From angiotensin-converting enzyme 2 disruption to thromboinflammatory microvascular disease: A paradigm drawn from COVID-19. (1st March 2021)

• Record Type: Journal Article
• Authors: Vinci, R.; Pedicino, D.; Andreotti, F.; Russo, G.; D'Aiello, A.; De Cristofaro, R.; Crea, F.; Liuzzo, G.
• Is Part Of: International journal of cardiology. Volume 326(2021)
• Page Start: 243
• Page End: 247
• Publication Date: 2021-03-01
• Subjects: 2019 coronavirus -- Renin-angiotensin system -- Thromboinflammatory microangiopathy -- Complement -- von Willebrand factor; ACE angiotensin-converting enzyme -- ACEI ACE inhibitors -- ANG angiotensin -- ARB angiotensin receptor blocker -- C complement component -- CCL C-C-motif chemokine ligand -- CD cluster of differentiation -- COVID-19 2019 coronavirus disease -- CRP C-reactive protein -- GCSF granulocyte-colony stimulating factor -- ICU intensive care unit -- IFN interferon -- IL interleukin -- IP interferon-gamma inducible protein -- MIP macrophage inflammatory protein -- MAC membrane attack complex -- MCP monocyte chemoattractant protein -- NO nitric oxide -- PAI-1 plasminogen activator inhibitor-1 -- PCT procalcitonin -- RAS renin-angiotensin system -- SARS-CoV severe acute respiratory syndrome coronavirus -- TF tissue factor -- TMPRSS2 transmembrane serine protease type II -- TNF tumor necrosis factor -- t-PA tissue-type plasminogen activator -- VWF von Willebrand factor; Cardiology -- Periodicals; Electronic journals; 616.12
• DOI: 10.1016/j.ijcard.2020.11.016
• Languages: English
• ISSNs: 0167-5273

Abstract

Abstract: 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. Highlights: SARS-CoV-2 entry into microvessels can disrupt the local renin-angiotensin-system. Complement and von Willebrand factor overexpression occur in COVID-19. COVID-19 patients show widespread thromboinflammatory microvascular disease. COVID-19 provides an important paradigm of potentially fatal microangiopathy.