Positive Association of Plasma Trimethylamine-N-Oxide and Atherosclerosis in Patient with Acute Coronary Syndrome
Aim. Atherosclerosis is the major cause of acute coronary syndrome (ACS) which is a significant contributor to both morbidity and mortality in the world. The microbiome-derived metabolite trimethylamine-N-oxide (TMAO) has aroused great interest and controversy as a risk factor of atherosclerosis. Th...
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| Vydané v: | Cardiovascular therapeutics Ročník 2022; s. 1 - 9 |
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| Hlavní autori: | , , , |
| Médium: | Journal Article |
| Jazyk: | English |
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Hindawi
03.11.2022
John Wiley & Sons, Inc Wiley |
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| ISSN: | 1755-5914, 1755-5922, 1755-5922 |
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| Abstract | Aim. Atherosclerosis is the major cause of acute coronary syndrome (ACS) which is a significant contributor to both morbidity and mortality in the world. The microbiome-derived metabolite trimethylamine-N-oxide (TMAO) has aroused great interest and controversy as a risk factor of atherosclerosis. Therefore, in this study, we aimed at investigating whether plasma TMAO can be a risk factor of atherosclerosis in coronary artery of patients with ACS and how this relates to lipids and proinflammatory cytokines in plasma. Methods. We enrolled consecutive patients with ACS who underwent percutaneous coronary intervention (PCI). Gensini scoring was used to evaluate angiographic atherosclerosis in the coronary artery of the patients. 13 patients were divided into low (Gensini score<25), 33 into intermediate (Gensini score 25-50), and 81 into severe atherosclerosis (Gensini score ≥50). Plasma TMAO, vasculitis factors, and cardiovascular biomarkers were measured by clinical biochemistry, intima-media thickness (IMT) of carotid artery was determined by the Color Doppler ultrasound, and the atherosclerotic lesion in coronary artery was assessed in PCI. Results. Plasma TMAO concentrations were positively associated with Gensini score (OR=0.629, p<0.001) and Gensini subgroup (R=0.604, p<0.001). Plasma TMAO concentrations in patients with severe coronary atherosclerosis were higher than those of patients with moderate coronary atherosclerosis, and the plasma TMAO concentrations of patients with moderate coronary atherosclerosis were higher than those of patients with mild coronary atherosclerosis, the difference was statistically significant [4.73 (3.13, 4.62) versus 1.13 (0.63, 3.34) versus 0.79 (0.20, 1.29), p<0.001], respectively. Furthermore, ROC analysis showed that plasma TMAO could identify the severity of atherosclerosis (p<0.001). The AUC of TMAO for severe atherosclerosis was 0.852 (95%CI=0.779−0.925). The sensitivity and specificity of TMAO for identifying severe atherosclerosis are 96.3% and 63.0% when the cut-off value of TMAO was set at 1.2715 pg/ml. Furthermore, logistic regression analysis showed plasma TMAO concentrations were positively associated with severity of atherosclerosis in coronary artery (OR=1.934, 95%CI=1.522−2.459, p<0.001). For all that, negatively association was observed between TMAO and age (OR=−0.224, p<0.05), B-type natriuretic peptide (BNP) (OR=−0.175, p<0.05), and interleukin-8 (IL-8) (OR=−0.324, p<0.001), while positive association was observed between TMAO and nitric oxide (NO) (OR=0.234, p<0.01). However, there is no obvious association was observed between Gensini score and cardiovascular biomarkers, vasculitis factors, and carotid IMT, respectively. Conclusion. Our cross-sectional observation suggested that plasma TMAO concentrations positively associated with coronary atherosclerosis in ACS patients and serve as a risk factor for severe atherosclerosis. Plasma TMAO also correlated with age, BNP, IL-8, and NO. However, no obvious association was found between atherosclerosis with vasculitis factors and cardiovascular biomarkers in this study, and there was no conclusive evidence showing TMAO enhance atherosclerosis via regulation of inflammation or lipid. |
