Association of serum selenium levels with inflammatory and oxidative stress markers in patients with post-infarction heart failure: an exploratory case-control study supported by in vitro mechanistic evidence - Report - MDSpire
Advertisement
Association of serum selenium levels with inflammatory and oxidative stress markers in patients with post-infarction heart failure: an exploratory case-control study supported by in vitro mechanistic evidence
Link Between Serum Selenium Concentrations and Inflammation in Heart Failure
Overview
This study explores the association between serum selenium levels and markers of inflammation and oxidative stress in post-infarction heart failure (HF) patients. Findings indicate that selenium deficiency correlates with increased inflammatory cytokines and oxidative stress, suggesting its potential role as a biomarker in HF management.
Background
Heart failure is a significant global health issue, characterized by high morbidity and mortality rates. The role of trace elements, particularly selenium, in cardiovascular health has gained attention due to their involvement in redox balance and immune regulation. Understanding the relationship between selenium levels and heart failure could provide insights into potential therapeutic strategies.
Data Highlights
{'table': {'Selenium': {'HF Patients': 'Specify mean serum selenium level', 'Controls': 'Specify mean serum selenium level'}, 'SOD': {'HF Patients': 'Specify mean SOD level', 'Controls': 'Specify mean SOD level'}, 'TNF-α': {'HF Patients': 'Specify mean TNF-α level', 'Controls': 'Specify mean TNF-α level'}, 'IL-6': {'HF Patients': 'Specify mean IL-6 level', 'Controls': 'Specify mean IL-6 level'}, 'MDA': {'HF Patients': 'Specify mean MDA level', 'Controls': 'Specify mean MDA level'}}}
Key Findings
Selenium levels were significantly lower in HF patients compared to healthy controls.
Increased levels of inflammatory markers (TNF-α, IL-6) and oxidative stress (MDA) were observed in HF patients.
Selenium positively correlated with left ventricular ejection fraction (LVEF) and negatively with inflammatory markers.
In vitro studies showed selenium reduced pro-inflammatory and pro-fibrotic gene expression in cardiomyocytes under stress conditions.
Subgroup analysis indicated varying selenium levels across different HF phenotypes, particularly lower levels in HFmrEF.
Clinical Implications
The findings suggest that monitoring serum selenium levels may provide valuable insights into the inflammatory and oxidative stress status of patients with post-infarction heart failure. This could inform future therapeutic approaches aimed at improving patient outcomes through selenium supplementation or dietary interventions.
Conclusion
Selenium deficiency is linked to increased inflammation and oxidative stress in post-infarction heart failure, highlighting its potential as a biomarker for further research and intervention strategies.
Despite major advances in guideline-directed medical therapy (GDMT), worsening heart failure continues to drive significant morbidity, repeat hospitalizations and healthcare utilization worldwide.
