Clinical implications of hyposelenium in heart failure with preserved ejection fraction

Background Selenium is an essential micronutrient required for selenoprotein synthesis, which regulates mitochondrial redox balance, antioxidant defence and inflammatory pathways. Selenium deficiency has been associated with adverse outcomes in heart failure with reduced ejection fraction; however, its clinical relevance in heart failure with preserved ejection fraction (HFpEF) remains insufficiently explored. Purpose To evaluate the prevalence, clinical characteristics and one-year outcomes of hyposelenium in patients with HFpEF and to determine whether low selenium levels independently predict adverse events. Methods In this single-centre cohort study, 168 patients with HFpEF (left ventricular ejection fraction ≥50%) admitted for first-onset acute heart failure between 2018 and 2022 were analysed. Serum selenium was measured at admission using atomic absorption spectrometry. Patients were classified into a low selenium group (<100 µg/L) and a normal selenium group (≥100 µg/L). The primary endpoints were one-year cardiovascular death and rehospitalisation for heart failure. Group comparisons were performed using Student’s t test and χ² test. Survival was analysed using the log-rank test. Independent predictors were assessed by multivariable logistic regression. Results Hyposelenium was observed in 75 patients (44.6%). Mean selenium levels were 81.3±11.2 µg/L in the low selenium group and 122.5±18.4 µg/L in the normal group. Age and body mass index did not differ between groups. The low selenium group had significantly lower serum albumin (3.2±0.5 vs 3.6±0.4 g/dL, p<0.001) and triglyceride levels (94.7±60.9 vs 123.4±69.3 mg/dL, p=0.02). Echocardiographic parameters were comparable. One-year cardiovascular mortality and heart failure rehospitalisation were significantly higher in the low selenium group (log-rank p<0.05 for both). Multivariable analysis identified serum selenium concentration as an independent predictor of cardiovascular death and rehospitalisation, together with age and renal function. Conclusion Selenium deficiency is common in HFpEF and is independently associated with adverse one-year outcomes. Hyposelenium may reflect both impaired antioxidant capacity and poor nutritional reserve. Assessment of selenium status could contribute to risk stratification in HFpEF, and correction of deficiency may represent a potential therapeutic target warranting further investigation.