COVID-19-Related Stroke

David C. Hess, Wael Eldahshan, Elizabeth Rutkowski

Research output: Contribution to journalComment/debate

33 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 languageEnglish (US)
Pages (from-to)322-325
Number of pages4
JournalTranslational Stroke Research
Volume11
Issue number3
DOIs
StatePublished - 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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