Zhang Ping, Shao Liang, Ma Jun
Department of Geriatrics & Neurology, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University.
Department of Cardiology, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University.
Int Heart J. 2018;59(1):64-70. doi: 10.1536/ihj.17-084.
Myocardial infarction (MI) can cause new-onset atrial fibrillation (AF) due to cardiac remodeling. As a recent study has shown, inflammatory factors are closely tied to cell death and survival in myocardial ischemia injury. Toll-like receptors (TLRs) have been shown to participate in the process of myocardial infarction as innate immune factors.The subjects were divided into 3 groups: healthy controls (n = 82), MI patients (n = 84), and AFMI (new-onset atrial fibrillation after myocardial infarction) patients (n = 85). Peripheral blood mononuclear cell (PBMC) TLR mRNA expression was detected by rt-PCR. Western blot was used to analyze PBMC TLRs and their downstream signal protein expression. PBMCs were presented as TLR2 expression or TLR4 expression using flow cytometry.From mRNA to protein detection, PBMC TLR2 and TLR4 were significantly higher in the AFMI group than in the control group and MI group. A similar tendency was also observed in the expression of downstream signaling proteins. When further analyzed with TLR2 and TLR4 antibodies by flow cytometry, PBMC levels also appeared to be higher in AFMI patients than those in MI patients and the healthy control group.In our study, PBMC TLRs and their downstream signaling proteins were significantly higher in the acute myocardial infarction patients with new-onset atrial fibrillation compared with healthy people and acute myocardial infarction patients without new-onset atrial fibrillation. They have the potential to be novel biomarkers for new-onset atrial fibrillation after acute myocardial infarction.
心肌梗死（MI）可因心脏重塑导致新发房颤（AF）。正如最近一项研究所显示的，炎症因子与心肌缺血损伤中的细胞死亡和存活密切相关。Toll样受体（TLRs）已被证明作为天然免疫因子参与心肌梗死过程。
研究对象分为3组：健康对照组（n = 82）、MI患者（n = 84）和AFMI（心肌梗死后新发房颤）患者（n = 85）。采用逆转录聚合酶链反应（rt-PCR）检测外周血单个核细胞（PBMC）TLR mRNA表达。用蛋白质印迹法分析PBMC TLRs及其下游信号蛋白表达。使用流式细胞术将PBMCs呈现为TLR2表达或TLR4表达。
从mRNA检测到蛋白质检测，AFMI组的PBMC TLR2和TLR4均显著高于对照组和MI组。在下游信号蛋白的表达中也观察到类似趋势。当通过流式细胞术用TLR2和TLR4抗体进一步分析时，AFMI患者的PBMC水平似乎也高于MI患者和健康对照组。
在我们的研究中，与健康人和无新发房颤的急性心肌梗死患者相比，新发房颤的急性心肌梗死患者的PBMC TLRs及其下游信号蛋白显著更高。它们有可能成为急性心肌梗死后新发房颤的新型生物标志物。
