不同剂量辛伐他汀治疗对急性冠状动脉综合征患者几种炎症因子的影响

Effects of simvastatin in deferent dosage on plasma levels of hs-CRP、Hcy and vWF in patients with acute coronary syndrome

目的观察急性冠状动脉综合征(ACS)患者使用两种剂量(20mg和40mg)的辛伐他汀治疗3天后对血浆高敏C反应蛋白(hsCRP)、同型半胱氨酸(Hcy)及遗传性血友病因子(vWF)的变化。方法对住院临床确诊为ACS的52例患者按随机原则分别入选常规治疗组(17例)不接受任何调脂药物治疗;辛伐他汀治疗组分别接受20mg(17例)和40mg(18例)辛伐他汀治疗3天。并测定各组治疗前后hsCRP、Hcy、vWF和血脂水平的变化。结果治疗3天后,20mg辛伐他汀治疗使血浆hsCRP、Hcy和vWF水平减低,但与常规治疗组比较差异无统计学意义;而40mg治疗组疗效则明显优于常规组,两组间的下降幅度差异有显著性(hsCRP为470%比43%,Hcy为366%比09%,vWF为190%比48%,P<005)。但三组治疗前后各血脂成分的变化差异均无显著性,而且40mg辛伐他汀治疗引起的血hsCRP、Hcy及vWF的降低与TC(r=0229,P=0361;r=0142,P=0574;r=0131,P=0605)、LDLC(r=-0020,P=0936;r=-0112,P=0659;r=-0321,P=0194)的下降百分数之间无相关关系。结论急性冠脉综合征患者大剂量辛伐他汀(40mg)治疗3天后,可明显控制血浆炎症因子、降低Hcy水平及改善内皮功能,从而有利于动脉粥样硬化斑块的稳定性。

Objective To observe whether intervention with two different dosage of simvastatin may benefit to plasma levels of high sensitive C reactive protein (hs CRP), homocysteine (Hcy) and Von Willebrand factor (vWF) in patients with acute coronary syndrome(ACS). Methods Patients with ACS were randomly assigned into three groups: the control group ( n =17) treated without lipid lowering drugs, 20 mg ( n =17) and 40 mg ( n =18) simvastatin group with 3 days of treatment. Before and after the treatment, the plasma levels of hs CRP, Hcy, vWF and lipid were detected. Results The treatments of 20 mg simvastatin did not decrease significantly the levels of hs CRP, Hcy and vWF. Compared to the control group, levels of hs CRP, Hcy and vWF were markedly reduced by 40 mg simvastatin (hs CRP 47 0% vs 4 3%,Hcy 36 6% vs. 0 9%, vWF 19 0% vs. 4 8%, P <0 05) No changes of lipid levels were observed in any group before and after treatment, whilst there were no relation between the decreaseing percentage of hs CRP, Hcy or vWF and that of TC( r =0 229, P =0 361; r =0 142, P =0 574; r =0 131, P =0 605)or LDL C( r = -0 020, P =0 936; r = -0 112, P =0 659; r = -0 321, P =0 194). Conclusion Treatments with high dose simvastatin (40 mg) for 3 days could reduce the levels of inflammatory factors and Hcy, and improved the function of vascular endothelium, which may promotes the stabilization of atherosclerotic plaque.