期刊文献+

不同剂量氟伐他汀对急性冠状动脉综合征患者血管内皮功能及炎症因子的影响 被引量:3

Effects of different dosage of fluvastatin on vascular endothelial function and inflammatory factors in patients with acute coronary syndrome
下载PDF
导出
摘要 目的探讨较大剂量与常规剂量氟伐他汀相比,对急性冠脉综合征(ACS)患者是否有进一步的改善血管内皮功能和抗炎的作用。方法收集本院ACS患者120例,常规治疗基础上随机给予氟伐他汀40mg(40mg组)或氟伐他汀80 mg(80 mg组),每晚睡前服用。治疗4周,测定治疗前后患者血清NO、Hs-CRP、IL-6、HSP60的水平,随访临床事件发生情况。结果两组患者治疗4周后血清NO水平均有所升高[40 mg组:(56.68±12.01)μmol/L比(74.49±12.38)μmol/L,P<0.05;80mg组:(51.29±14.67)μmol/L比(82.57±12.17)μmol/L,P<0.01],且80 mg组患者血清NO水平升高更明显(P<0.05)。两组患者血清Hs-CRP、IL-6、HSP60水平均有所下降[40mg组分别为:(14.79±12.68)mg/L比(6.17±4.68)mg/L,(47.96±37.54)ng/L比(36.21±20.06)ng/L,(6.36±1.24)μg/L比(3.14±1.09)μg/L,P<0.05;80 mg组分别为:(14.48±12.32)mg/L比(4.31±3.56)mg/L,(50.35±40.17)ng/L比(31.24±15.49)ng/L,(6.25±1.16)μg/L比(1.25±0.98)μg/L,P<0.01],且80mg组下降更明显(均为P<0.05)。临床事件的随访观察显示,40 mg组共有10例(16.67%)患者发生心血管事件,80 mg组仅有4例(6.67%)发生心血管事件,发生率两组间差异有统计学意义(P<0.05)。结论氟伐他汀可升高ACS患者血清NO水平,降低Hs-CRP、IL-6及HSP60水平,其改善血管内皮功能和抗炎作用在短期内呈剂量依赖性。较大剂量氟伐他汀早期强化治疗可以明显减少ACS患者近期心血管事件的发生率,且安全性良好。 Objective To investigate the effects of treatment with high dose or conventional dose fluvastatin on vascular endothelial function and inflammatory factors in patients with acute coronary syndrome (ACS). Methods From July 2009 to January 2010, 120 patients with ACS were enrolled in this study. Patients were randomly assigned to accept fluvastatin 40 mg once daily ( group A, n = 60) or fluvastatin 80 mg once daily ( group B, n = 60) and were followed up for 4 weeks. All patients accepted other conventional therapy for ACS. Serum nitric oxide ( NO ) , high sensitive C-reactive protein (Hs-CRP), interleukin-6 (IL-6) and heat shock protein 60 (HSP60) were measured at admission and 4 weeks later in all subjects. Results After 4 weeks treatment with fluvastatin, serum NO level was significantly increased and Hs- CRP, IL-6 and HSP60 levels significantly decreased both in group A and group B [ group A: serum NO level from (56. 68 ± 12. 01 ) μmol/L to (74. 49 ±12. 38 ) μmol/L, Hs-CRP from ( 14. 79 ± 12. 68 ) mg/L to ( 6. 17 ±4. 68 ) mg/L, IL-6 from (47.96 ± 37.54 ) ng/L to (36. 21±20.06 ) ng/L, HSP60 from ( 6. 36 ± 1.24 ) μg/L to ( 3.14 ± 1.09 ) μg/L ( ALL P 〈 0. 05 ). In group B : serum NO level from (51.29 ± 14. 67) μmol/L to (82. 57 ± 12. 17) μmol/L, Hs-CRP from ( 14.48±12. 32 )mg/L to (4. 31 ± 3.56) mg/L, IL-6 from (50. 35± 40. 17 )ng/L to (31.24 ± 15.49)ng/L, HSP60 from (6. 25 ± 1.16) μg/L to ( 1.25 ±0. 98 ) μg/L, All P 〈 0. 01 ] , especially in group B. Cardiovascular events rate was 16. 67% in Group A and 6. 67% in group B (P 〈0. 05) after 4 weeks of follow-up. Adverse events between two groups were similar. Conclusions Fluvastatin can increase serum NO level and decrease CRP, IL-6 and HSP60 levels in patients with ACS in a dose-dependent way. And 80 mg/d fluvastatin early intensive treatment in patients with ACS can reduce the incidence of cardiovascular events and has good safety.
出处 《中国心血管杂志》 2011年第5期356-359,共4页 Chinese Journal of Cardiovascular Medicine
关键词 冠状动脉硬化 一氧化氮 氟伐他汀 C反应蛋白 白细胞介素-6 热休克蛋白60 Coronary arteriosclerosis Nitric oxide Fluvastatin C-reactive protein Interleukin-6 Heat shock protein 60
  • 相关文献

