• Transl Res · May 2022

    Post-COVID-19 patients show an increased endothelial progenitor cell production.

    • Paula Poyatos, Neus Luque, Saioa Eizaguirre, Gladis Sabater, Laura Sebastián, Íria Francisco-Albesa, Míriam Peracaula, Mireia Boixadé, Ramon Orriols, and Olga Tura-Ceide.
    • Department of Pulmonary Medicine, Dr. Josep Trueta University Hospital of Girona, Santa Caterina Hospital of Salt and the Girona Biomedical Research Institute (IDIBGI), Girona, Spain; Department of Medical Sciences, Faculty of Medicine, University of Girona, Girona, Spain.
    • Transl Res. 2022 May 1; 243: 142014-20.

    AbstractSARS-CoV-2, the cause of COVID-19, has generated a global emergency. The endothelium is a target of SARS-CoV-2, generating endothelial dysfunction, an essential step for the development of cardiovascular complications. The number of endothelial progenitor cells acts as an indicator of vascular damage. However, its role in SARS-CoV-2 is unknown. The aim of this study was to quantify the number of endothelial colony forming cells (ECFCs) and assess for the first time if there is a significant increase after SARS-CoV-2 infection. This study also evaluates whether the number of ECFC is related to the presence of pulmonary embolism (PE), and if this increase correlates with any of the clinical parameters studied. A total of 63 subjects were recruited including 32 subjects 3-months after overcoming COVID-19 and 31 healthy controls. The results confirm the presence of vascular sequelae in post-COVID-19 patients, with an abnormal increase in the number of ECFCs in blood circulation compared to controls (2.81 ± 2.33 vs 1.23 ± 1.86, P = 0.001). There was no difference in ECFC production in COVID-19 who presented acute PE compared to those that did not (3.21 ± 2.49 vs 2.50 ± 2.23, P > 0.05). The appearance of ECFC colonies in COVID-19 patients was significantly related to male gender (P = 0.003), the presence of systemic hypertension (P = 0.01) and elevated hemoglobin levels (P = 0.02) at the time of ECFC isolation and lower PaO2 levels (P = 0.01) at admission. Whether these results indicate a prompt response of the patient to repair the damaged endothelium or reflect a postinfection injury that will persist in time is not known.Copyright © 2022 Elsevier Inc. All rights reserved.

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