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. 2020 Jun;11(3):322-325.
doi: 10.1007/s12975-020-00818-9. Epub 2020 May 7.

COVID-19-Related Stroke

David C Hess  1 , Wael Eldahshan  2 , Elizabeth Rutkowski  3
Affiliations

COVID-19-Related Stroke

David C Hess et al. Transl Stroke Res. 2020 Jun.

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.

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Conflict of interest statement

David C Hess MD is a consultant for Aruna Bio, Inc and receives fees for consultation and receives royalty payments from Athersys, Inc. Wael Eldahsahn PhD has no conflicts of interest/competing interests. Elizabeth Rutkowski has no conflicts of interest/competing interests.

Figures

Fig. 1
Fig. 1
ACE2 is expressed in human brain endothelium. SARS-CoV-2 binds ACE2, depleting ACE2 on the endothelium
See this image and copyright information in PMC

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