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目的:探讨高敏C反应蛋白(hs-CRP)与冠状动脉痉挛的关系以及调脂治疗对其影响。方法:根据入院时心绞痛特点,将经乙酰胆碱激发试验或非创伤性标准诊断为冠状动脉痉挛患者76例分为稳定型心绞痛(SAP)组和不稳定型心绞痛(UAP)组,并与非痉挛(乙酰胆碱试验阴性)患者作对照(对照组),测定3组患者血清LDL-C和hs-CRP水平。在阿司匹林和钙拮抗剂治疗基础上,42例因LDL-C高加用他汀类调脂治疗(调脂治疗组),其中18例来自UAP组,24例来自SAP组;另34例为非调脂治疗组。6个月后比较调脂治疗组、非调脂治疗组LDL-C和hs-CRP的变化情况。结果:SAP组和UAP组LDL-C均高于对照组(P<0.01),但SAP组与UAP组比较差异无统计学意义(P>0.05);UAP组hs-CRP显著高于SAP组,2组又显著高于对照组(均P<0.01);LDL-C与hs-CRP水平无显著相关性(P>0.05)。非调脂治疗组6个月后LDL-C无显著变化,但hs-CRP呈下降趋势(P<0.05);而调脂治疗组LDL-C及hs-CRP均显著降低(P<0.01)。结论:hs-CRP升高可能与不稳定的冠状动脉痉挛状态有关,在常规阿司匹林和钙拮抗剂基础之上加用调脂治疗可以更有效地降低血清hs-CRP。
Objective: To investigate the relationship between high-sensitivity C-reactive protein (hs-CRP) and coronary artery spasm and the effect of lipid-lowering therapy on it. Methods: According to the characteristics of angina at admission, 76 patients with coronary artery spasm diagnosed by acetylcholine provocation test or non-invasive standard were divided into stable angina pectoris (SAP) group and unstable angina pectoris (UAP) group, and were compared with non-spasmodic Acetylcholine test negative patients as control (control group), the determination of serum LDL-C and hs-CRP levels in three groups. On the basis of aspirin and calcium antagonist treatment, 42 patients were treated with statin lipid-lowering therapy (lipid-lowering treatment group) due to the high LDL-C level, of which 18 were from the UAP group, 24 from the SAP group and the other 34 were from the SAP group Lipid treatment group. After 6 months, the changes of LDL-C and hs-CRP in lipid-lowering treatment group and non-lipid-lowering treatment group were compared. Results: The levels of LDL-C in SAP group and UAP group were higher than those in control group (P <0.01), but there was no significant difference between SAP group and UAP group (P> 0.05). The hs-CRP in UAP group was significantly higher than that in SAP group 2 group was significantly higher than that of the control group (all P <0.01). There was no significant correlation between LDL-C and hs-CRP levels (P> 0.05). There was no significant change of LDL-C after 6 months in non-lipid-lowering treatment group, but hs-CRP showed a decreasing trend (P <0.05), while LDL-C and hs-CRP in lipid lowering treatment group were significantly decreased (P <0.01). CONCLUSIONS: The elevation of hs-CRP may be related to unstable coronary spasm. Serum hs-CRP can be more effectively reduced by adding lipid-lowering therapy on the basis of conventional aspirin and calcium antagonist.