Correlation Analysis of Gut Microbiota Derivatives with Coronary Artery Disease Severity and Prognosis

Previous research has highlighted a connection between gut microbiota derivatives and atherosclerosis. This study assesses the association between gut microbiota derivatives and coronary artery disease (CAD) to enhance CAD prevention and treatment strategies.

Patients presenting with suspected CAD were categorized into CAD and non-CAD groups. A propensity score matching analysis was performed to exclude confounding factors. Key differences in general characteristics and gut microbiota derivatives between these groups were also assessed. Additionally, the study explored the correlation between significant differences in the Gensini score and coronary flow reserve. Moreover, the potential of significant indicators to predict the diagnosis of coronary artery disease was analyzed.

After propensity score matching, the concentrations of interleukin-6 (IL-6) (47.23 ± 7.45 vs. 39.56 ± 7.37; p < 0.001), lipopolysaccharide (LPS) (12.79 ± 2.07 vs. 11.71 ± 1.88; p = 0.031), high-sensitivity C-reactive protein (hs-CRP) (13.58 ± 2.62 vs. 11.57 ± 2.49; p = 0.002), phenylacetyl glutamine (PAGIn) (619.20 ± 119.33 vs. 555.64 ± 109.29; p = 0.029), and trimethylamine-N-oxide (TMAO) (13.01 ± 2.19 vs. 11.70 ± 1.78; p = 0.011) in the CAD group were significantly elevated compared to those in the non-CAD group. Conversely, the serum levels of glucagon-like peptide-1 (GLP-1) (7.74 ± 2.07 vs. 9.06 ± 2.11; p = 0.012) were notably lower in the CAD group than in the non-CAD group. A positive association was observed between the serum concentrations of IL-6 (r = 0.410; p < 0.001), hs-CRP (r = 0.317; p < 0.007), TMAO (r = 0.311; p < 0.008), and coronary Gensini score. Moreover, IL-6 (b = 1.769, 95% confidence interval (CI): 0.256-3.282; p = 0.023) and TMAO (b = 10.735, 95% CI: 4.883-16.588; p < 0.001) had a direct positive impact on the coronary Gensini score. The highest diagnostic value for CAD was observed when the IL-6 cut-off value was 45.17 (sensitivity 69.6%, specificity 73.1%, area under curve 0.770; 95% CI: 0.662-0.879; p < 0.001). Meanwhile, the highest diagnostic value for CAD was noted when the TMAO cut-off value was 12.44 (sensitivity 65.2%, specificity 76.9%, the area under the curve 0.689; 95% CI: 0.564-0.814; p = 0.008). Serum TMAO was negatively correlated with coronary flow reserve (CFR) in CAD patients (r = -0.593; p = 0.009).

These findings suggest that serum IL-6, LPS, hs-CRP, PAGIn, TMAO, and GLP-1 levels can be used as clinical markers for predicting CAD severity. Among these, IL-6, hs-CRP, and TMAO are identified as independent risk factors influencing the severity of CAD-elevated levels of IL-6 and TMAO exhibit predictive utility for CAD diagnosis. Furthermore, serum TMAO is a potential clinical marker for forecasting a CAD prognosis.