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Thrombosis in Coronavirus disease 2019 (COVID-19) through the prism of Virchow's triad.
Ahmed, Sakir; Zimba, Olena; Gasparyan, Armen Yuri.
  • Ahmed S; Department of Clinical Immunology and Rheumatology, Kalinga Institute of Medical Sciences (KIMS), KIIT University, Bhubaneswar, India.
  • Zimba O; Department of Internal Medicine No. 2, Danylo Halytsky Lviv National Medical University, Lviv, Ukraine.
  • Gasparyan AY; Departments of Rheumatology and Research and Development, Dudley Group NHS Foundation Trust (Teaching Trust of the University of Birmingham, UK) Russells Hall Hospital, Pensnett Road, Dudley, West Midlands, DY1 2HQ, UK. a.gasparyan@gmail.com.
Clin Rheumatol ; 39(9): 2529-2543, 2020 Sep.
Article in English | MEDLINE | ID: covidwho-640445
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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Full text: Available Collection: International databases Database: MEDLINE Main subject: Pneumonia, Viral / Thrombosis / Endothelium, Vascular / Coronavirus Infections / Peptidyl-Dipeptidase A / Thrombophilia Type of study: Prognostic study Topics: Long Covid Language: English Journal: Clin Rheumatol Year: 2020 Document Type: Article Affiliation country: S10067-020-05275-1

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Full text: Available Collection: International databases Database: MEDLINE Main subject: Pneumonia, Viral / Thrombosis / Endothelium, Vascular / Coronavirus Infections / Peptidyl-Dipeptidase A / Thrombophilia Type of study: Prognostic study Topics: Long Covid Language: English Journal: Clin Rheumatol Year: 2020 Document Type: Article Affiliation country: S10067-020-05275-1