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目的探讨不稳定型心绞痛(UA)与炎症指标高敏C反应蛋白(hs-CRP)的关系以及早期阿托伐他汀干预对UA患者血清hs-CRP水平的影响。方法采用颗粒增强免疫透射比浊法测定60例UA患者、53例稳定型心绞痛患者(SA组)以及50例健康对照者(对照组)的血清hs-CRP水平。采用随机开放法将UA组分成常规组和阿托伐他汀组进行为期4周的干预,比较治疗前后的血清hs-CRP及血脂水平变化。选择性冠状动脉造影采用Judkin’s法,共有78例患者和29例健康对照者完成造影。结果UA组血清hs-CRP基础水平明显高于SA组及对照组(P<0.01)。血清hs-CRP水平与依照Gensini积分评估的冠状动脉病变严重程度显著相关。UA患者治疗4周后,阿托伐他汀组血清hs-CRP及LDL-C水平均明显下降(P<0.01),而常规组无明显变化。相关分析显示,阿托伐他汀组血清hs-CRP水平的下降与LDL-C下降无相关性。结论UA的发生与机体炎症反应激活有关。血清hs-CRP水平与冠状动脉病变范围及程度有一定关系。阿托伐他汀快速降低血清hs-CRP水平,在UA的早期治疗中具有重要意义。
Objective To investigate the relationship between unstable angina pectoris (UA) and hypersensitive C-reactive protein (hs-CRP) and the effect of early atorvastatin on serum hs-CRP level in UA patients. Methods The levels of serum hs-CRP in 60 UA patients, 53 patients with stable angina pectoris (SA group) and 50 healthy controls (control group) were determined by particle-enhanced immuno-turbidimetry. UA group was divided into routine group and atorvastatin group by randomized open-ended method for a period of 4 weeks of intervention, before and after treatment of serum hs-CRP and blood lipid levels. Selective coronary angiography using the Judkin’s method, a total of 78 patients and 29 healthy controls to complete the contrast. Results The basic level of hs-CRP in UA group was significantly higher than that in SA group and control group (P <0.01). Serum hs-CRP levels were significantly associated with the severity of coronary artery disease as assessed by Gensini score. Serum levels of hs-CRP and LDL-C in atorvastatin group were significantly decreased after UA treatment for 4 weeks (P <0.01), but no significant changes were found in the conventional group. Correlation analysis showed no significant correlation between serum hs-CRP levels and LDL-C decline in atorvastatin group. Conclusion The occurrence of UA is related to the activation of inflammatory reaction in the body. Serum hs-CRP levels and extent of coronary lesions have a certain relationship. Atorvastatin rapidly reduces serum hs-CRP level, which is of great significance in the early treatment of UA.