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Front. Med.    2023, Vol. 17 Issue (6) : 1047-1067    https://doi.org/10.1007/s11684-023-1041-7
Epidemiology, pathogenesis, and management of coronavirus disease 2019-associated stroke
Lu Liu1,2, Chenxia Zhou1,2, Huimin Jiang3, Huimin Wei4, Yifan Zhou3, Chen Zhou3,5(), Xunming Ji2,3,6()
1. Department of Neurology, Xuanwu Hospital, Capital Medical University, Beijing 100032, China
2. Neurology and Intracranial Hypertension and Cerebral Venous Disease Center, National Health Commission of China, Xuanwu Hospital, Capital Medical University, Beijing 100032, China
3. Beijing Institute of Brain Disorders, Capital Medical University, Beijing 100069, China
4. Beijing Advanced Innovation Center for Big Data-Based Precision Medicine, School of Biological Science and Medical Engineering, Beihang University, Beijing 100191, China
5. Department of Neurology, Beijing Shijitan Hospital, Capital Medical University, Beijing 100038, China
6. Department of Neurosurgery, Xuanwu Hospital, Capital Medical University, Beijing 100032, China
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Abstract

The coronavirus disease 2019 (COVID-19) epidemic has triggered a huge impact on healthcare, socioeconomics, and other aspects of the world over the past three years. An increasing number of studies have identified a complex relationship between COVID-19 and stroke, although active measures are being implemented to prevent disease transmission. Severe COVID-19 may be associated with an increased risk of stroke and increase the rates of disability and mortality, posing a serious challenge to acute stroke diagnosis, treatment, and care. This review aims to provide an update on the influence of COVID-19 itself or vaccines on stroke, including arterial stroke (ischemic stroke and hemorrhagic stroke) and venous stroke (cerebral venous thrombosis). Additionally, the neurovascular mechanisms involved in SARS-CoV-2 infection and the clinical characteristics of stroke in the COVID-19 setting are presented. Evidence on vaccinations, potential therapeutic approaches, and effective strategies for stroke management has been highlighted.
Keywords SARS-CoV-2      ischemic stroke      stroke      hemorrhagic stroke      cerebral venous thrombosis      vaccination     
Corresponding Author(s): Chen Zhou,Xunming Ji   
Just Accepted Date: 28 November 2023   Online First Date: 29 December 2023    Issue Date: 06 February 2024
 Cite this article:   
Lu Liu,Chenxia Zhou,Huimin Jiang, et al. Epidemiology, pathogenesis, and management of coronavirus disease 2019-associated stroke[J]. Front. Med., 2023, 17(6): 1047-1067.
 URL:  
https://academic.hep.com.cn/fmd/EN/10.1007/s11684-023-1041-7
https://academic.hep.com.cn/fmd/EN/Y2023/V17/I6/1047
Fig.1  Overview of stroke in patients with COVID-19. CVT, cerebral venous thrombosis; NIHSS, National Institutes of Health Stroke Scale; ICU, Intensive Care Unit; PF4, platelet factor 4.
Fig.2  Main mechanisms of COVID-19-associated stroke. The ACE2 receptor on the endothelial cells interacts with the spike protein of SARS-CoV-2. This interaction reduces productive ACE2 and increases Ang II levels. Pathogen-associated antigens activate monocytes, releasing a proinflammatory cytokine storm, which increases TF expression and fibrinogen production and promotes platelet hyperactivation. TF activates the extrinsic coagulation pathway and promotes the expression of coagulation factor VII/VIIa. The impaired endothelium also exposes vWF, which exacerbates platelet aggregation. NET formation generates a thrombotic-inflammatory response and facilitates thrombosis. The interaction among cytokine storm, endothelial cell damage, ACE/Ang II /AT1R, and coagulation dysfunction ultimately leads to thrombosis and hemorrhage. ACE2, angiotensin-converting enzyme 2; Ang II, angiotensin II; TF, tissue factor; vWF, von Willebrand factor; NETs, neutrophil extracellular traps.
Aspect Stroke with COVID-19 Stroke without COVID-19 References
Demographics More young patients (≤50 years) Older (average age > 50 years) [21, 62, 114]
Male predisposition Higher incidence in older men
Risk factors Fewer vascular risk factors Nonmodifiable risk factors: age, sex, genetics [21, 40, 114, 172, 209, 210]
Combined risks could increase disease severity Modifiable factors: hypertension, hyperlipidemia, etc.
More severe infectious disease Common risks in young: extracranial arterial dissections, inflammatory arteriopathies, cardiomyopathy, antiphospholipid syndrome
Stroke subtype and imaging characteristics Larger vessel occlusion, cryptogenic stroke, followed by cardioembolic stroke More small vessel disease [21, 26, 29, 62, 107, 109, 113, 150, 209, 211]
Men: more likely to suffer lacunar infarction
Less small artery stroke Women: more likely to suffer cardioembolic stroke
Multiple arterial territory involvement Children under 15 years old : congenital heart disease, nonatherosclerotic vasculopathies, infection, and hematologic defects, such as sickle cell disease, etc.
No significant difference between different populations due to limited data Patients between 15–35 years old: dissection, cardio embolism, nonatherosclerotic vasculopathies, and prothrombotic states, etc.
Clinical symptoms and severity during hospital Common neurological manifestation: fatigue, fever Adults: the sudden onset of a focal clinical deficit: hemiparesis, hemianesthesia, aphasia, homonymous hemianopsia, and hemispatial inattention, etc. [209, 212, 213]
Higher NIHSS score and in-hospital mortality, longer hospital stays Children: atypical presentations
Often requiring intubation, ICU admissions
Clinical prognosis Worse prognosis, higher 90-day mortality Younger patients: lower short-term mortality rates, long-term follow-up revealed a surplus of mortality [82, 94, 172, 209, 214]
Mortality correlation with age, especially > 25 years old Older patients: excess long-term mortality
Tab.1  Discrepancies among different stroke populations
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