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| AbstractList | Atherosclerosis is the major cause of acute coronary syndrome (ACS) which is a significant contributor to both morbidity and mortality in the world. The microbiome-derived metabolite trimethylamine-N-oxide (TMAO) has aroused great interest and controversy as a risk factor of atherosclerosis. Therefore, in this study, we aimed at investigating whether plasma TMAO can be a risk factor of atherosclerosis in coronary artery of patients with ACS and how this relates to lipids and proinflammatory cytokines in plasma.AimAtherosclerosis is the major cause of acute coronary syndrome (ACS) which is a significant contributor to both morbidity and mortality in the world. The microbiome-derived metabolite trimethylamine-N-oxide (TMAO) has aroused great interest and controversy as a risk factor of atherosclerosis. Therefore, in this study, we aimed at investigating whether plasma TMAO can be a risk factor of atherosclerosis in coronary artery of patients with ACS and how this relates to lipids and proinflammatory cytokines in plasma.We enrolled consecutive patients with ACS who underwent percutaneous coronary intervention (PCI). Gensini scoring was used to evaluate angiographic atherosclerosis in the coronary artery of the patients. 13 patients were divided into low (Gensini score < 25), 33 into intermediate (Gensini score 25-50), and 81 into severe atherosclerosis (Gensini score ≥50). Plasma TMAO, vasculitis factors, and cardiovascular biomarkers were measured by clinical biochemistry, intima-media thickness (IMT) of carotid artery was determined by the Color Doppler ultrasound, and the atherosclerotic lesion in coronary artery was assessed in PCI.MethodsWe enrolled consecutive patients with ACS who underwent percutaneous coronary intervention (PCI). Gensini scoring was used to evaluate angiographic atherosclerosis in the coronary artery of the patients. 13 patients were divided into low (Gensini score < 25), 33 into intermediate (Gensini score 25-50), and 81 into severe atherosclerosis (Gensini score ≥50). Plasma TMAO, vasculitis factors, and cardiovascular biomarkers were measured by clinical biochemistry, intima-media thickness (IMT) of carotid artery was determined by the Color Doppler ultrasound, and the atherosclerotic lesion in coronary artery was assessed in PCI.Plasma TMAO concentrations were positively associated with Gensini score (OR = 0.629, p < 0.001) and Gensini subgroup (R = 0.604, p < 0.001). Plasma TMAO concentrations in patients with severe coronary atherosclerosis were higher than those of patients with moderate coronary atherosclerosis, and the plasma TMAO concentrations of patients with moderate coronary atherosclerosis were higher than those of patients with mild coronary atherosclerosis, the difference was statistically significant [4.73 (3.13, 4.62) versus 1.13 (0.63, 3.34) versus 0.79 (0.20, 1.29), p < 0.001], respectively. Furthermore, ROC analysis showed that plasma TMAO could identify the severity of atherosclerosis (p < 0.001). The AUC of TMAO for severe atherosclerosis was 0.852 (95%CI = 0.779 - 0.925). The sensitivity and specificity of TMAO for identifying severe atherosclerosis are 96.3% and 63.0% when the cut-off value of TMAO was set at 1.2715 pg/ml. Furthermore, logistic regression analysis showed plasma TMAO concentrations were positively associated with severity of atherosclerosis in coronary artery (OR = 1.934, 95%CI = 1.522 - 2.459, p < 0.001). For all