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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 plasma adhesion factor in patients with coronary heart disease before and after treatment with atorvastatin. Methods 89 cases were divided into acute coronary syndrome (ACS) group, stable angina pectoris (SAP) group and control group. The ACS group was divided into AMI group and UAP group. ACS group and SAP group were treated with atorvastatin 20 mg daily for 8 weeks . The control group did not take statins. The levels of soluble intercellular adhesion molecule-1 (s ICAM-1) and soluble vascular cell adhesion molecule-1 (sVCAM-1) in plasma were measured by enzyme linked immunosorbent assay (ELISA) . Results The levels of s ICAM-1s in AMI group and UAP group were significantly higher than those in SAP group [(318.0 ± 86.4), (334.9 ± 122.6) μg / L] [(264.8 ± 86.6) μg / L vs 145.8) μg / L], the difference was statistically significant (P <0.01). The levels of VCAM-1 in AMI group, UAP group and SAP group were significantly higher than that in control group [(307.8 ± 182.1), (446.3 ± 160.4), (386.5 ± 104.2) μg / L] ], The difference was statistically significant (P <0.05). The levels of s ICAM-1 and s VCAM-1 in three groups after treatment were significantly lower than those before treatment. Conclusion The level of s ICAM-1 in patients with acute coronary syndrome is significantly increased, which reflects the unstable state of plaque. Atorvastatin can inhibit the expression of cell adhesion molecule and stabilize the atherosclerotic plaque.