Chunyu Zhang, Jinyu He, Yujia Huo, Lin Liu, Yong Xie, Yufei Meng, Gang Wei, Li Deng, Yang Jiang, Jian Feng
{"title":"肠道微生物代谢物三甲胺n -氧化物作为PCI术后不良心血管事件的新预测因子：系统评价和剂量反应荟萃分析","authors":"Chunyu Zhang, Jinyu He, Yujia Huo, Lin Liu, Yong Xie, Yufei Meng, Gang Wei, Li Deng, Yang Jiang, Jian Feng","doi":"10.1186/s12937-025-01159-9","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>Cardiovascular diseases are the leading cause of mortality worldwide, with acute coronary syndrome (ACS) being particularly fatal. Percutaneous coronary intervention (PCI) is a key treatment for ACS; however, major adverse cardiovascular events (MACE) frequently occur postoperatively. Trimethylamine N-oxide (TMAO), a gut microbiota-derived metabolite, has been proposed as an emerging risk factor for cardiovascular disease. This study aims to systematically evaluate TMAO's predictive value for MACE post-PCI and explore its dose-response relationship.</p><p><strong>Methods: </strong>A comprehensive literature search was conducted in four databases (PubMed, Web of Science, Embase, and the Cochrane Library), including retrospective or prospective cohort studies involving patients undergoing PCI. The primary outcome was MACE, and the secondary outcome was all-cause mortality. A dose-response analysis was conducted using a restricted cubic spline model to explore potential nonlinear associations between TMAO levels and outcomes. Heterogeneity was assessed using the Cochrane Q test and the I² statistic. Subgroup analysis and meta-regression were performed to identify sources of heterogeneity.</p><p><strong>Results: </strong>Eleven studies (comprising 13 independent cohorts) with 11,279 participants were included. Pooled analysis showed a significant association between elevated plasma TMAO levels and an increased risk of MACE after PCI (HR: 1.99, 95%CI: 1.68-2.35, 95%PI: 1.64-2.40, I² = 0%, p < 0.00001). Similarly, elevated plasma TMAO levels were significantly associated with an increased risk of all-cause mortality after PCI (HR: 1.76, 95%CI: 1.32-2.35, 95%PI: 0.79-3.90, I² = 65.1%, p < 0.00001). The dose-response analysis did not reveal a nonlinear relationship between TMAO and MACE or all-cause mortality. The linear model showed that each 1 µmol/L increase in plasma TMAO was associated with an 8.95% increased hazard of MACE (HR = 1.0895, 95%CI: 1.03-1.15), while all-cause mortality increased by 4% (HR = 1.04, 95%CI: 0.99-1.09).</p><p><strong>Conclusions: </strong>This study demonstrates that elevated plasma TMAO levels are significantly associated with an increased risk of MACE and all-cause mortality after PCI, with a dose-dependent effect on MACE risk. As a potential biomarker, TMAO may be used to predict the risk of adverse cardiovascular events after PCI, and future studies should further validate its clinical utility.</p><p><strong>Registration: </strong>PROSPERO CRD42024557486.</p>","PeriodicalId":19203,"journal":{"name":"Nutrition Journal","volume":"24 1","pages":"91"},"PeriodicalIF":3.8000,"publicationDate":"2025-06-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12168366/pdf/","citationCount":"0","resultStr":"{\"title\":\"Gut microbial metabolite trimethylamine N-oxide as a novel predictor for adverse cardiovascular events after PCI: a systematic review and dose-response meta-analysis.\",\"authors\":\"Chunyu Zhang, Jinyu He, Yujia Huo, Lin Liu, Yong Xie, Yufei Meng, Gang Wei, Li Deng, Yang Jiang, Jian Feng\",\"doi\":\"10.1186/s12937-025-01159-9\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Background: </strong>Cardiovascular diseases are the leading cause of mortality worldwide, with acute coronary syndrome (ACS) being particularly fatal. Percutaneous coronary intervention (PCI) is a key treatment for ACS; however, major adverse cardiovascular events (MACE) frequently occur postoperatively. Trimethylamine N-oxide (TMAO), a gut microbiota-derived metabolite, has been proposed as an emerging risk factor for cardiovascular disease. This study aims to systematically evaluate TMAO's predictive value for MACE post-PCI and explore its dose-response relationship.</p><p><strong>Methods: </strong>A comprehensive literature search was conducted in four databases (PubMed, Web of Science, Embase, and the Cochrane Library), including retrospective or prospective cohort studies involving patients undergoing PCI. The primary outcome was MACE, and the secondary outcome was all-cause mortality. A dose-response analysis was conducted using a restricted cubic spline model to explore potential nonlinear associations between TMAO levels and outcomes. Heterogeneity was assessed using the Cochrane Q test and the I² statistic. Subgroup analysis and meta-regression were performed to identify sources of heterogeneity.</p><p><strong>Results: </strong>Eleven studies (comprising 13 independent cohorts) with 11,279 participants were included. Pooled analysis showed a significant association between elevated plasma TMAO levels and an increased risk of MACE after PCI (HR: 1.99, 95%CI: 1.68-2.35, 95%PI: 1.64-2.40, I² = 0%, p < 0.00001). Similarly, elevated plasma TMAO levels were significantly associated with an increased risk of all-cause mortality after PCI (HR: 1.76, 95%CI: 1.32-2.35, 95%PI: 0.79-3.90, I² = 65.1%, p < 0.00001). The dose-response analysis did not reveal a nonlinear relationship between TMAO and MACE or all-cause mortality. The linear model showed that each 1 µmol/L increase in plasma TMAO was associated with an 8.95% increased hazard of MACE (HR = 1.0895, 95%CI: 1.03-1.15), while all-cause mortality increased by 4% (HR = 1.04, 95%CI: 0.99-1.09).