参考文献11

  • 1Ross R. The pathogenesis of atherosclerosis : a perspective for the 1990's. Nature, 1993, 362: 801-809.
  • 2不稳定性心绞痛诊断和治疗建议[J].中华心血管病杂志,2000,28(6):409-412. 被引量:2695
  • 3Davignon J, Ganz P. Role of endothelium dysfunction in atherosclerosis. Circulation, 2004, 109:Ⅲ27-Ⅲ32.
  • 4Russo G,Leopold J A, Loscalzo J. Vasoactive substance: nitric oxide and endothelial dysfunction in atherosclerosis. Vasc pharmacol, 2002, 38: 259-269.
  • 5Suwaidi JA,Hamasaki S, Higano ST, et al. Long-term follow-up of patients with mild coronary artery disease and endothelial dysfunction. Circulation, 2000, 101: 948-954.
  • 6Lauts U, Gertz K, Huang P, et al. Atorvastatin upregulates type Ⅲ nitric oxide synthase in thrombocytes, decreases platelet activation, and protects from cerebral ischemia in normocholesterolemic mice. Stroke, 2000, 31: 442-449.
  • 7Ridker PM, Morrow DA. C-reactive protein, inflammation, and coronary risk. Cardiol Clin, 2003, 21 : 315-325.
  • 8Yoshida M, Sawada T, Ishii H, et al. Hmg-CoA reductase inhibitor modulates monocyte-endothelial cell interaction under physiological flow conditions in vitro: involvement of Rho GTPase-dependent mechanism. Arterioscler Thromb Vasc Biol, 2001, 21: 1165-1171.
  • 9高旭光.脑血管病中如何合理应用调脂药?[J].中国全科医学,2007,10(7):599-599. 被引量:6
  • 10Amarenco P, Goldstein LB, Szarek M, et al. Effects of intense low-density lipoprotein cholesterol reduction in patients with stroke or transient ischemic attack: the Stroke Prevention by Aggressive Reduction in Cholesterol Levels (SPARCL) trial. Stroke, 2007, 38: 3198-3204.

二级参考文献10

  • 1Pederson JR,Olsson AG,Faergeman V,et al.Lipoprotein changes and reduction in the incidence of major coronary heart disease events in the Scandinavian Simvastatin Survival Study (4S)[].Circulation.1998
  • 2Flaker GC,Warnica JW,Sacks FM,et al.For the Cholesterol and Recurrent Event ( CARE) investigators.Pravastatin prevents clinical events in revascularized patients with average cholesterol concentrations[].Journal of the American College of Cardiology.1999
  • 3Dupuis J,Tardif JC,Cernack P,et al.Cholesterol reduction rapidly improves endothelial function after acute coronary syndromes: the RECIFE trial[].Circulation.1999
  • 4Dupuis J,Tardif JC,Cernacek P,et al.cholesterol reduction rapidly improves endothelial function after acute coronary syndromes.The RECIFE trial[].Circulation.1999
  • 5Corti R,Fayad ZA,Fuster V,et al.Effects of lipid-lowering by simvastatin on human ahterosclerotic lesions[].Circulation.2001
  • 6Sacks FM.Lipid-lowering therapy in acute coronary syndromes[].The Journal of The American Medical Association.2001
  • 7Williams JK,Sukhova GK,Herrington DM,et al.Pravastatin has cholesterol-lowering independent effects on the artery wall of atherosclerotic monkeys[].Journal of the American College of Cardiology.1998
  • 8Crisby M,Nordin FG,Shah PK,et al.Pravastatin treament increases collagen content and decreases lipid content, inflammation,metalloproteinases, and cell death in human carotid plaques: implications for plaque stabilization[].Circulation.2001
  • 9Rauch U,Osende JI,Chesebro JH,et al.Statin and cardiovascular diseases: the multiple effects of lipid-lowering therapy by statins[].Atherosclerosis.2000
  • 10Libby P.Current concepts of the pathogenesis of the acute coronary syndromes[].Circulation.2001

共引文献2721

同被引文献22

引证文献3

二级引证文献4

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部