COVID-19-Related Stroke

David C. Hess; Wael Eldahshan; Elizabeth Rutkowski

doi:10.1007/s12975-020-00818-9

COVID-19-Related Stroke

David C. Hess, Wael Eldahshan, Elizabeth Rutkowski

Neurology

Research output: Contribution to journal › Comment/debate › peer-review

270 Scopus citations

Abstract

The COVID-19 pandemic is associated with neurological symptoms and complications including stroke. There is hypercoagulability associated with COVID-19 that is likely a “sepsis-induced coagulopathy” and may predispose to stroke. The SARS-CoV-2 virus binds to angiotensin-converting enzyme 2 (ACE2) present on brain endothelial and smooth muscle cells. ACE2 is a key part of the renin angiotensin system (RAS) and a counterbalance to angiotensin-converting enzyme 1 (ACE1) and angiotensin II. Angiotensin II is proinflammatory, is vasoconstrictive, and promotes organ damage. Depletion of ACE2 by SARS-CoV-2 may tip the balance in favor of the “harmful” ACE1/angiotensin II axis and promote tissue injury including stroke. There is a rationale to continue to treat with tissue plasminogen activator for COVID-19-related stroke and low molecular weight heparinoids may reduce thrombosis and mortality in sepsis-induced coagulopathy.

Original language	English (US)
Pages (from-to)	322-325
Number of pages	4
Journal	Translational Stroke Research
Volume	11
Issue number	3
DOIs	https://doi.org/10.1007/s12975-020-00818-9
State	Published - Jun 1 2020

Keywords

Angiotensin-converting enzyme 2 (ACE2)
COVID-19
Coagulopathy
SARS-CoV-2
Sepsis
Stroke

ASJC Scopus subject areas

Neuroscience(all)
Clinical Neurology
Cardiology and Cardiovascular Medicine

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10.1007/s12975-020-00818-9

Cite this

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title = "COVID-19-Related Stroke",

abstract = "The COVID-19 pandemic is associated with neurological symptoms and complications including stroke. There is hypercoagulability associated with COVID-19 that is likely a “sepsis-induced coagulopathy” and may predispose to stroke. The SARS-CoV-2 virus binds to angiotensin-converting enzyme 2 (ACE2) present on brain endothelial and smooth muscle cells. ACE2 is a key part of the renin angiotensin system (RAS) and a counterbalance to angiotensin-converting enzyme 1 (ACE1) and angiotensin II. Angiotensin II is proinflammatory, is vasoconstrictive, and promotes organ damage. Depletion of ACE2 by SARS-CoV-2 may tip the balance in favor of the “harmful” ACE1/angiotensin II axis and promote tissue injury including stroke. There is a rationale to continue to treat with tissue plasminogen activator for COVID-19-related stroke and low molecular weight heparinoids may reduce thrombosis and mortality in sepsis-induced coagulopathy.",

keywords = "Angiotensin-converting enzyme 2 (ACE2), COVID-19, Coagulopathy, SARS-CoV-2, Sepsis, Stroke",

author = "Hess, {David C.} and Wael Eldahshan and Elizabeth Rutkowski",

note = "Funding Information: Colby Zhan, M.S. Medical Illustrator, Department of Neurosurgery, Augusta University for the Figure. Publisher Copyright: {\textcopyright} 2020, Springer Science+Business Media, LLC, part of Springer Nature.",

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AU - Eldahshan, Wael

AU - Rutkowski, Elizabeth

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PY - 2020/6/1

Y1 - 2020/6/1

N2 - The COVID-19 pandemic is associated with neurological symptoms and complications including stroke. There is hypercoagulability associated with COVID-19 that is likely a “sepsis-induced coagulopathy” and may predispose to stroke. The SARS-CoV-2 virus binds to angiotensin-converting enzyme 2 (ACE2) present on brain endothelial and smooth muscle cells. ACE2 is a key part of the renin angiotensin system (RAS) and a counterbalance to angiotensin-converting enzyme 1 (ACE1) and angiotensin II. Angiotensin II is proinflammatory, is vasoconstrictive, and promotes organ damage. Depletion of ACE2 by SARS-CoV-2 may tip the balance in favor of the “harmful” ACE1/angiotensin II axis and promote tissue injury including stroke. There is a rationale to continue to treat with tissue plasminogen activator for COVID-19-related stroke and low molecular weight heparinoids may reduce thrombosis and mortality in sepsis-induced coagulopathy.

AB - The COVID-19 pandemic is associated with neurological symptoms and complications including stroke. There is hypercoagulability associated with COVID-19 that is likely a “sepsis-induced coagulopathy” and may predispose to stroke. The SARS-CoV-2 virus binds to angiotensin-converting enzyme 2 (ACE2) present on brain endothelial and smooth muscle cells. ACE2 is a key part of the renin angiotensin system (RAS) and a counterbalance to angiotensin-converting enzyme 1 (ACE1) and angiotensin II. Angiotensin II is proinflammatory, is vasoconstrictive, and promotes organ damage. Depletion of ACE2 by SARS-CoV-2 may tip the balance in favor of the “harmful” ACE1/angiotensin II axis and promote tissue injury including stroke. There is a rationale to continue to treat with tissue plasminogen activator for COVID-19-related stroke and low molecular weight heparinoids may reduce thrombosis and mortality in sepsis-induced coagulopathy.

KW - Angiotensin-converting enzyme 2 (ACE2)

KW - COVID-19

KW - Coagulopathy

KW - SARS-CoV-2

KW - Sepsis

KW - Stroke

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COVID-19-Related Stroke

Abstract

Keywords

ASJC Scopus subject areas

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