Xinxin Liu1, Zulong Xie2, Meng Sun1, Xuedong Wang1, Ji Li1, Jinjin Cui1, Fengyun Zhang3, Li Yin1, Dan Huang1, Jingbo Hou1, Jinwei Tian4, Bo Yu5. 1. Department of Cardiology, 2nd Affiliated Hospital of Harbin Medical University, Harbin 150086, China; Key Laboratory of Myocardial Ischemia, Ministry of Education, Harbin Medical University, Harbin 150086, China. 2. Department of Cardiology, The Second Affiliated Hospital of Chongqing Medical University, Chongqing 400010, China. 3. Department of Cardiology, The Affiliated Hospital of Xuzhou Medical University, Xuzhou 221000, China. 4. Department of Cardiology, 2nd Affiliated Hospital of Harbin Medical University, Harbin 150086, China; Key Laboratory of Myocardial Ischemia, Ministry of Education, Harbin Medical University, Harbin 150086, China. Electronic address: tianjinweidr2009@163.com. 5. Department of Cardiology, 2nd Affiliated Hospital of Harbin Medical University, Harbin 150086, China; Key Laboratory of Myocardial Ischemia, Ministry of Education, Harbin Medical University, Harbin 150086, China. Electronic address: dryu_hmu@163.com.
Abstract
BACKGROUND: Plaque vulnerability indicates the risk of a cardiovascular event. In the present study, we sought to analyze the relationship between trimethylamine N-oxide (TMAO), a gut microbiota metabolite from dietary phosphatidylcholine, and vulnerable plaque characteristics in patients with coronary artery disease (CAD). METHODS: One hundred eighty non-culprit plaques from 90 patients with ACS or with stable angina were assessed by optical coherence tomography (OCT). The plasma TMAO levels were measured using rapid resolution liquid chromatography quadrupole time-of-flight mass spectrometry (RRLC-QTOF/MS). RESULTS: Patients were divided into two groups (high TMAO group and low TMAO group) according to the median plasma TMAO level (114.73 μg/L). The non-culprit plaques in the high TMAO group exhibited a thinner fibrous cap thickness (FCT) (65.97 ± 25.89 vs. 93.0 ± 28.28 μm, P < 0.001), higher frequency of microvessels (75.6% vs. 31.1%, P < 0.001, per-patient) and increased incidence of thin-cap fibroatheroma (TCFA) (69.2% vs. 18.4%, P < 0.001, per-patient) compared with the low TMAO group. Moreover, the level of TMAO was negatively associated with FCT (r = -0.418, P < 0.001). Furthermore, multivariate regression analysis results showed that TMAO (OR: 7.455, 95% CI: 2.753-20.189, P < 0.001) had a significant association with TCFA, with a cut-off point of 118.34 μg/L, specificity of 72.6% and sensitivity of 79.5% in predicting the prevalence of TCFA. CONCLUSIONS: In conclusion, these findings suggest that the level of TMAO is significantly correlated with the incidence of TCFA. New biomarkers acquired through non-invasive means, such as TMAO, offer the potential to improve risk stratification and clinical management in patients with CAD.
BACKGROUND: Plaque vulnerability indicates the risk of a cardiovascular event. In the present study, we sought to analyze the relationship between trimethylamine N-oxide (TMAO), a gut microbiota metabolite from dietary phosphatidylcholine, and vulnerable plaque characteristics in patients with coronary artery disease (CAD). METHODS: One hundred eighty non-culprit plaques from 90 patients with ACS or with stable angina were assessed by optical coherence tomography (OCT). The plasma TMAO levels were measured using rapid resolution liquid chromatography quadrupole time-of-flight mass spectrometry (RRLC-QTOF/MS). RESULTS:Patients were divided into two groups (high TMAO group and low TMAO group) according to the median plasma TMAO level (114.73 μg/L). The non-culprit plaques in the high TMAO group exhibited a thinner fibrous cap thickness (FCT) (65.97 ± 25.89 vs. 93.0 ± 28.28 μm, P < 0.001), higher frequency of microvessels (75.6% vs. 31.1%, P < 0.001, per-patient) and increased incidence of thin-cap fibroatheroma (TCFA) (69.2% vs. 18.4%, P < 0.001, per-patient) compared with the low TMAO group. Moreover, the level of TMAO was negatively associated with FCT (r = -0.418, P < 0.001). Furthermore, multivariate regression analysis results showed that TMAO (OR: 7.455, 95% CI: 2.753-20.189, P < 0.001) had a significant association with TCFA, with a cut-off point of 118.34 μg/L, specificity of 72.6% and sensitivity of 79.5% in predicting the prevalence of TCFA. CONCLUSIONS: In conclusion, these findings suggest that the level of TMAO is significantly correlated with the incidence of TCFA. New biomarkers acquired through non-invasive means, such as TMAO, offer the potential to improve risk stratification and clinical management in patients with CAD.
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