血浆丙酮酸激酶 M2 浓度升高与冠心病的临床严重程度和预后有关。

Biochemia medica Pub Date : 2024-02-15 Epub Date: 2023-12-15 DOI:10.11613/BM.2024.010704
Zi-Wen Zhao, Yi-Wei Xu, Xin-Tao Zhang, Hang-Hao Ma, Jing-Kun Zhang, Xue Wu, Yu Huang
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引用次数: 0

摘要

简介丙酮酸激酶M2(PKM2)参与动脉粥样硬化和冠状动脉疾病(CAD)的病理生理学。我们检测了血浆中PKM2的浓度是否与CAD患者的临床严重程度和主要不良心血管事件(MACE)相关:共招募了 2443 名 CAD 患者和 238 名对照者。随访时间为两年。血浆中 PKM2 的浓度通过酶联免疫吸附试验(ELISA)试剂盒(Cloud-Clone,中国武汉)和 SpectraMax i3x 多模式微孔板阅读器(Molecular Devices,美国圣何塞)进行检测。通过逻辑回归分析评估了急性冠状动脉综合征(ACS)的预测因素。不同四分位数的PKM2浓度与MACEs之间的关系通过Kaplan-Meier(KM)曲线、Log-rank检验和Cox比例危险模型进行评估。PKM2和一组常规风险因素的预测价值由接收器操作特征曲线(ROC)确定。利用净再分类改进(NRI)和综合辨别改进(IDI)来评估将PKM2加入包含一组常规风险因素的预测模型后对风险预测的增强作用:在CAD患者中,PKM2浓度是ACS的独立预测因子(P<0.001)。Kaplan-Meier累积生存曲线和Cox比例危险分析显示,与PKM2浓度较低的患者相比,PKM2浓度较高的患者MACE发生率更高(P < 0.001)。将PKM2加入一组常规风险因素后,其对MACEs的预后价值显著增加:结论:血浆PKM2基线浓度可预测CAD的临床严重程度和预后。
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Elevated plasma pyruvate kinase M2 concentrations are associated with the clinical severity and prognosis of coronary artery disease.

Introduction: Pyruvate kinase M2 (PKM2) was involved in the pathophysiology of atherosclerosis and coronary artery disease (CAD). We tested whether plasma PKM2 concentrations were correlated with clinical severity and major adverse cardiovascular events (MACEs) in CAD patients.

Materials and methods: A total of 2443 CAD patients and 238 controls were enrolled. The follow-up time was two years. Plasma PKM2 concentrations were detected by enzyme-linked immunosorbent assay (ELISA) kits (Cloud-Clone, Wuhan, China) using SpectraMax i3x Multi-Mode Microplate Reader (Molecular Devices, San Jose, USA). The predictors of acute coronary syndrome (ACS) were assessed by logistic regression analysis. The association between PKM2 concentration in different quartiles and MACEs was evaluated by Kaplan-Meier (KM) curves with log-rank test and Cox proportional hazard models. The predictive value of PKM2 and a cluster of conventional risk factors was determined by Receiver operating characteristic (ROC) curves. The net reclassification improvement (NRI) and the integrated discrimination improvement (IDI) were utilized to evaluate the enhancement in risk prediction when PKM2 was added to a predictive model containing a cluster of conventional risk factors.

Results: In CAD patients, PKM2 concentration was the independent predictor of ACS (P < 0.001). Kaplan-Meier cumulative survival curves and Cox proportional hazards analyses revealed that patients with a higher PKM2 concentration had higher incidence of MACEs compared to those with a lower PKM2 concentration (P < 0.001). The addition of PKM2 to a cluster of conventional risk factors significantly increased its prognostic value of MACEs.

Conclusion: Baseline plasma PKM2 concentrations predict the clinical severity and prognosis of CAD.

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