心肌梗死中与生物标志物相关的单核细胞炎症信号

R. Guimarães, J. Marchini, Luz Marina Gómez Gómez, R. S. Leite, Ó. Dutra, Iran Castro, A. Manica
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引用次数: 1

摘要

背景:单核细胞是炎症信号传导的重要组成部分,它们的募集在信号通路中起着至关重要的作用,它指导和决定了细胞对活化内皮的粘附。更好地了解急性冠脉综合征(ACS)动脉粥样硬化性疾病患者单核细胞亚群与炎症信号之间的相关性,对于开发更有效的预防和治疗心血管疾病的疗法至关重要。目的:分析缺血性心脏病患者生物标志物与单核细胞活化的差异。方法:这是一项病例对照研究,比较伴有和不伴有st段抬高的ACS患者与没有冠状动脉狭窄的患者之间的生物标志物和单核细胞亚群。非参数Kruskal-Wallis检验用于评估组间差异,Dunn事后检验用于确定哪些组存在差异。库兹克的有序群体趋势测试被用来评估下降或上升的趋势。参与者分为3组:对照组(0);非st段抬高型心肌梗死(NSTEMI) (1);st段抬高型心肌梗死(STEMI) D1(2)。结果:招募了47例ACS患者和19例对照组,冠状动脉造影无阻塞性病变。单核细胞谱评估在症状出现时间和有无动脉粥样硬化性疾病方面存在统计学差异(Kruskal-Wallis, p = 0.0009)。Dunn 's事后检验显示,对照组与STEMI D1组(p = 0.0014)、STEMI D3组(p = 0.0036)和STEMI D7组(p = 0.0195)之间存在显著差异,与对照组相比,经典(p = 0.0022)和非经典(p = 0.0031)单核细胞增加了2倍。对于经典单核细胞,对照组与所有STEMI组之间以及NSTEMI组与STEMI D1、D3和D7组之间存在差异。对于非经典单核细胞,对照组与STEMI D7组之间存在差异(p = 0.0056), NSTEMI组与STEMI D7组之间存在差异(p = 0.0166)。结论:本研究发现ACS患者急性心肌梗死时总单核细胞动员和经典单核细胞动员均增加。
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Biomarker-associated Monocyte Inflammatory Signaling in Myocardial Infarction
Background: Monocytes are essential components in inflammatory signaling, and their recruitment is crucial in the signaling pathway, which directs and determines cell adhesion to the activated endothelium. A better understanding of the correlation between monocyte subsets and inflammatory signaling in patients with atherosclerotic disease in acute coronary syndrome (ACS) is essential for the development of more effective therapies for the prevention and treatment of cardiovascular diseases. Objective: To analyze differences between biomarkers and monocyte activation in the setting of ischemic heart disease. Methods: This was a case-control study comparing biomarkers and monocyte subsets between patients with ACS with and without ST-segment elevation and individuals without coronary stenosis. The nonparametric Kruskal-Wallis test was used to assess differences between groups, and Dunn’s post hoc test was used to identify which groups were different. Cuzick’s test for ordered group trends was used to assess falling or rising trends. Participants were classified into 3 groups: control (0); non-ST-elevation myocardial infarction (NSTEMI) (1); ST-elevation myocardial infarction (STEMI) D1 (2). Results: Forty-seven patients with ACS and 19 controls with no obstructive lesions on coronary angiography were recruited. Monocyte profile assessment was statistically different regarding time of symptom onset and the presence or absence of atherosclerotic disease (Kruskal-Wallis, p = 0.0009). Dunn’s post hoc test showed a significant difference between the control group and the STEMI D1 (p = 0.0014), STEMI D3 (p = 0.0036), and STEMI D7 (p = 0.0195) groups, corresponding to a 2-fold increase in classical (p = 0.0022) and nonclassical (p = 0.0031) monocytes compared with controls. For classical monocytes, there was a difference between the control group and all STEMI groups and between the NSTEMI group and the STEMI D1, D3, and D7 groups. For nonclassical monocytes, there was a difference between the control group and the STEMI D7 group (p = 0.0056) and between the NSTEMI group and the STEMI D7 group (p = 0.0166). Conclusion: This study found that there was an increase in total and classical monocyte mobilization at the time of acute myocardial infarction in patients with ACS.
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