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目的探讨阿托伐他汀治疗不稳定型心绞痛(UA)的疗效及其对血清血脂,高敏C反应蛋白(hs-CRP)和同型半胱氨酸(Homocysteine,Hcy)水平的影响。方法选择90例诊断明确的不稳定型心绞痛患者,随机分成两组,对照组给予拜阿司匹林、氢氯吡格雷抗血小板聚集、低分子肝素抗凝治疗;治疗组在常规组基础上予阿托伐他汀40mg,每晚1次,口服。3月后比较两组观察患者用药前后血脂,hs-CRP和Hcy水平变化的变化。结果治疗后两组患者心绞痛症状有明显改善,治疗组有效率为93.33%,优于对照组的75.56%,差异有统计学意义(P<0.05)。治疗前两组血脂,hs-CRP和Hcy水平比较无显著性差异(P>0.05),治疗后两组TC、TG、LDL-C和hs-CRP水均较治疗前明显下降(P<0.01),HDL-C较治疗前明显升高(P<0.01),治疗组较对照组变化更为明显(P<0.01或P<0.05)。对照组在治疗后Hcy水平仅出现下降趋势(P>0.05),但治疗组较治疗前及对照组出现明显下降,差异有统计学意义(P<0.01)。结论阿托伐他汀可提高不稳定型心绞痛的疗效,能降低血中hs-CRP和Hcy水平,从而降低不稳定型心绞痛及动脉粥样硬化危险因素。
Objective To investigate the effects of atorvastatin on patients with unstable angina pectoris (UA) and its effects on serum lipids, hs-CRP and homocysteine (Hcy) levels. Methods Ninety patients with unstable angina pectoris were selected and randomly divided into two groups. The control group was treated with aspirin, clopidogrel antiplatelet and low molecular weight heparin anticoagulant therapy. The treatment group was treated with atorvastatin Statin 40mg, 1 night, orally. After 3 months, the changes of blood lipid, hs-CRP and Hcy in two groups before and after treatment were compared. Results After treatment, the symptoms of angina in both groups were significantly improved. The effective rate of the treatment group was 93.33%, which was better than that of the control group (75.56%), the difference was statistically significant (P <0.05). The levels of TC, TG, LDL-C and hs-CRP in the two groups before treatment were significantly lower than those before treatment (P <0.01) , HDL-C was significantly higher than before treatment (P <0.01), the treatment group more obvious changes than the control group (P <0.01 or P <0.05). The level of Hcy in the control group decreased only after treatment (P> 0.05), but there was a significant decrease in the treatment group compared with that before treatment and in the control group (P <0.01). Conclusions Atorvastatin can improve the curative effect of unstable angina pectoris and decrease the levels of hs-CRP and Hcy in blood, so as to reduce the risk factors of unstable angina pectoris and atherosclerosis.