小剂量阿托伐他汀联合阿司匹林对脑梗死患者颈动脉粥样硬化斑块及血液生化指标的影响

目的观察阿托伐他汀联合阿司匹林对脑梗死患者颈动脉粥样硬化斑块、血小板膜表面P选择素（CD62P）、血小板糖蛋白GPⅡb-Ⅲa复合物（PAC-1）及超敏C反应蛋白（hs—CRP）的影响。方法将104例经超声检查证实、有颈动脉粥样硬化斑块的急性脑梗死患者随机分为干预1组（34例）、干预2组（32例）及对照组（38例）。干预1组和2组分别口服阿托伐他汀10、20mg／d，同时加服拜阿司匹林100mg／d；对照组1：3服拜阿司匹林100mg／d。治疗后3周检测血中CD62P、PAC-1、hs—CRP；治疗后6个月时超声检查斑块及血脂情况。结果干预1、2组及对照组比较：①斑块大小变化差异无统计学意义。②治疗前，3组不稳定性斑块数分别为54、46、49个，稳定性斑块为5、6、4个，治疗后不稳定性斑块分别为44、34、50个，稳定性斑块为15、17、5个。与治疗前自身和对照组比较，两个干预组变化差异均有统计学意义，对照组治疗前后以及两个干预组间差异均无统计学意义。③两个干预组治疗后，CD62P、PAC-1及hs—CRP较自身治疗前及对照组均显著性降低（P〈0．01），对照组治疗前后以及两个干预组间差异均无统计学意义。④治疗后两个干预组血脂水平均显著降低（P〈0．01）。总胆固醇〈4．0mmol／L者，干预1、2组治疗前分别为2例和1例，治疗后为7例和14例（P〈0．05）。对照组各项指标变化差异均无统计学意义。⑤治疗后急性脑血管事件，对照组3例，干预1组1例，干预2组0例。干预2组药物不良反应有6例（18．8％），干预1组有1例（2．9％），两组比较差异有统计学意义（P〈0．05）。结论阿托伐他汀联合阿司匹林可抑制血小板活化及炎性反应，对颈动脉粥样硬化斑块具有一定的稳定作用。阿司匹林联合10mg／d的阿托伐他汀较20mg／d更安全。

Effects of low-dose atorvastatin in combination with aspirin on carotid atherosclerotic plaques and blood biochemical parameters in patients with cerebral infarction

Objective To observe the effects of low-dose atorvastatin in combination with aspirin on carotid atheroselerotic plaques, platelets surface P-seleetin （CD62P） , platelet glyeoprotein ]] b/m a receptor complex （ PAC-1 ） , and high sensitivity C-reactive protein （hs-CRP） in patients with cerebral infarction. Methods A total 104 patients with acute cerebral infarction whose carotid atherosclerotic plaques were confirmed by ultrasonography were randomly assigned into three groups ： the intervention group 1 （ n = 34） , intervention group 2 （n = 32） and the control group （n = 38）. Patients in intervention groups 1 and group 2 received oral atorvastatin 10 and 20 mg/d separately, and also received Bayaspirin 100 mg/d at the same time, while the control group only received Bayaspirin 100 mg/d. The plasma CD62P, PAC-1 and hs-CRP were detected 3 weeks after treatment ; and the changes of carotid atherosclerotic plaques and lipid were examined with ultrasonography at 6 months. Results As compared between the 2 intervention groups, and the control group： （1）There was no significant difference in the size of carotid atherosclerotic plaques. （2）Before treatment, the numbers of unstable plaque in the 3 groups were 54, 46 and 49, and the numbers of stable plaque were 5, 6 and 4 respectively. After treatment, the numbers of unstable plaque were 44, 34 and 50, and the numbers of stable plaque were 15, 17 and 5 respectively. As compared with themselves and the control group before treatment, there were significant differences in both intervention groups. There were no significant differences before and after treatment in the control group and between the two intervention groups. （3）After treatment, the CD62P, PAC-1, and hs-CRP in the 2 intervention groups were reduced significantly than themselves before treatment and the control group （P 〈 0.01 ）.（4）After treatment, the mean lipid levels in the two intervention groups were reduced （P 〈0.01 ）. There were 2 and 1 patients with total cholesterol 〈 4.0 mmol/L in the intervention groups 1 and 2 before treatment, and there were 7 and 14 patients after treatment （P 〈0.05）. The changes of all the indices in the control group did not have statistical difference. （5）After treatment, the acute cerebrovasctdar events in the control group were 3 cases, in the intervention group 1 was 1 case, and in the intervention group 2 was 0 case. There were 6 patients （18.8%） experienced adverse drug reaction in the intervention group 2, while there was only 1 （2.9%） in the intervention group 1. There was significant difference between the two groups （P 〈 0. 05）. Conclusion Atorvastatin in combination with aspirin inhibits platelet activation and inflammatory response. It has a certain effect on the stability of carotid atherosclerotic plaques. Aspirin in combination with atorvastatin 10 mg/d is more safe than 20 mg/d.