Publication date: Jul 17, 2025

endothelial cells may be a primary source for the initiation and spread of Acute Respiratory Distress Syndrome (ARDS) caused by SARS-CoV-2, resulting in severe endothelial injury and widespread thrombosis. The objective of this study was to evaluate the influence of lung function on the vascular response of patients with long COVID. This is an observational and cross-sectional study. Only one visit was performed, during which the evaluation form was completed and the post-COVID-19 Functional Status Scale (PCFS) was applied. In addition, participants underwent the assessment of flow-mediated vasodilation in the brachial artery and the assessment of pulmonary function. A total of 32 participants were included, of which 19 (59 %) were women. The mean age was 55. 8 +/- 8. 6 years, with a mean weight of 88. 96 +/- 21. 66 kg. The participants had an average time of 32. 25 months since the acute phase. The patients had an average of FEV₁/FVC 81. 15+/-14. 7 ( %) and KCO 93. 72+/-7. 95 ( %). FMD had an average of -0. 21+/-11. 24 ( %), indicating still impaired endothelial function. We found correlation between basal diameter (-0. 21 [-4. 26 to 3. 84]) vs lung function variables, especially with the variable KCO ( %) (p < 0. 001; r = 0. 560). When we perform simple linear regression KCO ( %) indicates that this variable alone influences 29 % of the response to the basal diameter of the participants. Two years after recovery from COVID-19 infection, the patients present changes in endothelial function, which have important implications for individuals when it comes to cardiovascular health.

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