that, negatively association was observed between TMAO and age (OR = -0.224, p < 0.05), B-type natriuretic peptide (BNP) (OR = -0.175, p < 0.05), and interleukin-8 (IL-8) (OR = -0.324, p < 0.001), while positive association was observed between TMAO and nitric oxide (NO) (OR = 0.234, p < 0.01). However, there is no obvious association was observed between Gensini score and cardiovascular biomarkers, vasculitis factors, and carotid IMT, respectively.ResultsPlasma TMAO concentrations were positively associated with Gensini score (OR = 0.629, p < 0.001) and Gensini subgroup (R = 0.604, p < 0.001). Plasma TMAO concentrations in patients with severe coronary atherosclerosis were higher than those of patients with moderate coronary atherosclerosis, and the plasma TMAO concentrations of patients with moderate coronary atherosclerosis were higher than those of patients with mild coronary atherosclerosis, the difference was statistically significant [4.73 (3.13, 4.62) versus 1.13 (0.63, 3.34) versus 0.79 (0.20, 1.29), p < 0.001], respectively. Furthermore, ROC analysis showed that plasma TMAO could identify the severity of atherosclerosis (p < 0.001). The AUC of TMAO for severe atherosclerosis was 0.852 (95%CI = 0.779 - 0.925). The sensitivity and specificity of TMAO for identifying severe atherosclerosis are 96.3% and 63.0% when the cut-off value of TMAO was set at 1.2715 pg/ml. Furthermore, logistic regression analysis showed plasma TMAO concentrations were positively associated with severity of atherosclerosis in coronary artery (OR = 1.934, 95%CI = 1.522 - 2.459, p < 0.001). For all that, negatively association was observed between TMAO and age (OR = -0.224, p < 0.05), B-type natriuretic peptide (BNP) (OR = -0.175, p < 0.05), and interleukin-8 (IL-8) (OR = -0.324, p < 0.001), while positive association was observed between TMAO and nitric oxide (NO) (OR = 0.234, p < 0.01). However, there is no obvious association was observed between Gensini score and cardiovascular biomarkers, vasculitis factors, and carotid IMT, respectively.Our cross-sectional observation suggested that plasma TMAO concentrations positively associated with coronary atherosclerosis in ACS patients and serve as a risk factor for severe atherosclerosis. Plasma TMAO also correlated with age, BNP, IL-8, and NO. However, no obvious association was found between atherosclerosis with vasculitis factors and cardiovascular biomarkers in this study, and there was no conclusive evidence showing TMAO enhance atherosclerosis via regulation of inflammation or lipid.ConclusionOur cross-sectional observation suggested that plasma TMAO concentrations positively associated with coronary atherosclerosis in ACS patients and serve as a risk factor for severe atherosclerosis. Plasma TMAO also correlated with age, BNP, IL-8, and NO. However, no obvious association was found between atherosclerosis with vasculitis factors and cardiovascular biomarkers in this study, and there was no conclusive evidence showing TMAO enhance atherosclerosis via regulation of inflammation or lipid. Aim. Atherosclerosis is the major cause of acute coronary syndrome (ACS) which is a significant contributor to both morbidity and mortality in the world. The microbiome-derived metabolite trimethylamine-N-oxide (TMAO) has aroused great interest and controversy as a risk factor of atherosclerosis. Therefore, in this study, we aimed at investigating whether plasma TMAO can be a risk factor of atherosclerosis in coronary artery of patients with ACS and how this relates to lipids and proinflammatory cytokines in plasma. Methods. We enrolled consecutive patients with ACS who underwent percutaneous coronary intervention (PCI). Gensini scoring was used to evaluate angiographic atherosclerosis in the coronary artery of the patients. 