阿托伐他汀对颈动脉粥样硬化斑块患者血浆高敏C反应蛋白的影响

目的观察应用阿托伐他汀干预后颈动脉粥样硬化患者颈动脉粥样硬化斑块及血浆高敏C反应蛋白（hs—CRP）的变化。探讨他汀类药物预防缺血性脑血管病的机制。方法收集2006年7月-2008年10月福建省立医院门诊及住院的有颈动脉粥样硬化患者80例，随机分为阿托伐他汀药物干预组（A组，40例）及非他汀药物干预组（B组，40例）。并设无颈动脉粥样硬化对照组（C组，40例）。A组在饮食控制的基础上给予阿托伐他汀20mg口服，1次／日，疗程16周。B组采用饮食控制，加强体育运动，减轻体重等方法。干预8周后，观察血脂及血浆hs—CRP的变化，8周、16周后复查颈动脉多普勒超声，并进行统计分析。结果干预前A纽与B组两组间血浆血脂、hs—CRP水平无明显差异。两组血浆、血脂、hs—CRP水平均高于对照组（P〈0．05）。干预8周后A组血浆血脂、hs—CRP水平明显低于B组（P〈0．05）。干预8周时两组患者颈动脉粥样硬化斑块无明显改变，16周后药物干预组颈动脉粥样硬化斑块明显变小，易损癍块减少。结论他汀类药物在治疗颈动脉粥样斑块中不仅有降脂的作用，还有降低血浆hs—CRP起到抗炎稳定斑块的作用，从而起到预防缺血性脑血管病的作用。

Effects of Atorvastatin on Plasma hs - C - reactive Protein in Patients with Carotid Atherosclerosis

Objective To observe the effects of atorvastatin on carotid atheroselerotic plaques and plasma high sensitive C- reactive protein（hs- CRP） in patients with carotid atherosclerosis. Methods From July 2006 to October 2008, eighty patients with carotid atherosclerosis were selected from Fujian Provincial Hospital and divided randomly into two groups： Atorvastatin intervention group（n = 40） treated with atorvastatin based on diet control,and normal intervention group（n= 40） received diet control and athletic sports for 16 weeks. After treatment for 8 weeks,the changes of plasma hs - CRP and blood lipid were observed. After treatment for 8 weeks and 16 weeks,carotid Doppler ultrasonography was carried out. Results There was no difference in the levels of blood lipid and hs -CRP between atorvastatin intervention group and normal intervention group pre- treatment（P〉0.05）. The levels of blood lipid and plasma hs - CRP in intervention groups were higher than that in control group（P〈0.05）. After treatment for 8 weeks,the levels of blood lipid and plasma hs - CRP in atorvastatin intervention groups were lower than that in normal intervention group（P〈0.05）. After treatment for 16 weeks, the carotid atherosclerotic plaque size and vulnerable plaque rate reduced in atorvastatin intervention groups（P〈 0.05）. Conclusion Atorvastatin had preventive effect on stroke by stabilizing atherosclerotic plaques,reducing the hs- CRP level and lipid in patients with carotid atherosclerosis.