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COVID-19-Related Stroke

David C Hess1, Wael Eldahshan2, Elizabeth Rutkowski3

  • 1Department of Neurology, Medical College of Georgia, Augusta University, Augusta, GA, 30912, USA. Dhess@augusta.edu.

Translational Stroke Research
|May 8, 2020
PubMed

Insights

COVID-19 can cause stroke due to hypercoagulability, potentially linked to sepsis-induced coagulopathy. SARS-CoV-2 virus interaction with ACE2 may disrupt the renin-angiotensin system, favoring harmful pathways that lead to stroke.

Area of Science:

  • Neurology
  • Virology
  • Cardiovascular Science

Background:

  • COVID-19 is linked to neurological complications, notably stroke.
  • Hypercoagulability in COVID-19 patients resembles sepsis-induced coagulopathy, increasing stroke risk.

Discussion:

  • SARS-CoV-2 binds to ACE2 on brain cells, disrupting the renin-angiotensin system (RAS).
  • This interaction may shift the balance towards the pro-inflammatory and vasoconstrictive ACE1/angiotensin II axis, promoting stroke.
  • ACE2 depletion by SARS-CoV-2 could be a mechanism for COVID-19-related neurological injury.

Key Insights:

  • COVID-19-associated stroke may stem from viral disruption of the ACE2/RAS pathway.
  • Understanding this mechanism provides rationale for specific stroke treatments in COVID-19 patients.

Outlook:

  • Continued use of tissue plasminogen activator for COVID-19 stroke is supported.
  • Low molecular weight heparinoids show promise in mitigating thrombosis and mortality in sepsis-induced coagulopathy, including COVID-19 cases.

Keywords:
Angiotensin-converting enzyme 2 (ACE2)COVID-19CoagulopathySARS-CoV-2SepsisStroke

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