13 patients were divided into low (Gensini score<25), 33 into intermediate (Gensini score 25-50), and 81 into severe atherosclerosis (Gensini score ≥50). Plasma TMAO, vasculitis factors, and cardiovascular biomarkers were measured by clinical biochemistry, intima-media thickness (IMT) of carotid artery was determined by the Color Doppler ultrasound, and the atherosclerotic lesion in coronary artery was assessed in PCI. Results. Plasma TMAO concentrations were positively associated with Gensini score (OR=0.629, p<0.001) and Gensini subgroup (R=0.604, p<0.001). Plasma TMAO concentrations in patients with severe coronary atherosclerosis were higher than those of patients with moderate coronary atherosclerosis, and the plasma TMAO concentrations of patients with moderate coronary atherosclerosis were higher than those of patients with mild coronary atherosclerosis, the difference was statistically significant [4.73 (3.13, 4.62) versus 1.13 (0.63, 3.34) versus 0.79 (0.20, 1.29), p<0.001], respectively. Furthermore, ROC analysis showed that plasma TMAO could identify the severity of atherosclerosis (p<0.001). The AUC of TMAO for severe atherosclerosis was 0.852 (95%CI=0.779−0.925). The sensitivity and specificity of TMAO for identifying severe atherosclerosis are 96.3% and 63.0% when the cut-off value of TMAO was set at 1.2715 pg/ml. Furthermore, logistic regression analysis showed plasma TMAO concentrations were positively associated with severity of atherosclerosis in coronary artery (OR=1.934, 95%CI=1.522−2.459, p<0.001). For all that, negatively association was observed between TMAO and age (OR=−0.224, p<0.05), B-type natriuretic peptide (BNP) (OR=−0.175, p<0.05), and interleukin-8 (IL-8) (OR=−0.324, p<0.001), while positive association was observed between TMAO and nitric oxide (NO) (OR=0.234, p<0.01). However, there is no obvious association was observed between Gensini score and cardiovascular biomarkers, vasculitis factors, and carotid IMT, respectively. Conclusion. Our cross-sectional observation suggested that plasma TMAO concentrations positively associated with coronary atherosclerosis in ACS patients and serve as a risk factor for severe atherosclerosis. Plasma TMAO also correlated with age, BNP, IL-8, and NO. However, no obvious association was found between atherosclerosis with vasculitis factors and cardiovascular biomarkers in this study, and there was no conclusive evidence showing TMAO enhance atherosclerosis via regulation of inflammation or lipid. Aim. Atherosclerosis is the major cause of acute coronary syndrome (ACS) which is a significant contributor to both morbidity and mortality in the world. The microbiome-derived metabolite trimethylamine-N-oxide (TMAO) has aroused great interest and controversy as a risk factor of atherosclerosis. Therefore, in this study, we aimed at investigating whether plasma TMAO can be a risk factor of atherosclerosis in coronary artery of patients with ACS and how this relates to lipids and proinflammatory cytokines in plasma. Methods. We enrolled consecutive patients with ACS who underwent percutaneous coronary intervention (PCI). Gensini scoring was used to evaluate angiographic atherosclerosis in the coronary artery of the patients. 13 patients were divided into low (Gensiniscore<25), 33 into intermediate (Gensini score 25-50), and 81 into severe atherosclerosis (Gensini score≥50). Plasma TMAO, vasculitis factors, and cardiovascular biomarkers were measured by clinical biochemistry, intima-media thickness (IMT) of carotid artery was determined by the Color Doppler ultrasound, and the atherosclerotic lesion in coronary artery was assessed in PCI. Results. Plasma TMAO concentrations were positively associated with Gensini score (OR=0.629, p<0.001) and Gensini subgroup (R=0.604, p<0.001). Plasma TMAO concentrations in patients with severe coronary atherosclerosis