目的:探讨冠心病患者血清中趋化因子CX3CL1的表达在冠心病中的临床意义。方法:采用病例-对照的研究方法,依据临床症状收集经冠脉造影显示确诊为冠心病的患者250例,其中临床症状诊断为稳定性心绞痛患者75例,不稳定型心绞痛患者75例,急性心肌梗死患者100例(其中包含ST段抬高型急性心肌梗死和非ST段抬高型急性心肌梗死患者各50例)。同期收集对照组200例,对照组为冠状动脉造影显示为正常。ELISA方法检测上述不同人群血清中趋化因子CX3CL1表达变化,利用流式细胞仪检测上述不同人群血清中CD4^+CD28~-CX3CR1+T细胞表达含量的变化。结果:冠心病患者组血清趋化因子CX3CL1表达明显高于对照组(P〈0.05);与稳定型冠心病组患者相比较,不稳定型冠心病组和急性心肌梗死组患者血清中趋化因子CX3CL1水平明显高于稳定型冠心病患者组(P〈0.05);ST段抬高型急性心肌梗死患者血清CX3CL1表达水平高于非ST段抬高型急性心肌梗死患者(P〈0.05)。不稳定型心绞痛患者冠状动脉介入手术后即刻抽取患者的静脉血,血清中CX3CL1表达含量明显高于冠状动脉介入手术前血清中的表达含量。冠心病患者CD4^+CD28~-CX3CR1+T细胞受体的表达含量明显增高,在急性ST段抬高型心肌梗死患者血清中的表达最高(P〈0.05)。结论:趋化因子CX3CL1可能参与冠心病动脉粥样硬化不稳定斑块的形成,并且可能成为外周血中预测不稳定型斑块的血清生物学标志物。
Objective: To explore the clinical significance of serum CX3CL1 level for coronary artery disease. Methods: The study was conducted in 250 cases of coronary artery disease patients(75 patients with stable angina pectoria,75 patients with unstable angina pectoris,50 patients with ST-elevation acute myocardial infarction,50 non ST-elevation acute myocardial infarction patients) and 200 cases of control subjects(normal coronay artery) in a case-control study. The CX3CL1 level in different groups were analyzed by ELISA and CX3CR1 expression on CD4^+CD28~-T cells was analyzed by flow cytometry. Results: The serum CX3CL1 level increased markedly in coronary artery disease patients compared with the control subjects(P〈0.05). The serum CX3CL1 level of patients with stable unstable angina was increased in the patients with ST-elevation acute myocardial infarction than those with the non ST-elevation acute myocardial infarction patients(P〈0.05). An increased number of CD4^+CD28~-CX3CR1+T cells was found in the patients with coronary artery disease patients than the control group especially in the ST-elevation acute myocardial infarction patient(P〈0.05). Conclusion: CX3CL1 might be involved in the formation of coronary atherosclerotic plaque and played an important role in the atherosclerotic procession,which might be useful to predict the stability of plaque in the early stage of coronary artery disease.