Circulating endothelial cells (CEC) are stressed cells detached from injured vessels, which are low in count in healthy individuals. Increased counts of CEC provide a direct proof of endothelial damage during the course of severe COVID-19 and are clinically informative biomarkers of disease severity. Future studies are required to define the usefulness of CEC as a biomarker.

Michigan State University

University of Michigan - Ann Arbor

Endothelial dysfunction is a cardiac condition that is the precursor of atherosclerosis.  It is controlled by the so called "cardiovascular risk factors", and when these risk factors are treated, this condition can be reversed.  Endothelial dysfunction leads to:

- plaque buildup in vascular tissue
- thrombosis
- vasoconstriction
- inflammation
- oxidative stress 
- vascular tissue remodeling

Endothelial dysfunction is a comorbidity of conditions that have been shown to aggravate a SARS-CoV-2, including obesity.  It also causes phenomena that might mechanistically enhance COVID-19.

Endothelial Dysfunction and COVID-19

Guervilly, C., Burtey, S., Sabatier, F., Cauchois, R., Lano, G., Abdili, E., Daviet, F., Arnaud, L., Brunet, P., Hraiech, S., Jourde-Chiche, N., Koubi, M., Lacroix, R., Pietri, L., Berda, Y., Robert, T., Degioanni, C., Velier, M., Papazian, L., Kaplanski, G., … Dignat-George, F. (2020). Circulating Endothelial Cells as a Marker of Endothelial Injury in Severe COVID -19. The Journal of infectious diseases, 222(11), 1789–1793. https://doi.org/10.1093/infdis/jiaa528

Circulating Endothelial Cells as a Marker of Endothelial Injury in Severe COVID -19

Endothelial dysfunction is associated with obesity and has been shown to lead to inflammation, oxidative stress, and vascular endothelial cell apoptosis.  These conditions may contribute to cytokine storm syndrome which is known to exacerbate COVID-19.  Additionally, the chronic inflammation and impaired ability to break down blood clots caused by endothelial dysfunction may lead to thrombosis, a condition that is thought to be mechanistically involved in severe lung damage and death in SARS-CoV-2 infections.  

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