阿托伐他汀治疗冠心病前后患者血浆黏附因子浓度变化的观察

Effects of atorvastatin on the changes of the levels of plasma soluble ICAM-1 and soluble VCAM-1 in patients with coronary heart disease

目的观察阿托伐他汀治疗冠心病前后患者血浆黏附因子浓度的变化。方法将89例研究对象分为急性冠状动脉综合征(ACS)组、稳定型心绞痛(SAP)组和对照组。ACS组又分为急性心肌梗死(AMI)组、不稳定型心绞痛(UAP)组两个亚组,ACS组和SAP组在常规治疗的基础上每日口服20 mg阿托伐他汀,共8周。对照组未服用他汀类药物。酶联免疫吸附分析(ELISA)方法分别测定研究对象入选当日和治疗8周后血浆中可溶性细胞间黏附因子-1(s ICAM-1)和可溶性血管细胞黏附因子-1(s VCAM-1)水平。结果 AMI组和UAP组的s ICAM-1s水平[(318.0±86.4)、(334.9±122.6)μg/L]明显高于SAP组[(264.8±86.6)μg/L]和对照组[(279.8±145.8)μg/L],差异有统计学意义(P<0.01)。AMI组、UAP组和SAP组s VCAM-1水平[(407.8±182.1)、(446.3±160.4)、(386.5±104.2)μg/L]均显著高于对照组[(307.7±23.2)μg/L],差异有统计学意义(P<0.05)。治疗后三组s ICAM-1和s VCAM-1水平较治疗前显著下降。结论急性冠状动脉综合征患者s ICAM-1水平显著升高,反映斑块的不稳定状态;阿托伐他汀具有抑制细胞黏附因子表达、稳定粥样硬化斑块的作用。

Objective To observe the changes of the levels of plasma soluble intercellular adhesion molecule-1（ ICAM-1） and soluble vascular cell adhesion molecule-1（ VCAM-1）,and investigate the effects of atorvastatin on expression of them in patients with coronary heart disease（ CHD）. Methods The concentrations of plasma s ICAM-1 and s VCAM-1 were measured by ELISA in 58 patients with acute coronary syndrome（ ACS group） and 16 patients with stable angina pectoris（ SAP group） and 15 health people（ control group）. ACS group was divided into two subgroups： acute myocardial infarction（ AMI group） and unstable angina pectoris（ UAP group）. Patients with ACS and SAP were treated with atorvastatin 20 mg per day for 8 weeks. Before and after treatment,the concentrations of plasma s ICAM-1 and s VCAM-1 were examined.Results The levels of plasma s ICAM-1 in patients with ACS were higher than those with SAP（ P 0. 05）. The levels of s VCAM-1 were significantly higher in AMI group,UAP group and SAP group than those in control group（ P 0. 05）. After being treated,the levels of s ICAM-1 and s VCAM-1 were reduced siginificantly in all groups. Conclusion The levels of plasma s ICAM-1 are higher in patients with ACS than those with SAP,and atorvastatin may inhibit expression of cell adhesion molecule and stabilize the plaque of atherosclerosis.