Key result
Mitral stenosis links to higher circulating HIF-2α levels that correlate with pulmonary artery pressure.
Why the study?
Mitral stenosis causes chronic pressure overload and secondary pulmonary hypertension associated with hypoxia-inducible pathways, prompting investigation into circulating HIF-2α levels and their relationship with MS severity.
Cross-Sectional (n=138)
Circulating HIF-2α levels are modestly elevated in patients with rheumatic mitral stenosis and correlate with pulmonary hypertension and cardiac stress, suggesting the involvement of hypoxia-inducible pathways in the disease's pathophysiology.
Should not yet change mitral stenosis management; hypothesis-generating for hypoxia-inducible pathways in pulmonary hypertension.
Mitral 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. This 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. HIF-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. Elevated 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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Kan et al. (2026) conducted a cross-sectional in Rheumatic mitral stenosis (n=138). Mitral Stenosis (Exposure) vs. Healthy controls was evaluated on Circulating HIF-2α levels (ng/ml) (p=0.0275). Circulating HIF-2α levels were significantly higher in patients with mitral stenosis compared to healthy controls (median 5.2 vs. 4.7 ng/ml) and correlated with pulmonary artery pressure.
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