Thrombosis in Coronavirus disease 2019 (COVID-19) through the prism of Virchow’s triad
Open accessAbstract
The pathogenesis of Coronavirus disease 2019 (COVID-19) is gradually being comprehended. A high number of thrombotic episodes are reported, along with the mortality benefits of heparin. COVID-19 can be viewed as a prothrombotic disease. We overviewed the available evidence to explore this possibility. We identified various histopathology reports and clinical case series reporting thromboses in COVID-19. Also, multiple coagulation markers support this. COVID-19 can be regarded as a risk factor for thrombosis. Applying the principles of Virchow's triad, we described abnormalities in the vascular endothelium, altered blood flow, and platelet function abnormalities that lead to venous and arterial thromboses in COVID-19. Endothelial dysfunction, activation of the renin-angiotensin-aldosterone system (RAAS) with the release of procoagulant plasminogen activator inhibitor (PAI-1), and hyperimmune response with activated platelets seem to be significant contributors to thrombogenesis in COVID-19. Stratifying risk of COVID-19 thromboses should be based on age, presence of comorbidities, D-dimer, CT scoring, and various blood cell ratios. Isolated heparin therapy may not be sufficient to combat thrombosis in this disease. There is an urgent need to explore newer avenues like activated protein C, PAI-1 antagonists, and tissue plasminogen activators (tPA). These should be augmented with therapies targeting RAAS, antiplatelet drugs, repurposed antiinflammatory, and antirheumatic drugs. Key Points • Venous and arterial thromboses in COVID-19 can be viewed through the prism of Virchow's triad. • Endothelial dysfunction, platelet activation, hyperviscosity, and blood flow abnormalities due to hypoxia, immune reactions, and hypercoagulability lead to thrombogenesis in COVID-19. • There is an urgent need to stratify COVID-19 patients at risk for thrombosis using age, comorbidities, D-dimer, and CT scoring. • Patients with COVID-19 at high risk for thrombosis should be put on high dose heparin therapy.
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Vascular dysfunction and thrombotic complications are hallmark features of COVID-19.
“Vascular dysfunction and thrombotic complications are hallmark features of COVID-19 (55).”
From Lung epithelial and endothelial damage, loss of tissue repair, inhibition of fibrinolysis, and cellular senescence in fatal COVID-19 (2021) · cites this paper as [55]
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Behcet's Disease as a Model of Venous Thrombosis~!2009-11-07~!2009-12-07~!2010-02-22~!
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D’Agnillo, F., Walters, K.-A., Xiao, Y., Sheng, Z.-M., Scherler, K., Park, J., Gygli, S., Rosas, L. A., Sadtler, K., Kalish, H., et al. (2021) · Science Translational Medicine · doi:10.1126/scitranslmed.abj7790 · Cited by 237 · see citing works
Hamidi, S. H., Kadamboor Veethil, S., & Hamidi, S. H. (2021) · Pharmacological Reports · doi:10.1007/s43440-021-00255-x · Cited by 50 · see citing works
- Authors
- Ahmed, S., Zimba, O., & Gasparyan, A. Y.
- Affiliations
- KIIT University (IN)
- Danylo Halytsky Lviv National Medical University (UA)
- Russells Hall Hospital (GB)
- Corresponding author
- Gasparyan, Armen Yuri
- Venue
- Clinical Rheumatology
- Published
- 2020-07-11
- Volume
- 39
- Issue
- 9
- Pages
- 2529-2543
- ISSN
- 0770-3198 (ISSN-L)
- 1434-9949
- PMC
- PMC7353835
- OpenAlex
- W3041022255
- Cited by
- 251
- References
- 177
- Citations by year
- 2026: 8 · 2025: 10 · 2024: 24 · 2023: 41 · 2022: 57 · 2021: 87 · 2020: 22
- FWCI
- 2.45
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Clinical Rheumatology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Infectious Diseases › COVID-19 Clinical Research Studies
- Health Sciences › Medicine › Hematology › Blood Coagulation and Thrombosis Mechanisms
- Health Sciences › Medicine › Internal Medicine › Venous Thromboembolism Diagnosis and Management
- Keywords
- COVID-19 pandemic, thrombosis, Virchow's triad, endothelial dysfunction, platelet activation, hypercoagulability, renin-angiotensin-aldosterone system, plasminogen activator inhibitor-1, D-dimer, thrombosis risk stratification, heparin therapy, activated protein C, tissue plasminogen activator, antiplatelet agents, drug repurposing
- MeSH terms
- Betacoronavirus, Angiotensin-Converting Enzyme 2, COVID-19, SARS-CoV-2, Angiotensin-Converting Enzyme Inhibitors, Anticoagulants, Blood Platelets, Blood Viscosity, Endothelium, Vascular, Fibrin Fibrinogen Degradation Products, Fibrinogen, Fibrinolytic Agents, Heparin, Humans, Peptidyl-Dipeptidase A, Tissue Plasminogen Activator, Platelet Aggregation Inhibitors, Pneumonia, Viral, Severity of Illness Index, Thrombosis, Platelet Activation, Plasminogen Activator Inhibitor 1, Coronavirus Infections, Thrombophilia, Angiotensin Receptor Antagonists, Pandemics
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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