Background and Objective <p>Inflammation plays a pivotal role in the progression of coronary artery disease (CAD). High-sensitivity C-reactive protein (hsCRP) serves as a well-established biomarker for assessing cardiovascular inflammation risk. However, the specific intestinal microbiota alteration contributing to increased inflammation remains unclear. Therefore, the present study investigated the correlation between the intestinal microbiota and inflammation in patients with unstable angina (UA).</p> Methods <p>A cohort of 92 patients with UA was recruited for this study. The plasma hsCRP level was measured via a CardioPhase hsCRP assay, fecal samples were collected after admission, and 16S rRNA sequencing was conducted to identify the fecal microbial profile. The participants were classified into two groups according to the median hsCRP level (1.11&#xa0;mg/L). The composition of the fecal microbiota was compared between patients with hsCRP ≥ 1.11&#xa0;mg/L and those with hsCRP &lt; 1.11&#xa0;mg/L. Additionally, the correlations between the fecal microbiota and clinical characteristics were analyzed.</p> Results <p>A notable reduction in the relative abundance of <i>Akkermansia</i> was observed in patients with hsCRP ≥ 1.11&#xa0;mg/L, whereas the diversity of the fecal microbiota was not significantly different between patients with hsCRP ≥ 1.11&#xa0;mg/L and those with hsCRP &lt; 1.11&#xa0;mg/L. Furthermore, the abundance of <i>Akkermansia</i> was negatively correlated with hsCRP levels.</p> Conclusion <p>This study suggested a significant association between decreased levels of <i>Akkermansia</i> and inflammatory risk in patients with UA. These findings underscore the potential role of the intestinal microbiota in contributing to inflammation in UA patients. Further work is needed on the mechanism by which the microbiota contributes to inflammatory risk.</p>

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Association of Decreased Fecal Microbiota Akkermansia with Increased High-Sensitivity C-Reactive Protein Levels in Patients with Unstable Angina

  • Yuan-fan Yuan,
  • Ji-yu Zhang,
  • Jia-hao Xu,
  • Xin-yi Xia,
  • Miao Yu,
  • Ling-feng Zha,
  • De-sheng Hu,
  • Wei-min Wang,
  • Chao-long Wang,
  • Qing Wang,
  • Chen Chen,
  • Zhi-lei Shan,
  • Fen Yang,
  • Xiang Cheng

摘要

Background and Objective

Inflammation plays a pivotal role in the progression of coronary artery disease (CAD). High-sensitivity C-reactive protein (hsCRP) serves as a well-established biomarker for assessing cardiovascular inflammation risk. However, the specific intestinal microbiota alteration contributing to increased inflammation remains unclear. Therefore, the present study investigated the correlation between the intestinal microbiota and inflammation in patients with unstable angina (UA).

Methods

A cohort of 92 patients with UA was recruited for this study. The plasma hsCRP level was measured via a CardioPhase hsCRP assay, fecal samples were collected after admission, and 16S rRNA sequencing was conducted to identify the fecal microbial profile. The participants were classified into two groups according to the median hsCRP level (1.11 mg/L). The composition of the fecal microbiota was compared between patients with hsCRP ≥ 1.11 mg/L and those with hsCRP < 1.11 mg/L. Additionally, the correlations between the fecal microbiota and clinical characteristics were analyzed.

Results

A notable reduction in the relative abundance of Akkermansia was observed in patients with hsCRP ≥ 1.11 mg/L, whereas the diversity of the fecal microbiota was not significantly different between patients with hsCRP ≥ 1.11 mg/L and those with hsCRP < 1.11 mg/L. Furthermore, the abundance of Akkermansia was negatively correlated with hsCRP levels.

Conclusion

This study suggested a significant association between decreased levels of Akkermansia and inflammatory risk in patients with UA. These findings underscore the potential role of the intestinal microbiota in contributing to inflammation in UA patients. Further work is needed on the mechanism by which the microbiota contributes to inflammatory risk.