were higher than those of patients with moderate coronary atherosclerosis, and the plasma TMAO concentrations of patients with moderate coronary atherosclerosis were higher than those of patients with mild coronary atherosclerosis, the difference was statistically significant [4.73 (3.13, 4.62) versus 1.13 (0.63, 3.34) versus 0.79 (0.20, 1.29), p<0.001], respectively. Furthermore, ROC analysis showed that plasma TMAO could identify the severity of atherosclerosis (p<0.001). The AUC of TMAO for severe atherosclerosis was 0.852 (95%CI=0.779-0.925). The sensitivity and specificity of TMAO for identifying severe atherosclerosis are 96.3% and 63.0% when the cut-off value of TMAO was set at 1.2715pg/ml. Furthermore, logistic regression analysis showed plasma TMAO concentrations were positively associated with severity of atherosclerosis in coronary artery (OR=1.934, 95%CI=1.522-2.459, p<0.001). For all that, negatively association was observed between TMAO and age (OR=-0.224, p<0.05), B-type natriuretic peptide (BNP) (OR=-0.175, p<0.05), and interleukin-8 (IL-8) (OR=-0.324, p<0.001), while positive association was observed between TMAO and nitric oxide (NO) (OR=0.234, p<0.01). However, there is no obvious association was observed between Gensini score and cardiovascular biomarkers, vasculitis factors, and carotid IMT, respectively. Conclusion. Our cross-sectional observation suggested that plasma TMAO concentrations positively associated with coronary atherosclerosis in ACS patients and serve as a risk factor for severe atherosclerosis. Plasma TMAO also correlated with age, BNP, IL-8, and NO. However, no obvious association was found between atherosclerosis with vasculitis factors and cardiovascular biomarkers in this study, and there was no conclusive evidence showing TMAO enhance atherosclerosis via regulation of inflammation or lipid. Aim. Atherosclerosis is the major cause of acute coronary syndrome (ACS) which is a significant contributor to both morbidity and mortality in the world. The microbiome-derived metabolite trimethylamine-N-oxide (TMAO) has aroused great interest and controversy as a risk factor of atherosclerosis. Therefore, in this study, we aimed at investigating whether plasma TMAO can be a risk factor of atherosclerosis in coronary artery of patients with ACS and how this relates to lipids and proinflammatory cytokines in plasma. Methods. We enrolled consecutive patients with ACS who underwent percutaneous coronary intervention (PCI). Gensini scoring was used to evaluate angiographic atherosclerosis in the coronary artery of the patients. 13 patients were divided into low ( Gensini score < 25 ), 33 into intermediate (Gensini score 25-50), and 81 into severe atherosclerosis (Gensini score ≥50). Plasma TMAO, vasculitis factors, and cardiovascular biomarkers were measured by clinical biochemistry, intima-media thickness (IMT) of carotid artery was determined by the Color Doppler ultrasound, and the atherosclerotic lesion in coronary artery was assessed in PCI. Results. Plasma TMAO concentrations were positively associated with Gensini score ( OR = 0.629 , p < 0.001 ) and Gensini subgroup ( R = 0.604 , p < 0.0 01). Plasma TMAO concentrations in patients with severe coronary atherosclerosis were higher than those of patients with moderate coronary atherosclerosis, and the plasma TMAO concentrations of patients with moderate coronary atherosclerosis were higher than those of patients with mild coronary atherosclerosis, the difference was statistically significant [4.73 (3.13, 4.62) versus 1.13 (0.63, 3.34) versus 0.79 (0.20, 1.29), p < 0.001 ], respectively. Furthermore, ROC analysis showed that plasma TMAO could identify the severity of atherosclerosis ( p < 0.001 ). The AUC of TMAO for severe atherosclerosis was 0.852 ( 95 % CI = 0.779 − 0.925 ). The sensitivity