead of print.
From angiotensin-converting enzyme 2 disruption to thromboinflammatory microvascular disease: A paradigm drawn from COVID-19
R Vinci[SUP] 1 [/SUP], D Pedicino[SUP] 2 [/SUP], F Andreotti[SUP] 3 [/SUP], G Russo[SUP] 4 [/SUP], A D'Aiello[SUP] 1 [/SUP], R De Cristofaro[SUP] 5 [/SUP], F Crea[SUP] 4 [/SUP], G Liuzzo[SUP] 4 [/SUP]
Affiliations
Abstract
We concisely review the 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.
Keywords: 2019 coronavirus; Complement; Renin-angiotensin system; Thromboinflammatory microangiopathy; von Willebrand factor.
. 2020 Nov 9;S0167-5273(20)34090-0.
doi: 10.1016/j.ijcard.2020.11.016. Online ahead of print.
From angiotensin-converting enzyme 2 disruption to thromboinflammatory microvascular disease: A paradigm drawn from COVID-19
R Vinci[SUP] 1 [/SUP], D Pedicino[SUP] 2 [/SUP], F Andreotti[SUP] 3 [/SUP], G Russo[SUP] 4 [/SUP], A D'Aiello[SUP] 1 [/SUP], R De Cristofaro[SUP] 5 [/SUP], F Crea[SUP] 4 [/SUP], G Liuzzo[SUP] 4 [/SUP]
Affiliations
- PMID: 33181158
- DOI: 10.1016/j.ijcard.2020.11.016
Abstract
We concisely review the 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.
Keywords: 2019 coronavirus; Complement; Renin-angiotensin system; Thromboinflammatory microangiopathy; von Willebrand factor.