ArticleBMC cardiovascular disorders2026
Mitral stenosis severity and the hypoxic response: potential role of hypoxia-inducible factor-2α - a cross-sectional study.
Article in BMC cardiovascular disorders, 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
backgroundMitral stenosis (MS) causes chronic pressure overload and secondary pulmonary hypertension, which are associated with activation of hypoxia-inducible pathways. This study investigated the circulating levels of hypoxia-inducible factor-2α (Endothelial PAS domain protein 1-EPAS1) in patients with MS and their relationship with disease severity.
methodsThis prospective study included 69 patients diagnosed with rheumatic MS and an equal number of age- and sex-matched healthy individuals. Hypoxia-inducible factor-2α (HIF-2α) levels were assessed using an enzyme-linked immunosorbent assay (ELISA) along with conventional biomarkers, and all patients underwent echocardiographic assessments. Statistical comparisons were performed using appropriate parametric or non-parametric tests, and relationships were evaluated using Spearman’s rank correlation coefficients.
resultsHIF-2α levels were significantly higher in patients with MS than in the controls (median 5.2 vs. 4.7; p = 0.0275). Patients with MS also had higher high-sensitivity cardiac troponin T levels (median 7.7 vs. 4.9, p = 0.0328) than controls. HIF-2α was weakly positively correlated with systolic pulmonary artery pressure (ρ = 0.28, p = 0.001), left atrial diameter (ρ = 0.22, p = 0.012), and N-terminal pro-B-type natriuretic peptide level (ρ = 0.29, p = 0.014). HIF-2α levels did not significantly correlate with the mitral valve area or mean transmitral gradient.
conclusionElevated HIF-2α levels in patients with MS are correlated with pulmonary hypertension and cardiac stress. These findings support the involvement of hypoxia-inducible pathways in the pathophysiology of MS. However, HIF-2α elevation is modest and its clinical utility as a biomarker for MS is currently limited.
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