Key result
Lower serum selenium in post-infarction HF is linked to greater inflammatory and oxidative stress.
Why the study?
Selenium is essential for antioxidant defense and immune regulation, but its influence on post-infarction heart failure remains underexplored.
Is serum Selenium associated with inflammatory and oxidative stress markers in patients with post-infarction heart failure?
Case-Control (n=89)
Is serum Selenium associated with inflammatory and oxidative stress markers in patients with post-infarction heart failure?
p-value: p=<0.05
Selenium deficiency is associated with greater inflammatory and oxidative stress burden in post-infarction HF, supported by in vitro evidence of reduced pro-inflammatory and pro-fibrotic gene expression with Selenium treatment.
Selenium deficiency may associate with oxidative stress and inflammation in post-MI HF; leaves open any supplementation benefit pending trials.
Background As a trace element, Selenium is essential for antioxidant defense and immune regulation; however, its influence on post-infarction heart failure (HF) remains underexplored. Methods The present study used a hybrid approach, combining a retrospective case-control analysis with in vitro mechanistic assays. Serum Selenium, inflammatory cytokines (TNF-α, IL-6), oxidative stress markers (MDA, SOD), and left ventricular ejection fraction (LVEF) were assessed in 46 patients with post-infarction HF and 43 healthy controls. In parallel, H9C2 cardiomyocytes exposed to either lipopolysaccharide (LPS) or palmitic acid (PA) were assessed for inflammatory and fibrotic gene expression, with and without Selenium treatment. Results HF subjects had significantly lower Selenium and SOD levels than controls (all p < 0.05), and increased TNF-α, IL-6, and MDA. Selenium as an anti-inflammatory element was positively associated with LVEF and negatively associated with TNF-α, IL-6, and MDA. In vitro , Selenium was associated with decreased expression of pro-inflammatory (TNF-α, IL-1β and IL-6) and pro-fibrotic (Collagen I, III, and α -SMA) genes during stress. Exploratory subgroup analysis suggested heterogeneous distributions of Selenium and oxidative stress markers across HF phenotypes, with the lowest Selenium levels observed in the HFmrEF subgroup. In vitro , Selenium reduced stress-induced expression of pro-inflammatory (TNF-a, IL-1b) and pro-fibrotic (Collagen I, Collagen III, a-SMA) genes. Conclusion Selenium deficiency was associated with greater inflammatory and oxidative stress burden in post-infarction HF. In vitro findings indicates that Selenium may contribute to cardiac injury via inflammation and fibrotic signaling. These data support serum Selenium as an exploratory biomarker for further study in HF and provide a rationale for future longitudinal and interventional research.
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Lessomo et al. (2026) conducted a case-control in post-infarction heart failure (n=89). Serum Selenium levels vs. Healthy controls was evaluated on Serum Selenium, inflammatory cytokines (TNF-α, IL-6), oxidative stress markers (MDA, SOD), and left ventricular ejection fraction (LVEF) (p=<0.05). Post-infarction heart failure patients had significantly lower serum selenium levels than healthy controls (p<0.05), which was associated with greater inflammatory and oxidative stress burden.
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