J Clin Neurol.  2021 Apr;17(2):155-163. 10.3988/jcn.2021.17.2.155.

Pathomechanism and Management of Stroke in COVID-19: Review of Immunopathogenesis, Coagulopathy, Endothelial Dysfunction, and Downregulation of ACE2

Affiliations
  • 1Department of Neurology, Udayana University, Sanglah General Hospital, Denpasar, Bali, Indonesia
  • 2Department of Neurology, Udayana University, Udayana University Hospital, Bali, Indonesia

Abstract

Coronavirus disease 2019 (COVID-19) can reportedly manifest as an acute stroke, with most cases presenting as large vessel ischemic stroke in patients with or without comorbidities. The exact pathomechanism of stroke in COVID-19 remains ambiguous. The findings of previous studies indicate that the most likely underlying mechanisms are cerebrovascular pathological conditions following viral infection, inflammation-induced endothelial dysfunction, and hypercoagulability. Acute endothelial damage due to inflammation triggers a coagulation cascade, thrombosis propagation, and destabilization of atherosclerosis plaques, leading to largevessel occlusion and plaque ulceration with concomitant thromboemboli, and manifests as ischemic stroke. Another possible mechanism is the downregulation of angiotensin-converting enzyme 2 as the target action of severe acute respiratory syndrome-coronavirus-2 (SARSCoV-2). Acute stroke management protocols need to be modified during the COVID-19 pandemic in order to adequately manage stroke patients with COVID-19.

Keyword

stroke; COVID-19; hypercoagulability; inflammation; renin-angiotensin system.
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