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氧化三甲胺(TMAO)作为大动脉粥样硬化性缺血性脑卒中患者主要血管不良事件和复发的新预测因子。

TMAO as a Novel Predictor of Major Adverse Vascular Events and Recurrence in Patients with Large Artery Atherosclerotic Ischemic Stroke.

机构信息

Department of Neurology, Nanjing Drum Tower Hospital, Clinical College of Nanjing Medical University, Nanjing, China.

Department of Neurology, 89657The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.

出版信息

Clin Appl Thromb Hemost. 2022 Jan-Dec;28:10760296221090503. doi: 10.1177/10760296221090503.

DOI:10.1177/10760296221090503
PMID:35345908
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8969508/
Abstract

OBJECTIVES

To explore the association of plasma trimethylamine N-oxide (TMAO) concentration with large artery atherosclerotic (LAA) ischemic stroke and its role in predicting neurological outcome and major vascular event recurrence.

MATERIALS AND METHODS

We performed a case-control study that included patients with first-ever LAA stroke as cases (n = 291) and asymptomatic patients as controls (n = 235). Clinical data and venous blood samples were collected within 72 hours after stroke. All subjects were followed for 3 months. TMAO level was detected by liquid chromatography mass spectrometry (LC-MS). Logistic and Cox proportional hazard regression were performed to evaluate plasma TMAO concentration as a predictor of LAA stroke and major vascular event recurrence, respectively. Kaplan-Meier survival analysis was performed to compare major vascular event recurrence between patients with high and low TMAO concentration.

RESULTS

After adjusting for traditional stroke risk factors, the plasma TMAO level was significantly higher in the LAA stroke group than the control group (OR = 1.031, 95% CI 1.024-1.037,  < .001). At a cutoff level of 106.9 pg/ml, TMAO had a sensitivity of 63.23% and specificity of 80.00% in discriminating the LAA stroke subjects from the controls in Receiver operator characteristic (ROC) analysis. Kaplan-Meier survival analysis demonstrated TMAO plasma concentration was significantly relevant with recurrent vascular events (Log Rank,  = .006). Moreover, this association was still existed after adjusting for traditional risks (adjusted HR, 3.128; 95% CI, 1.018-9.610) in Cox regression model. But TMAO plasma levels were not relevant with functional disability after 3 months of the LAA stroke.

CONCLUSION

Elevated plasma TMAO concentration was independently associated with LAA ischemic stroke. The risk of major vascular event recurrence increased by 2.128 times in the LAA stroke subjects with plasma TMAO level higher than 126.83 pg/mL. Plasma TMAO concentration might be a potential biomarker of major vascular event recurrence.

摘要

目的

探讨血浆三甲胺 N-氧化物(TMAO)浓度与大动脉粥样硬化性(LAA)缺血性卒中的关系及其在预测神经功能结局和主要血管事件复发中的作用。

材料与方法

我们进行了一项病例对照研究,纳入了首次发生 LAA 卒中的患者作为病例(n=291)和无症状患者作为对照(n=235)。在卒中后 72 小时内采集临床数据和静脉血样。所有患者均随访 3 个月。采用液相色谱-质谱联用(LC-MS)法检测 TMAO 水平。采用 logistic 和 Cox 比例风险回归分别评估血浆 TMAO 浓度作为 LAA 卒中及主要血管事件复发的预测因子。Kaplan-Meier 生存分析比较了 TMAO 浓度高和低的患者之间主要血管事件复发的差异。

结果

在校正传统卒中危险因素后,LAA 卒中组患者的血浆 TMAO 水平明显高于对照组(OR=1.031,95%CI 1.024-1.037, < .001)。在截断值为 106.9 pg/ml 时,TMAO 在 ROC 分析中鉴别 LAA 卒中患者和对照组的敏感性为 63.23%,特异性为 80.00%。Kaplan-Meier 生存分析显示,TMAO 血浆浓度与复发性血管事件显著相关(Log Rank,  = .006)。此外,在 Cox 回归模型中校正传统危险因素后,这种相关性仍然存在(调整后的 HR,3.128;95%CI,1.018-9.610)。但 TMAO 血浆水平与 LAA 卒中后 3 个月的功能残疾无关。

结论

血浆 TMAO 浓度升高与 LAA 缺血性卒中独立相关。在 LAA 卒中患者中,TMAO 水平高于 126.83 pg/ml 时,主要血管事件复发的风险增加 2.128 倍。血浆 TMAO 浓度可能是主要血管事件复发的潜在生物标志物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1924/8969508/e92dff84cd43/10.1177_10760296221090503-fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1924/8969508/61a127120fb0/10.1177_10760296221090503-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1924/8969508/ba5030c0dbc8/10.1177_10760296221090503-fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1924/8969508/bc27ab39e0c3/10.1177_10760296221090503-fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1924/8969508/e92dff84cd43/10.1177_10760296221090503-fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1924/8969508/61a127120fb0/10.1177_10760296221090503-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1924/8969508/ba5030c0dbc8/10.1177_10760296221090503-fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1924/8969508/bc27ab39e0c3/10.1177_10760296221090503-fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1924/8969508/e92dff84cd43/10.1177_10760296221090503-fig4.jpg

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