</p><p><strong>Conclusions: </strong>This study demonstrates that elevated plasma TMAO levels are significantly associated with an increased risk of MACE and all-cause mortality after PCI, with a dose-dependent effect on MACE risk. As a potential biomarker, TMAO may be used to predict the risk of adverse cardiovascular events after PCI, and future studies should further validate its clinical utility.</p><p><strong>Registration: </strong>PROSPERO CRD42024557486.</p>\",\"PeriodicalId\":19203,\"journal\":{\"name\":\"Nutrition Journal\",\"volume\":\"24 1\",\"pages\":\"91\"},\"PeriodicalIF\":3.8000,\"publicationDate\":\"2025-06-16\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12168366/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Nutrition Journal\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1186/s12937-025-01159-9\",\"RegionNum\":2,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"NUTRITION & DIETETICS\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Nutrition Journal","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1186/s12937-025-01159-9","RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"NUTRITION & DIETETICS","Score":null,"Total":0}
Gut microbial metabolite trimethylamine N-oxide as a novel predictor for adverse cardiovascular events after PCI: a systematic review and dose-response meta-analysis.
Background: Cardiovascular diseases are the leading cause of mortality worldwide, with acute coronary syndrome (ACS) being particularly fatal. Percutaneous coronary intervention (PCI) is a key treatment for ACS; however, major adverse cardiovascular events (MACE) frequently occur postoperatively. Trimethylamine N-oxide (TMAO), a gut microbiota-derived metabolite, has been proposed as an emerging risk factor for cardiovascular disease. This study aims to systematically evaluate TMAO's predictive value for MACE post-PCI and explore its dose-response relationship.
Methods: A comprehensive literature search was conducted in four databases (PubMed, Web of Science, Embase, and the Cochrane Library), including retrospective or prospective cohort studies involving patients undergoing PCI. The primary outcome was MACE, and the secondary outcome was all-cause mortality. A dose-response analysis was conducted using a restricted cubic spline model to explore potential nonlinear associations between TMAO levels and outcomes. Heterogeneity was assessed using the Cochrane Q test and the I² statistic. Subgroup analysis and meta-regression were performed to identify sources of heterogeneity.
Results: Eleven studies (comprising 13 independent cohorts) with 11,279 participants were included. Pooled analysis showed a significant association between elevated plasma TMAO levels and an increased risk of MACE after PCI (HR: 1.99, 95%CI: 1.68-2.35, 95%PI: 1.64-2.40, I² = 0%, p < 0.00001). Similarly, elevated plasma TMAO levels were significantly associated with an increased risk of all-cause mortality after PCI (HR: 1.76, 95%CI: 1.32-2.35, 95%PI: 0.79-3.90, I² = 65.1%, p < 0.00001). The dose-response analysis did not reveal a nonlinear relationship between TMAO and MACE or all-cause mortality. The linear model showed that each 1 µmol/L increase in plasma TMAO was associated with an 8.95% increased hazard of MACE (HR = 1.0895, 95%CI: 1.03-1.15), while all-cause mortality increased by 4% (HR = 1.04, 95%CI: 0.99-1.09).
Conclusions: This study demonstrates that elevated plasma TMAO levels are significantly associated with an increased risk of MACE and all-cause mortality after PCI, with a dose-dependent effect on MACE risk. As a potential biomarker, TMAO may be used to predict the risk of adverse cardiovascular events after PCI, and future studies should further validate its clinical utility.
期刊介绍：
Nutrition Journal publishes surveillance, epidemiologic, and intervention research that sheds light on i) influences (e.g., familial, environmental) on eating patterns; ii) associations between eating patterns and health, and iii) strategies to improve eating patterns among populations. The journal also welcomes manuscripts reporting on the psychometric properties (e.g., validity, reliability) and feasibility of methods (e.g., for assessing dietary intake) for human nutrition research. In addition, study protocols for controlled trials and cohort studies, with an emphasis on methods for assessing dietary exposures and outcomes as well as intervention components, will be considered.
Manuscripts that consider eating patterns holistically, as opposed to solely reductionist approaches that focus on specific dietary components in isolation, are encouraged. Also encouraged are papers that take a holistic or systems perspective in attempting to understand possible compensatory and differential effects of nutrition interventions. The journal does not consider animal studies.
In addition to the influence of eating patterns for human health, we also invite research providing insights into the environmental sustainability of dietary practices. Again, a holistic perspective is encouraged, for example, through the consideration of how eating patterns might maximize both human and planetary health.
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