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Monitoring Changes in Human Umbilical Vein Endothelial Cells upon Viral Infection Using Impedance-Based Real-Time Cell Analysis
Published on: May 5, 2023
Coagulation Disorders and Thrombosis in COVID-19 Patients and a Possible Mechanism Involving Endothelial Cells: A
An-Tian Chen1,2, Chen-Yu Wang1, Wen-Ling Zhu1
11Department of Cardiology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100730, China.
Insights
Coronavirus disease 2019 (COVID-19) significantly impacts older adults, causing coagulation disorders and thrombosis in up to 95% of patients. Endothelial cell dysfunction is a key factor in COVID-19-related clot formation and poor outcomes.
Area of Science:
- Medical Research
- Infectious Diseases
- Hematology
Background:
- Coronavirus disease 2019 (COVID-19) is a global pandemic disproportionately affecting older adults.
- COVID-19 is associated with increased risks of organ dysfunction, mortality, and significant coagulation disorders.
Purpose of the Study:
- To investigate the role of coagulation disorders and thrombosis in COVID-19 pathophysiology.
- To explore the mechanisms linking endothelial cell dysfunction to hypercoagulation in COVID-19 patients.
Main Methods:
- Review of existing literature on COVID-19, coagulation abnormalities, and endothelial cell function.
- Analysis of laboratory findings in COVID-19 patients, including D-dimer levels, prothrombin time, and platelet counts.
- Examination of the impact of SARS-CoV-2 on endothelial cells and related inflammatory pathways.
Main Results:
- Up to 95% of COVID-19 patients exhibit coagulation disorders, such as elevated D-dimer and low platelet counts.
- Thrombosis is prevalent in severe COVID-19 cases, correlating with increased mortality.
- SARS-CoV-2 infection activates endothelial cells, leading to inflammation, dysfunction, and promoting clot formation.
Conclusions:
- Coagulation disorders and thrombosis are critical indicators of poor prognosis in COVID-19, particularly in severe cases.
- Endothelial cell activation and dysfunction are central to the development of hypercoagulation in COVID-19.
- Further research is needed to fully elucidate the mechanisms of coagulopathy in COVID-19.
Abstract:
Coronavirus disease 2019 (COVID-19) is still an ongoing pandemic worldwide. COVID-19 is an age-related disease with a higher risk of organ dysfunction and mortality in older adults. Coagulation disorders and thrombosis are important pathophysiological changes in COVID-19 infection. Up to 95% of COVID-19 patients have coagulation disorders characterized by an elevated D-dimer, a prolonged prothrombin time, a low platelet count and other laboratory abnormalities. Thrombosis is found in critical cases with an increased risk of death. Endothelial cells are prone to be affected by the novel SARS-CoV-2 and express angiotensin-converting enzyme 2. The evidence, such as the presence of the virus, has been identified, leading to the inflammation and dysfunction. Endothelial cell activation and dysfunction play a pivotal role in the hypercoagulation status in COVID-19 patients. In addition to the direct exposure of subendothelial tissue to blood, Weibel-Palade bodies within the endothelium containing coagulants can be released into the circulation. Endothelial nitric oxide synthase may be impaired, thus facilitating platelet adhesion. Moreover, anti-β2-glycoprotein I antibodies may also contribute to the coagulopathy in COVID-19 by inducing the upregulation of proinflammatory mediators and adhesion molecules. To conclude, coagulation disorders and thrombosis are vital and predict a poor outcome in COVID-19 patients, especially in severe cases. Endothelial cell activation and dysfunction may play an important role in causing clot formation. More basic and clinical research is warranted to further our understanding of the role of coagulopathy and their possible mechanism in COVID-19 patients.
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