冠状动脉性心脏病合并2型糖尿病患者的内皮细胞微粒水平

Circulatory endothelial microparticle in patients with coronary artery heart disease and type 2 diabetes mellitus

目的探讨冠状动脉性心脏病合并2型糖尿病患者的血浆内皮细胞微粒(EMP)水平,及其与单纯冠状动脉性心脏病患者及健康者的差异。方法选择单纯冠状动脉性心脏病患者(A组)78例,冠状动脉性心脏病合并2型糖尿病患者(B组)96例,健康者(C组)30名。采用生化法检测受试者的血脂水平,应用流式微球技术检测血浆EMP水平,酶联免疫吸附试验(ELISA)检测内皮素-1(ET-1)和细胞间黏附分子-1(ICAM-1)水平,并对A组和B组的患者进行Gensini评分。比较各组间血脂、EMP、ET-1和ICAM-1水平的差异。结果 B组的三酰甘油(TG)水平显著高于A组和C组(P值均<0.01),高密度脂蛋白胆固醇(HDL-C)水平显著低于A组和C组(P值均<0.01),A组与C组间血脂水平的差异均无统计学意义(P值均>0.05)。A组和B组的血EMP水平及血清ET-1和ICAM-1水平均显著高于C组(P值均<0.01),B组上述指标均显著高于A组(P值均<0.01)。结论冠状动脉性心脏病患者存在一定程度的血管内皮功能异常,且冠状动脉性心脏病合并2型糖尿病患者进一步加重,提示高血糖和胰岛素抵抗加重了冠状动脉性心脏病患者血管内皮损伤程度。

Objective To determine the differences of circulatory endothelial microparticle among the patients with coronary artery heart disease（CAD）and diabetes mellitus（DM）,CAD patients and healthy individuals.Methods A total of 78 CAD patients without DM（group A）,96 CAD patients with type 2 DM（group B）and 30 healthy subjects（group C）were enrolled in this study.Their serum lipid profile was detected by biochemistry.Plasma level of endothelial microparticle was determined by a novel cytometry bead assay,and the levels of endothelin-1（ET-1）and intercellular adhesion molecule-1（ICAM-1）were measured by enzyme-linked immunosorbent assay（ELISA）.The differences of lipid profile,levels of endothelial microparticle（EMP）,ET-1 and ICAM-1 and their Gensini scores were analyzed between the 3 groups.Results The patients of group B had highest TG level and lowest HDL-C level compared with the patients of group A and group C（P0.01）.There was no statistical difference in lipid profiles between group A and group C（P0.05）.The levels of EMP,ET-1 and ICAM-1 in group A and group B were significantly higher than those in group C（P0.01）,and those of group B were significantly higher than those in group A（P0.01）.Conclusion CAD patients suffer from endothelial dysfunction,which is more severe in those combined with DM.Our results indicate that the disturbance of glucose metabolism and insulin resistance deteriorate endothelial impairment in CAD patients.