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氧化应激和炎症生物标志物与非 ST 段抬高型心肌梗死患者及不同程度肾功能的心肌坏死和心力衰竭的关系。

Association between Biomarkers of Oxidative Stress and Inflammation with Cardiac Necrosis and Heart Failure in Non-ST Segment Elevation Myocardial Infarction Patients and Various Degrees of Kidney Function.

机构信息

Division of Nephrology and Hypertension, 1st Department of Internal Medicine, AHEPA Hospital, School of Medicine, Aristotle University of Thessaloniki, 54636 Thessaloniki, Greece.

Department for Biochemistry, Faculty of Medicine, University of Nis, 18000 Nis, Serbia.

出版信息

Oxid Med Cell Longev. 2021 Nov 1;2021:3090120. doi: 10.1155/2021/3090120. eCollection 2021.

DOI:10.1155/2021/3090120
PMID:34760045
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8575633/
Abstract

The aim of this study was to explore the possible association between markers of inflammation and oxidative stress (OS) and markers of cardiac function and necrosis in 100 NSTEMI (non-ST-elevation myocardial infarction) patients with various degrees of kidney dysfunction. At admission, ejection fraction (EF), brain natriuretic peptide (BNP), troponin (TnI), creatinine phosphokinase (CPK), alanine transaminase (ALT), aspartate transaminase (AST), high-sensitive C-reactive protein (hs-CRP), interleukins 6 and 10 (IL-6, IL10), myeloperoxidase (MPO), transforming growth factor beta (TGF-1), glomerular filtration rate (GFR), and albuminuria were assessed. Study participants were divided into 2 subgroups based on the median level of EF. Compared to the high, patients in the low EF group had higher GFR, BNP, CPK, hs-CRP, IL-10, IL-6, and MPO values and lower albuminuria levels. The levels of EF decreased in parallel with the progression of CKD, whereas the levels of BNP, IL-6, and TGF- were significantly higher in late stages of CKD. Spearman's rho correlation analysis showed that EF was inversely correlated with MPO ( = -0.20, = 0.05) BNP ( = -0.30, = 0.002), hs-CRP ( = -0.38, < 0.0001), IL-10 ( = -0.30, = 0.003), and IL-6 ( = -0.24, = 0.02) and positively with GFR ( = 0.27, = 0.008). TnI was correlated with CPK ( = 0.44, < 0.0001), CPK-MB ( = 0.31, = 0.002), ALT ( = 0.50, < 0.0001), AST ( = 0.29, = 0.004), IL-10 ( = 0.22, = 0.03), and MPO ( = -0.28, = 0.006). In multivariate regression analysis, only BNP ( = -0.011, = 0.004), hs-CRP ( = -0.11, = 0.001), and GFR ( = 0.12, = 0.0029) were independent determinants of EF. Similarly, MPO ( = -1.69, = 0.02), IL-10 ( = 0.15, = 0.006), and AST ( = 0.04, = 0.001) were the 3 major determinants of TnI. Based on these associations, we built a predictive model including markers of inflammation and OS (MPO, IL-10, and hs-CRP) to identify patients with the most severe cardiac injury (combined EF below median and troponin above median values). Receiver-operator characteristic (ROC) analysis showed that the area under the ROC curve of this model to detect patients with low EF and high TnI was 0.67 ( = 0.015, 95%confidence interval = 0.53-0.81).

摘要

这项研究的目的是探索炎症和氧化应激(OS)标志物与心脏功能和坏死标志物在 100 名不同程度肾功能障碍的 NSTEMI(非 ST 段抬高心肌梗死)患者中的可能相关性。入院时,评估了射血分数(EF)、脑钠肽(BNP)、肌钙蛋白(TnI)、肌酸磷酸激酶(CPK)、丙氨酸转氨酶(ALT)、天冬氨酸转氨酶(AST)、高敏 C 反应蛋白(hs-CRP)、白细胞介素 6 和 10(IL-6、IL10)、髓过氧化物酶(MPO)、转化生长因子 β(TGF-1)、肾小球滤过率(GFR)和蛋白尿。根据 EF 的中位数,将研究参与者分为 2 个亚组。与高 EF 组相比,低 EF 组患者的 GFR、BNP、CPK、hs-CRP、IL-10、IL-6 和 MPO 值更高,而蛋白尿水平更低。EF 水平随着 CKD 的进展而降低,而 BNP、IL-6 和 TGF-β在 CKD 的晚期水平显著升高。Spearman rho 相关分析显示 EF 与 MPO( = -0.20, = 0.05)、BNP( = -0.30, = 0.002)、hs-CRP( = -0.38, < 0.0001)、IL-10( = -0.30, = 0.003)和 IL-6( = -0.24, = 0.02)呈负相关,与 GFR( = 0.27, = 0.008)呈正相关。TnI 与 CPK( = 0.44, < 0.0001)、CPK-MB( = 0.31, = 0.002)、ALT( = 0.50, < 0.0001)、AST( = 0.29, = 0.004)、IL-10( = 0.22, = 0.03)和 MPO( = -0.28, = 0.006)相关。在多变量回归分析中,只有 BNP( = -0.011, = 0.004)、hs-CRP( = -0.11, = 0.001)和 GFR( = 0.12, = 0.0029)是 EF 的独立决定因素。同样,MPO( = -1.69, = 0.02)、IL-10( = 0.15, = 0.006)和 AST( = 0.04, = 0.001)是 TnI 的 3 个主要决定因素。基于这些关联,我们构建了一个包含炎症和 OS 标志物(MPO、IL-10 和 hs-CRP)的预测模型,以识别心脏损伤最严重的患者(EF 中位数以下和肌钙蛋白中位数以上的患者)。接收器工作特征(ROC)分析显示,该模型检测 EF 低和 TnI 高的患者的 ROC 曲线下面积为 0.67( = 0.015,95%置信区间= 0.53-0.81)。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d088/8575633/cbec811b1212/OMCL2021-3090120.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d088/8575633/d3890f28dd97/OMCL2021-3090120.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d088/8575633/cbec811b1212/OMCL2021-3090120.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d088/8575633/d3890f28dd97/OMCL2021-3090120.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d088/8575633/cbec811b1212/OMCL2021-3090120.002.jpg

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