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Updated: Oct 9, 2025

Monitoring Changes in Human Umbilical Vein Endothelial Cells upon Viral Infection Using Impedance-Based Real-Time Cell Analysis
Published on: May 5, 2023
Sustained inflammation, coagulation activation and elevated endothelin-1 levels without macrovascular dysfunction at
L H Willems1, M Nagy2, H Ten Cate3
1Department of Surgery, Radboud University Medical Centre, Nijmegen, the Netherlands.
Insights
Three months after COVID-19, macrovascular function was normal, but endothelial cells showed persistent inflammation and coagulation activation. Further research is needed on SARS-CoV-2 vascular effects.
Area of Science:
- Cardiovascular Medicine
- Infectious Diseases
- Immunology
Background:
- COVID-19 can cause endothelial damage and thrombosis, potentially impacting long-term cardiovascular health.
- Limited data exists on the persistent effects of COVID-19 on vascular function beyond the acute phase.
Purpose of the Study:
- To investigate endothelial dysfunction, coagulation, and inflammation three months after COVID-19 infection.
- To assess long-term cardiovascular implications in patients recovering from COVID-19.
Main Methods:
- A cohort study of 203 COVID-19 patients and 312 historical controls.
- Macrovascular dysfunction assessed via carotid artery diameter response to cold stimulus.
- Plasma endothelin-1, coagulation enzyme:inhibitor complexes, and inflammatory cytokines were measured.
Main Results:
- No significant difference in macrovascular dysfunction prevalence between COVID-19 survivors and controls.
- Significantly elevated endothelin-1 levels persisted three months post-COVID-19.
- Elevated markers of coagulation (thrombin:antithrombin, FVIIa:AT, Von Willebrand Factor) and inflammation (IL-18, IL-6, IL-1ra) were observed.
Conclusions:
- While macrovascular function may recover, sustained endothelial cell involvement, coagulation activity, and inflammation are evident three months post-COVID-19.
- These findings underscore the need for further research into SARS-CoV-2-related vascular inflammation and thrombosis.
- Longer follow-up studies are crucial for understanding the long-term vascular consequences of COVID-19.
Introduction:
Endothelial damage and thrombosis caused by COVID-19 may imperil cardiovascular health. More than a year since the WHO declared COVID-19 pandemic, information on its effects beyond the acute phase is lacking. We investigate endothelial dysfunction, coagulation and inflammation, 3 months post-COVID-19.
Materials And Methods:
A cohort study was conducted including 203 patients with prior COVID-19. Macrovascular dysfunction was assessed by measuring the carotid artery diameter in response to hand immersion in ice-water. A historic cohort of 312 subjects served as controls. Propensity score matching corrected for baseline differences. Plasma concentrations of endothelin-1 were measured in patients post-COVID-19, during the acute phase, and in matched controls. Coagulation enzyme:inhibitor complexes and inflammatory cytokines were studied.
Results And Conclusions:
The prevalence of macrovascular dysfunction did not differ between the COVID-19 (18.6%) and the historic cohort (22.5%, RD -4%, 95%CI: -15-7, p = 0.49). Endothelin-1 levels were significantly higher in acute COVID-19 (1.67 ± 0.64 pg/mL) as compared to controls (1.24 ± 0.37, p < 0.001), and further elevated 3 months post-COVID-19 (2.74 ± 1.81, p < 0.001). Thrombin:antithrombin(AT) was high in 48.3%. Markers of contact activation were increased in 16-30%. FVIIa:AT (35%) and Von Willebrand Factor:antigen (80.8%) were elevated. Inflammatory cytokine levels were high in a majority: interleukin(IL)-18 (73.9%), IL-6 (47.7%), and IL-1ra (48.9%). At 3 months after acute COVID-19 there was no indication of macrovascular dysfunction; there was evidence, however, of sustained endothelial cell involvement, coagulation activity and inflammation. Our data highlight the importance of further studies on SARS-CoV-2 related vascular inflammation and thrombosis, as well as longer follow-up in recovered patients.
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