Coronary Plaque Characterization Assessed by Optical Coherence Tomography and Plasma Trimethylamine-N-oxide Levels in Patients With Coronary Artery Disease

Fu, Qiang; Zhao, Mingming; Wang, Dezhao; Hu, Hongyu; Guo, Caixia; Chen, Wei; Li, Qun; Zheng, Lemin; Chen, Buxing

doi:10.1016/j.amjcard.2016.07.071

Cited by 62 publications

(44 citation statements)

References 18 publications

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“…In line with the previous reports, plasma TMAO levels were significantly higher in patients with ruptured plaque (8.6 ± 4.8 μM) compared to those without plaque rupture (4.2 ± 2.4 μM). These data suggest that circulating TMAO level may reflect coronary plaque vulnerability and progression (Fu et al, ).…”

Section: Tmao Enhances the Risk Of Inflammation Obesity And Atherosmentioning

confidence: 93%

Trimethylamine N‐oxide: breathe new life

Subramaniam

Fletcher

2017

British J Pharmacology

143

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Section: Tmao Enhances the Risk Of Inflammation Obesity And Atherosmentioning

confidence: 93%

Trimethylamine N‐oxide: breathe new life

Subramaniam

Fletcher

2017

British J Pharmacology

143

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“…22, 59–62 Circulating TMAO was associated with the presence of vulnerable coronary plaque, plaque rupture, and long-term risks of incident cardiovascular events in patients with acute coronary syndrome. 63, 64 Mechanistic studies in animal model studies also reveal TMAO alters platelet calcium signalling, and elicits a pro-thrombotic effect in vivo. 10 These observations suggest that TMAO could be a marker for coronary plaque vulnerability and progression, and a direct participant in enhanced risk for myocardial infarction.…”

Section: Pathogenic Mechanism Of Gut Microbiota and Metabolites In Camentioning

confidence: 99%

Gut Microbiota in Cardiovascular Health and Disease

Tang

Kitai

Hazen

2017

Circulation Research

1,250

941

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Significant interest in recent years has focused on gut microbiota-host interaction because accumulating evidence has revealed that intestinal microbiota play an important role in human health and disease, including cardiovascular diseases. Changes in the composition of gut microbiota associated with disease, referred to as dysbiosis, have been linked to pathologies such as atherosclerosis, hypertension, heart failure, chronic kidney disease, obesity and type 2 diabetes mellitus. In addition to alterations in gut microbiota composition, the metabolic potential of gut microbiota has been identified as a contributing factor in the development of diseases. Recent studies revealed that gut microbiota can elicit a variety of effects on the host. Indeed, the gut microbiome functions like an endocrine organ, generating bioactive metabolites, that can impact host physiology. Microbiota interact with the host through a number of pathways, including the trimethylamine (TMA)/ trimethylamine N-oxide (TMAO) pathway, short-chain fatty acids pathway, and primary and secondary bile acids pathways. In addition to these “metabolism dependent” pathways, metabolism independent processes are suggested to also potentially contribute to CVD pathogenesis. For example, heart failure associated splanchnic circulation congestion, bowel wall edema and impaired intestinal barrier function are thought to result in bacterial translocation, the presence of bacterial products in the systemic circulation and heightened inflammatory state. These are believed to also contribute to further progression of heart failure and atherosclerosis. The purpose of the current review is to highlight the complex interplay between microbiota, their metabolites and the development and progression of cardiovascular diseases. We will also discuss the roles of gut microbiota in normal physiology and the potential of modulating intestinal microbial inhabitants as novel therapeutic targets.

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“…Considering the role of TMAO in pathogenesis of atherosclerosis, several lines of evidence have explored the relationship between plasm TMAO levels and the instability of coronary plaque. In a cohort study of patients with coronary artery disease (CAD), the results suggested that TMAO levels in the plaque rupture group were dramatically higher than those in nonplaque rupture group (). The study further divided all patients into a thin‐cap fibroatheroma (TCFA) group and a non‐TCFA group according to the definition of TCFA (a plaque with lipid component in ≥ 2 quadrants with the thinnest thickness of fibrous cap ≤ 65 μm).…”

Section: Plaque Instabilitymentioning

confidence: 99%

Gut microbiota in atherosclerosis: focus on trimethylamine N‐oxide

Zhu

Jiang

2020

APMIS

125

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in atherosclerosis: focus on trimethylamine N-oxide. APMIS 2020; 128: 353-366.The increasing prevalence of cardiovascular diseases cannot adequately be explained by traditional risk factors. Recently, accumulating evidence has suggested that gut microbiota-derived numerous metabolites are contributors to atherosclerotic events. Among them, the role of trimethylamine N-oxide (TMAO) in promoting atherosclerosis has gained attention. TMAO is reported to exert the proatherogenic effects by impacting on the traditional risk factors of atherosclerosis and is associated with high risk of cardiovascular events. Besides that, TMAO is involved in the complex pathological processes of atherosclerotic lesion formation, such as endothelial dysfunction, platelet activation and thrombus generation. In light of these promising findings, TMAO may serve as a potential target for atherosclerosis prevention and treatment, which is conceptually novel, when compared with existing traditional treatments. It is likely that regulating TMAO production and associated gut microbiota may become a promising strategy for the anti-atherosclerosis therapy.

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Coronary Plaque Characterization Assessed by Optical Coherence Tomography and Plasma Trimethylamine-N-oxide Levels in Patients With Coronary Artery Disease

Cited by 62 publications

References 18 publications

Trimethylamine N‐oxide: breathe new life

Trimethylamine N‐oxide: breathe new life

Gut Microbiota in Cardiovascular Health and Disease

Gut microbiota in atherosclerosis: focus on trimethylamine N‐oxide

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