急性冠脉综合征患者内皮祖细胞及C反应蛋白的变化

Changes of levels of endothelial progenitor cells and C-reactive protein in patients with acute coronary syndrome

目的:观察急性冠脉综合征(ACS)患者外周血中内皮祖细胞(EPCs)及C反应蛋白的变化。方法:入选40例ACS(不稳定型心绞痛18例、急性心肌梗死22例)患者与20例行冠状动脉造影术排除冠心病的正常人(正常对照组),取所有研究对象外周血100μl分别加入CD34-PE、AC133-异硫氰酸荧光素(FITC)荧光抗体使与EPCs表面CD34、AC133抗原结合,通过流式细胞仪检测PE、FITC阳性细胞的数量。同时检测高敏C反应蛋白(hsCRP)浓度。结果:与正常对照组比较,不稳定型心绞痛、急性心肌梗死患者外周血中EPCs数量显著增多[(0.48±0.04)%比(0.84±0.31)%比(1.57±0.62)%,P<0.001],hsCRP浓度明显升高[(0.63±011)mg/L比(7.8±0.59)mg/L比(11.2±0.46)mg/L,P<0.001],且上述指标在急性心肌梗死组明显高于不稳定心绞痛组(P<0.001),所有患者外周血中EPCs数量与hsCRP浓度正相关(r=0.82,P<0.001)。结论:急性冠脉综合征患者外周血中内皮祖细胞数量显著增多,可能与炎症因子激活骨髓干细胞分化为内皮祖细胞,参与血管修复有关。

Objective： To investigate changes of levels of endothelial progenitor cells （EPCs） and C--reactive protein （CRP） in peripheral blood in patients with acute coronary syndrome （ACS）. Methods： A total of 40 ACS patients [18 cases with unstable angina pectoris （UAP） and 22 cases with acute myocardial infarction （AMI）] and 20 normal subjects （normal control group） who were excluded coronary heart disease by coronary angiography were enrolled. 100 peripheral blood of each subject was obtained, and CD34--PE, AC133-- fluorescein isothiocyanate （FITC） fluorescent antibodies were added to combine with CD34 and AC133 antigens on surface of EPCs respectively. Num- ber of PE and FITC positive cells was detected by flow cytometer. And concentration of high sensitive C--reactive protein （hsCRP） was measured. Results： Compared with normal control group, there were significant increase in UAP patients and AMI patients, in number of EPCs [（0.48＋0.04）% vs. （0.84＋0.31）% vs. （1.57＋0.62）%] and concentration of hsCRP [ （0.63＋011） mg/L vs. （7.8＋0.59） mg/L vs. （11.2＋0.46） mg/L] in peripheral blood P〈0. 001 both. Levels of above indicators in AMI group were significantly higher than those of UAP group （P（ 0. 001）. Number of EPCs in peripheral blood was positively correlated with concentration of hsCRP in all patients （r =0.82, P〈0. 001）. Conclusion： Number of EPCs significantly increases in peripheral blood of ACS patients, its possible cause may be myeloid stem cells differentiated into EPCs after stimulation from inflammatory factors, and then takes part in vascular repair.