and specificity of TMAO for identifying severe atherosclerosis are 96.3% and 63.0% when the cut-off value of TMAO was set at 1.2715 pg/ml. Furthermore, logistic regression analysis showed plasma TMAO concentrations were positively associated with severity of atherosclerosis in coronary artery ( OR = 1.934 , 95 % CI = 1.522 − 2.459 , p < 0.001 ). For all that, negatively association was observed between TMAO and age ( OR = − 0.224 , p < 0.05 ), B-type natriuretic peptide (BNP) ( OR = − 0.175 , p < 0.05 ), and interleukin-8 (IL-8) ( OR = − 0.324 , p < 0.001 ), while positive association was observed between TMAO and nitric oxide (NO) ( OR = 0.234 , p < 0.01 ). However, there is no obvious association was observed between Gensini score and cardiovascular biomarkers, vasculitis factors, and carotid IMT, respectively. Conclusion. Our cross-sectional observation suggested that plasma TMAO concentrations positively associated with coronary atherosclerosis in ACS patients and serve as a risk factor for severe atherosclerosis. Plasma TMAO also correlated with age, BNP, IL-8, and NO. However, no obvious association was found between atherosclerosis with vasculitis factors and cardiovascular biomarkers in this study, and there was no conclusive evidence showing TMAO enhance atherosclerosis via regulation of inflammation or lipid. |
| Audience | Academic |
| Author | Lin, Ying Kong, Wanwen Ma, Junyi Chen, Weiyu |
| AuthorAffiliation | 1 Department of Cardiology, Shunde Hospital, Guangzhou University of Traditional Chinese Medicine, China 3 The Heart Research Institute, The University of Sydney, Australia 2 Guangzhou University of Traditional Chinese Medicine, China |
| AuthorAffiliation_xml | – name: 3 The Heart Research Institute, The University of Sydney, Australia – name: 2 Guangzhou University of Traditional Chinese Medicine, China – name: 1 Department of Cardiology, Shunde Hospital, Guangzhou University of Traditional Chinese Medicine, China |
| Author_xml | – sequence: 1 givenname: Wanwen surname: Kong fullname: Kong, Wanwen organization: Department of CardiologyShunde HospitalGuangzhou University of Traditional Chinese MedicineChinagzucm.edu.cn – sequence: 2 givenname: Junyi surname: Ma fullname: Ma, Junyi organization: Guangzhou University of Traditional Chinese MedicineChinagzucm.edu.cn – sequence: 3 givenname: Ying surname: Lin fullname: Lin, Ying organization: Guangzhou University of Traditional Chinese MedicineChinagzucm.edu.cn – sequence: 4 givenname: Weiyu orcidid: 0000-0002-1507-1843 surname: Chen fullname: Chen, Weiyu organization: The Heart Research InstituteThe University of SydneyAustraliasydney.edu.au |
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| ContentType | Journal Article |
| Copyright | Copyright © 2022 Wanwen Kong et al. COPYRIGHT 2022 John Wiley & Sons, Inc. Copyright © 2022 Wanwen Kong et al. This is an open access article distributed under the Creative Commons Attribution License (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. https://creativecommons.org/licenses/by/4.0 Copyright © 2022 Wanwen Kong et al. 2022 |
| Copyright_xml | – notice: Copyright © 2022 Wanwen Kong et al. – notice: COPYRIGHT 2022 John Wiley & Sons, Inc. – notice: Copyright © 2022 Wanwen Kong et al. This is an open access article distributed under the Creative Commons Attribution License (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. https://creativecommons.org/licenses/by/4.0 – notice: Copyright © 2022 Wanwen Kong et al. 2022 |
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| References | 24 Y. Wang (1) 2019; 35 J. Bu (2) 2020; 43 25 26 27 28 29 Y. Tan (22) 2019; 12 M. W. Xia (13) 2019; 11 K. Zuo (23) 2019; 8 30 31 10 32 11 33 12 34 14 Y. Huo (15) 2019 16 17 19 3 4 5 6 7 G. H. Ma (18) 2017; 37 8 9 20 21 |
