IMR Press / RCM / Volume 22 / Issue 1 / DOI: 10.31083/j.rcm.2021.01.299
Open Access Original Research
Trimethylamine N-oxide is associated with coronary atherosclerotic burden in non-ST-segment myocardial infarction patients: SZ-NSTEMI prospective cohort study
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1 Department of Cardiology, Fuwai Hospital Chinese Academy of Medical Sciences Shenzhen, 518055 Shenzhen, P. R. China
2 Shenzhen Key Laboratory of Biomimetic Materials and Cellular Immunomodulation, Institute of Biomedicine and Biotechnology, Shenzhen Institute of Advanced Technology, Chinese Academy of Sciences, 518055 Shenzhen, P. R. China
3 Department of Cardiology, The First Affiliated Hospital of Dalian Medical University, 116011 Dalian, P. R. China
4 Guangdong Cardiovascular Institute, Guangdong General Hospital, Guangdong Academy of Medical Sciences, 510080 Guangzhou, P. R. China
5 Tianjin Key Laboratory of Ionic-Molecular Function of Cardiovascular Disease, Department of Cardiology, Tianjin Institute of Cardiology, Second Hospital of Tianjin Medical University, 300211 Tianjin, P. R. China
6 Department of Cardiology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, 200080 Shanghai, P. R. China
7 Department of Cardiology, Rehman Medical Institute, 25000 Peshawar, Pakistan
Rev. Cardiovasc. Med. 2021, 22(1), 231–238;
Submitted: 7 January 2021 | Revised: 11 March 2021 | Accepted: 12 March 2021 | Published: 30 March 2021

Trimethylamine N-oxide (TMAO) is reported to accelerate atherosclerosis and the development of adverse cardiac outcomes. Relationship between coronary atherosclerotic burden and TMAO has been examined in stable coronary artery disease and ST-segment elevation myocardial infarction, but not in non-ST-segment elevation myocardial infarction (NSTEMI). We examined the association between TMAO and coronary atherosclerotic burden in NSTEMI. In this prospective cohort study, two groups including NSTEMI (n = 73) and age-sex matched Healthy (n = 35) individuals were enrolled between 2019 and 2020. Coronary atherosclerotic burden was stratified based on the number of diseased coronary vessels and clinical risk scores including SYNTAX and GENSINI. Fasting plasma TMAO was measured by isotope dilution high-performance liquid chromatography. The median plasma TMAO levels were significantly higher in the NSTEMI group than in the Healthy group, respectively (0.59 μM; interquartile range [IQR]: 0.43-0.78 versus 0.42 μM; IQR: 0.33-0.64; P = 0.006). Within the NSTEMI group, higher TMAO levels were observed in the multivessel disease (MVD) versus single vessel disease (P = 0.002), and intermediate-high risk (score 23) versus low risk (score < 23) of SYNTAX (P = 0.003) and GENSINI (P = 0.005). TMAO level remained an independent predictor of MVD (odds ratio [OR]: 5.94, P = 0.005), intermediate-high risk SYNTAX (OR: 3.61, P = 0.013) and GENSINI scores (OR: 4.60, P = 0.008) following adjustment for traditional risk factors. Receiver operating characteristic curve (AUC) analysis for TMAO predicted MVD (AUC: 0.73, 95% confidence interval [Cl]: 0.60-0.86, P = 0.002), intermediate-high SYNTAX score (AUC: 0.70, 95% Cl: 0.58-0.82, P = 0.003) and GENSINI score (AUC: 0.70, 95% Cl: 0.57-0.83, P = 0.005). In all, TMAO levels are independently associated with high coronary atherosclerotic burden in NSTEMI.

Trimethylamine N-oxide
Non-ST-segment elevation myocardial infarction
Coronary atherosclerotic burden
SYNTAX score
Multivessel disease
Fig. 1.
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