ArticleJournal of thrombosis and thrombolysis2026
Severity-associated endothelial dysfunction in post-COVID-19 patients: flow-mediated dilation and vasoactive biomarkers.
Article in Journal of thrombosis and thrombolysis, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
COVID-19 is frequently associated with endothelial dysfunction, characterized by an imbalance between vasodilatory and vasoconstrictive mediators. This study evaluated endothelial function in the early post-COVID-19 period across groups of acute disease severity using flow-mediated dilation (FMD), circulating vasoactive biomarkers, and echocardiography. Serum endothelin-1 (ET-1), arginase-1 (Arg1), thromboxane A₂ (TxA₂)-related immunoreactivity, and prostacyclin (PGI₂)-related immunoreactivity were measured by enzyme-linked immunosorbent assay. An impaired FMD response was defined as < 10% brachial artery dilation from baseline. Overall, 502 post-COVID-19 patients were classified by acute COVID-19 severity as mild (n = 262), moderate (n = 183), severe (n = 41), or critical (n = 16); 27 healthy individuals served as a reference group. Impaired FMD responses were more frequent after severe (90.24%) and critical (100.00%) disease than in the reference group (18.52%). Greater acute disease severity was associated with progressively lower FMD values, smaller absolute brachial artery diameter changes, higher ET-1, Arg1, and TxA₂-related immunoreactivity, and lower PGI₂-related immunoreactivity. After adjustment for age, sex, body mass index, systolic blood pressure, smoking, diabetes mellitus, pre-existing cardiovascular disease, and post-COVID-19 interval, acute disease severity remained associated with impaired FMD (adjusted odds ratio 3.32, 95% confidence interval 2.29-4.82; p < 0.001 per one-category increase). Biomarker-FMD correlations were generally weak. Among patients assessed during the early post-COVID-19 period, greater acute COVID-19 severity was associated with greater impairment of endothelium-dependent vasodilation and an altered profile of circulating vasoactive biomarkers. These findings indicate associated functional and biochemical vascular abnormalities without establishing causality or a mechanistic relationship. Prospective longitudinal studies are needed to clarify their temporal evolution and clinical significance.
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