| References_xml | – ident: 3 doi: 10.1016/S0140-6736(17)32154-2 – start-page: 103 volume-title: Training Materials for Interventional Therapy of Coronary Heart Disease, 2018 ed year: 2019 ident: 15 – ident: 29 doi: 10.3390/ijms20143570 – ident: 30 doi: 10.1002/jcp.29518 – ident: 5 doi: 10.1007/s13238-018-0549-0 – ident: 6 doi: 10.1056/NEJMoa1109400 – ident: 24 doi: 10.1373/clinchem.2016.264853 – ident: 9 doi: 10.1016/j.biopha.2017.11.016 – ident: 14 doi: 10.1016/j.clinbiochem.2020.10.008 – ident: 16 doi: 10.1161/JAHA.118.010606 – ident: 28 doi: 10.1161/JAHA.115.002767 – volume: 12 start-page: 281 issue: 1 year: 2019 ident: 22 article-title: Plasma trimethylamine N-oxide as a novel biomarker for plaque rupture in patients with ST-segment-elevation myocardial infarction publication-title: Circulation: Cardiovascular Interventions – volume: 8 start-page: 58 issue: 6 year: 2019 ident: 23 article-title: Disordered gut microbiota and alterations in metabolic patterns are associated with atrial fibrillation publication-title: Gigascience – ident: 25 doi: 10.1093/eurheartj/ehw582 – ident: 19 doi: 10.1007/s11739-020-02470-5 – ident: 17 doi: 10.1097/MD.0000000000014309 – volume: 35 start-page: 601 issue: 7 year: 2019 ident: 1 article-title: Coronary artery lesion and carotid atherosclerosis study on the correlation between vulnerability of sclerotic plaque publication-title: Chinese Journal of Ultrasound Medicine – ident: 12 doi: 10.3389/fcvm.2021.778615 – ident: 32 doi: 10.1016/j.pharmthera.2014.06.003 – volume: 43 start-page: 129 issue: 3 year: 2020 ident: 2 article-title: Metabolic abnormalities and prevention and treatment of cardiovascular diseases in Chinese adults publication-title: Shanghai Medical Journal – ident: 27 doi: 10.1161/JAHA.117.006347 – ident: 31 doi: 10.5830/CVJA-2011-068 – ident: 11 doi: 10.1016/S0002-9149(83)80105-2 – volume: 11 start-page: 63 year: 2019 ident: 13 article-title: Correlation of platelet parameters and serum IL-6 levels with severity of coronary lesions in coronary heart disease publication-title: Chinese Journal of Evidence-Based Medicine – volume: 37 start-page: 8451 issue: 71 year: 2017 ident: 18 article-title: Trimethylamine N-oxide in atherogenesis: impairing endothelial self-repair capacity and enhancing monocyte adhesion publication-title: Bioscience Reports – ident: 34 doi: 10.1002/clc.23246 – ident: 7 doi: 10.3390/nu10101398 – ident: 21 doi: 10.1007/s11883-021-00910-x – ident: 20 doi: 10.3389/fcvm.2021.628471 – ident: 33 doi: 10.1007/s11883-020-0819-1 – ident: 4 doi: 10.1001/jamacardio.2019.3355 – ident: 26 doi: 10.1161/ATVBAHA.118.311023 – ident: 8 doi: 10.1038/s41569-018-0108-7 – ident: 10 doi: 10.1016/j.bbrc.2016.11.017 |
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| Snippet | Aim. Atherosclerosis is the major cause of acute coronary syndrome (ACS) which is a significant contributor to both morbidity and mortality in the world. The... Atherosclerosis is the major cause of acute coronary syndrome (ACS) which is a significant contributor to both morbidity and mortality in the world. The... |
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| SubjectTerms | Acute coronary syndromes Analysis Angina pectoris Atherosclerosis Biomarkers Cardiac patients Cardiovascular disease Cholesterol Coronary heart disease Coronary vessels Cross-sectional studies Cytokines Dehydrogenases Electrocardiography Health aspects Health risks Heart attacks Hospitals Hypertension Kinases Laboratories Medical imaging Metabolism Metabolites Mortality Natriuretic peptides Nitric oxide Plasma Risk factors Traditional Chinese medicine Transluminal angioplasty Veins & arteries |
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| Title | Positive Association of Plasma Trimethylamine-N-Oxide and Atherosclerosis in Patient with Acute Coronary Syndrome |
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