期刊
TRANSLATIONAL STROKE RESEARCH
卷 11, 期 3, 页码 322-325出版社
SPRINGER
DOI: 10.1007/s12975-020-00818-9
关键词
COVID-19; SARS-CoV-2; Stroke; Sepsis; Coagulopathy; Angiotensin-converting enzyme 2 (ACE2)
资金
- [R01 NS099455]
- [1UO1NS113356]
- [R01NS112511]
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.
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