Changes in circulating lipopolysaccharide and zonulin following acute myocardial infarction: The impact of smoking.

BACKGROUND

Serum lipopolysaccharide (LPS), a marker of gut dysbiosis and endotoxemia is associated with myocardial infarction (MI). We investigated factors affecting LPS changes in MI patients treated with percutaneous coronary intervention (PCI) and aimed to establish factors associated with the degree of LPS decrease following MI.

METHODS

In 46 PCI-treated MI patients (mean age 57.2 [8.6]) years we measured LPS and zonulin, a marker of gut permeability, on admission, 30 and 60 days thereafter, inflammatory markers (interleukin [IL]-6, IL-18), P-selectin, and 8-isoprostaglandin F2α (8-isoPGF2α).

RESULTS

The median initial LPS concentration was 44.0 (37.0-57.0) pg/mL and it fell by 11.3 % at 1 month, with a further 8.3 % drop after the second month, in association with zonulin, but not with P-selectin or inflammatory markers. LPS and zonulin at baseline correlated positively with 8-isoPGF2α. A < 10 % decrease in LPS was recorded in 20 (43.5 %) patients and was more frequent in smokers, those with a complete occlusion of the infarct-related artery (IRA) and a shorter symptom duration before PCI. LPS decrease <10 % was associated with a decline in IL-10 concentrations 30- and 60-days post MI. On multivariate analysis only current smoking and an initial complete IRA occlusion were independently associated with <10 % decrease in LPS at 1 month (OR 10.44; 95 % CI 2.13-51.21; p = 0.004 and OR 6.59; 95 % CI 1.21-35.88; p = 0.029, respectively).

CONCLUSIONS

This study is the first to show factors affecting post-MI changes in LPS, highlighting the role of smoking and initial complete IRA occlusion in persistent low-grade endotoxemia following MI.