期刊文献+

替米沙坦对轻度心力衰竭心肌纤维化和心功能的影响 被引量:1

Effects of telmisartan on myocardial fibrosis and left ventricular function in patients with mild heart failure
下载PDF
导出
摘要 目的探讨替米沙坦对轻度心力衰竭心肌纤维化和心功能的影响。方法选择轻度心力衰竭患者(NYHA分级为Ⅰ~Ⅱ级)72例为观察组,随机分为常规治疗组和替米沙坦组,每组36例;另选健康体检者30例为对照组,治疗前和治疗3个月时采用放射免疫法测定血清Ⅲ型前胶原氨基末端肽(PⅢNP)和血浆脑钠肽(BNP)浓度,并应用心脏彩声超声测定心功能变化。结果观察组血清PⅢNP和血浆BNP浓度均高于正常对照组(P<0.01);3个月后与治疗前比较:替米沙坦组血PⅢNP和BNP均明显下降(P<0.01);且较常规治疗组亦明显下降(P<0.05)。结论替米沙坦治疗轻度心力衰竭患者可以起到抗心肌纤维化、改善心功能的作用。 Objective To evaluate the effects of telmisartan on myocardial fibrosis and left ventricular function in patients with mild chronic heart failure.Methods The 72 patients were randomly divided into two groups,routine treatment group (n=36) and telmisartan group (n=36),and 30 healthy subjects were enrolled as control group.The serum levels of aminoterminal propeptide of typeⅢ procollagen(PⅢNP)and brain natriuretic peptide (BNP)were detected by radioimmunoassay.After 3-month therapy,PⅢNP and BNP were rechecked and the parameters of ventricular function were detected by echocardiography.Results The serum levels of PⅢNP and BNP in routine treatment group and telmisartan group were significantly higher than those of control group (P0.01).After 3-month treatment,the levels of PⅢNP and BNP were significantly decreased in telmisartan group,as compared with those before treatment (P0.01),which were also significantly lower than those of routine treatment group(P0.05).Conclusion The telmisartan therapy can relieve myocardial fibrosis and improve left ventricular function in old patients with mild heart failure.
作者 王仁忠
出处 《河北医药》 CAS 2010年第17期2333-2334,共2页 Hebei Medical Journal
关键词 心力衰竭 替米沙坦 心内膜心肌纤维化症 heart failure telmisartan endomyocardial fibrosis
  • 相关文献

参考文献3

二级参考文献28

  • 1[10]Beggah AT,Escoubet B,Puttini S,et al.From the cover:reversible cardiac fibrosis and heart failure induced by conditional expression of an antisense mRNA of the mineralocorticoid receptor in cardiomyocytes.Proc Nat Acad Sci U S A 2002;99:7160-5.
  • 2[11]Sabbah HN,Sharov VG,Lesch M,et al.Progression of heart failure:a role for interstitial fibrosis.Mol Cell Biochem 1995;147:29-34.
  • 3[12]Zannad F,Alla F,Dousset B,et al.Limitation of excessive extracellular matrix turnover may contribute to survival benefit of spironolactone therapy in patients with congestive heart failure:insights from the randomized aldactone evaluation study(RALES).Circulation 2000;102:2700-6.
  • 4[13]Zannad F,Dousset B,Alla F.Treatment of congestive heart failure:interfering the aldosterone-cardiac extracellular matrix relationship.Hypertension 2001;38:1227-32.
  • 5[14]Querejeta R,Lopez B,Gonzalez A,et al.Increased collagen type Ⅰ synthesis in patients with heart failure of hypertensive origin:relation to myocardial fibrosis.Circulation 2004;110:1263-8.
  • 6[1]Banff C,Cavalca V,Veglia F,et al.Neurohormonal activation is associated with increased levels of plasma matrix metalloproteinase-2 in human heart failure.Eur Heart J 2005;26:481-8.
  • 7[2]Reinhardt D,Sigusch HH,Hensse J,et al.Cardiac remodelling in end stage heart failure:upregulation of matrix metalloproteinase(MMP)irrespective of the underlying disease,and evidence for a direct inhibitory effect of ACE inhibitors on MMP.Heart2002;88:525-30.
  • 8[3]Yamazaki T,Lee JD,Shimizu H,et al.Circulating matrix metalloproteinase-2 is elevated in patients with congestive heart failure.Eur J Heart Fail 2004;6:41-5.
  • 9[4]Wilson EM,Gunasinghe HR,Coker ML,et al.Plasma matrix metalloproteinase and inhibitor profiles in patients with heart failure.J Card Fail 2002;8:390-8.
  • 10[5]Spinale FG,Coker ML,Heung LJ,et al.A matrix metalloproteinase induction/activation system exists in the human left ventricular myocardium and is upregulated in heart failure.Circulation 2000;102:1944-9.

共引文献28

同被引文献4

引证文献1

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