This observational analysis shows elevated LPS levels correlate with lower ejection fraction in myocardial infarction patients, suggesting endotoxemia may hinder recovery.
Background: Atherosclerosis is the main cause of coronary heart disease, which frequently precedes the onset of heart failure. Lipopolysaccharide (LPS), a pro-inflammatory endotoxin produced by Gram-negative bacteria, exacerbates atherosclerotic processes and negatively impacts myocardial function, particularly in the context of activating low grade inflammation. Zonulin, a key regulator of the blood-gut barrier, modulates tight junction permeability, potentially facilitating the translocation of microbial-derived compounds, including LPS, into the circulation. Given these interactions, we investigated serum levels of lipopolysaccharide and zonulin in patients following myocardial infarction. This study aimed to assess serum levels of zonulin and lipopolysaccharide (LPS) in patients who had experienced a myocardial infarction (MI) and to evaluate the association between these biomarkers and ejection fraction (EF) across different patient groups. Methods: 78 patients (22 women and 56 men) diagnosed with MI, who underwent primary PCI (percutaneous coronary intervention), were included in the study. The blood samples were collected between 24 and 48 h after PCI. Results: Post-myocardial infarction patients with an ejection fraction ≤ 40% exhibited significantly elevated serum lipopolysaccharide levels compared to those with an ejection fraction > 40%. However, no significant differences in zonulin levels were observed between the study groups. Conclusions: Our findings suggest that elevated serum lipopolysaccharide levels may be associated with a reduction in post-infarction ejection fraction. This observation highlights a potential link between endotoxemia and impaired myocardial function following MI, warranting further investigation.
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Olędzki et al. (2025) studied this question.
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