The emerging association between COVID-19 and acute stroke

Laura K Stein, Naomi A Mayman, Mandip S Dhamoon, Johanna T Fifi, Laura K Stein, Naomi A Mayman, Mandip S Dhamoon, Johanna T Fifi

Abstract

Prior to COVID-19, only two human-tropic coronaviruses resulted in epidemics and cerebrovascular disease was rarely reported. Evidence now suggests that 1-6% of hospitalized COVID-19 patients develop stroke. According to some reports, stroke risk is more than sevenfold greater in patients with COVID-19 than influenza. Concerningly, outcomes of COVID-19-related stroke are often worse than in stroke patients without COVID-19 from the same cohorts. In this review, we highlight the emerging association between COVID-19 and stroke and discuss putative pathogenetic mechanisms. Etiology of stroke in COVID-19 patients is likely multifactorial, related to coagulopathy, inflammation, platelet activation, and alterations to the vascular endothelium. Significant work remains to be done to better understand the pathogenesis of COVID-19-related stroke and for designing optimal primary and secondary prevention strategies.

Keywords: SARS-COV-2; cerebrovascular disease; coronavirus; pandemic; thrombectomy; thrombolysis; thrombosis.

Conflict of interest statement

The authors declare no competing interests in relation to this work.

Copyright © 2021 Elsevier Ltd. All rights reserved.

Figures

Figure 1
Figure 1
The pathogenesis of ischemic stroke in coronavirus disease 2019 (COVID-19), similar to other arterial thromboses seen in this disease, such as peripheral arterial thrombosis and myocardial infarction, is likely multifactorial, stemming from inflammation and coagulopathy. There is an emerging body of evidence demonstrating the association between COVID-19 and stroke and highlighting the difference in affected population, clinical presentation, and outcomes between COVID-19 positive and COVID-19 negative stroke patients. This figure highlights the major putative mechanisms. Severe acute respiratory syndrome coronavirus 2 (SARS-COV-2) binds to ACE2 receptors in various tissues, entering the body and activating the immune system, resulting in inflammation via release of cytokines. This inflammation directly induces a hypercoagulable state. Direct effects on the endothelium also occur, which results in local inflammation and platelet activation, potentially causing plaque rupture. Finally, cardioembolic sources of stroke can be caused by the virus’s direct inflammatory effect on the muscle or injury due to increased oxygen demand.

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Source: PubMed

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