摘要
目的探讨急性心肌梗死急诊经皮冠状动脉介入治疗（PCI）术前给予负荷剂量瑞舒伐他汀对内皮功能及炎症因子的影响，、方法选取2叭2年5月-2013年5月我院急救中心收治的76例急性心肌梗死患者，将患者随机分为两组，试验组（PCI术前使用瑞舒伐他汀＋常规治疗）38例，对照组（常规治疗）38例。分别在PCI术前、PCI术后24h、PCI术后4周测定hs-CRP，ET-1。NO水平。结果两组患者入院时hs-CRP，ET-1，NO浓度差异无显著性。术后24h两组hs-CRP水平较入院时明显升高（P〈0．05），对照组升高更明显（P〈0．05）；ET-1水平较入院时明显升高（P〈0．05），对照组升高更明显（P〈0．05）；NO水平较PCI术前升高，试验组升高更明显，差异有显著性（P〈0．05）。术后4周时两组hs-CRP，ET-1水平均较PCI术前及术后24h降低，试验组较对照组降低更明显（P〈0．05），NO水平较PCI术前及术后24h明显升高，试验组升高更明显，差异有显著性（P〈0．05）。结论急性心肌梗死急诊PCI前口服负荷剂量瑞舒伐他汀可减轻AMI患者PCI术后炎症反应，改善冠脉内皮功能。
Objective To observe the effects of rosuvastatin on tile vascular endothelial funetinn and inflammatory factors in pa- lients wilh acute myocardial infarction. Methods Seventy-six patients with acute myocardial infarction in our hospital were enrolled. They were randomly divided into the control group （ not taking preoperative statins ） and the trial group （ preoperative loading dose of rosuvastatin 20rag） with 38 cases in each group. The levels of hs-CRP,ET-1 ,NO were measured at before PCI and ＇after 24 hours,4weeks. Results The difference of hs-CRP, ET-I and NO levels between the two groups were not significantly different before PCI（P 〉 0.05）. At 24 hours after PCI ,the levels of hs-CRP and ET-I were highly increased （ P 〈 0.05 ） , the levels of the conlrol group were increased than that of the trial group（ P 〈0.05） ; the level of NO was highly increased more significantly in the trial group compared with the control group（ P 〈0.05）. In the four week postoperatively,the levels hs-CRP aud ET-I were decreased significantly and the level of NO was increased eompa,＇ed with be- fore PCI and 24 hours after PCI ,the level of hs-CRP and ET-I in trial group were obviously lower than control group（ P 〈0.05 ） ,and the level of NO was nbvionsly higher than control group（ P 〈 0.05 ）. Conclusion Rosuvastatin could inhibit inflammatory, reaction in patients with AMl,and improve the vascuhlar endothelial tunction.
出处
《潍坊医学院学报》
2014年第1期73-75,共3页
Acta Academiae Medicinae Weifang
关键词
瑞舒伐他汀
心肌梗死
急性
内皮功能
炎症因子
Rosuvaslatin
Acute myocardial infarction
The vascular endothelial function
Inflammatory
factors
