Cited by 251COVID-19 Clinical Research StudiesBlood Coagulation and Thrombosis MechanismsVenous Thromboembolism Diagnosis and Management

Thrombosis in Coronavirus disease 2019 (COVID-19) through the prism of Virchow’s triad

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Ahmed, Sakir, Zimba, Olena, Gasparyan, Armen Yuri·2020·Clinical Rheumatology

Abstract

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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  1. [7]Zhou F Yu T Du R Clinical course and risk factors for mortality of adult inpatients with COVID-19 in Wuhan, China: a retrospective cohort study Lancet 2020 395 1054 1062 10.1016/S0140-6736(20)30566-3 32171076 PMC7270627 · DOI · Paper page

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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
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
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

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