我们的网站为什么显示成这样?

可能因为您的浏览器不支持样式,您可以更新您的浏览器到最新版本,以获取对此功能的支持,访问下面的网站,获取关于浏览器的信息:

|本期目录/Table of Contents|

急性心肌梗死患者MMP-9水平与心室重构的相关性及其缬沙坦的干预效果

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2010年第5期
页码:
727-729
栏目:
临床研究
出版日期:
2010-06-22

文章信息/Info

Title:
Effects of valsartan on plasma matrix metalloproteinase-9 in patients with acute myocardial infarction
作者:
赵瑞平孙凯李永明
内蒙古包头市中心医院心内科,内蒙古 包头 014040
Author(s):
ZHAO Rui-ping SUN Kai LI Yong-ming
Department of Cardiology, Baotou Central Hospital, Baotou 014040, Inner Mongolia, China
关键词:
心肌梗死急性基质金属蛋白酶缬沙坦
Keywords:
myocardial infarction acute matrix metalloproteinase-9 valsartan
分类号:
R541.4
DOI:
-
文献标识码:
A
摘要:
目的: 探讨急性心肌梗死(AMI)患者基质金属蛋白酶-9(MMP-9)的变化及与心室重构的相关性,并观察缬沙坦对其干预的效果。方法: 选AMI患者90例,随机分为常规治疗组和缬沙坦组,正常体检者45例为正常对照组,AMI患者于入选时检测MMP-9,测定超声心动图指标[左室收缩末期容积(LVESV)、舒张末期容积(LVEDV)和左室射血分数(LVEF)],服药1周、4周、12周后再测定MMP-9、超声心动图指标,正常对照组病例入选后测定MMP-9。比较各组病例MMP-9值;比较两治疗组患者用药1周及4周后MMP-9值、用药4周及12周后超声心动图指标及其变化。结果: AMI患者与正常对照组MMP-9值、超声心动图指标比较,差异有统计学意义(P<0.05);用药1周时B组较A组MMP-9值减小(P<0.05);用药4周时A、B两组MMP-9值均减小,而超声心动图指标差异无统计学意义,12周后A、B两组超声心动图指标发生变化(P<0.05);用药1周后、4周后两组MMP-9值均较用药前减小(P<0.05)。结论: 缬沙坦能降低AMI患者MMP-9的表达,降低心室重构发生率。
Abstract:
AIM: To observe the changes of plasma MMP-9 in acute myocardial infarction (AMI) patients and the effect of valsartan on MMP-9. METHODS: Ninety AMI patients and 45 control cases were recruited. The patients were randomly divided into two groups: group A (routine treatment group, n=45) and group B (valsartan treatment group, n=45). Plasma MMP-9 and echocardiographic indices were measured in all groups and MMP-9 and echocardiographic indices were measured in patient groups at 1 week, 4 weeks and 12 weeks after treatment. RESULTS: No statistical difference was observed in MMP-9 and echocardiographic indices between groups (P>0.05). MMP-9 in group A was statistically lower than in group B 1 week post-treatment. After 4 weeks, MMP-9 returned to normal in both groups and no statistical difference was found in echocardiographic indices between groups. Twelve weeks after treatment, changes were found in echocardiographic indices in both groups. CONCLUSION: Valsartan reduces the expression of MMP-9 and degrades the incidence of ventricular remodeling in AMI patients.

参考文献/References

[1]Nishiya D, Enomoto S, Omura T, et al. The long-acting Ca2+-channel blocker azelnidipine prevents left ventricular remodeling after myocardial infarction[J]. J Pharmacol Sci, 2007, 103(4):391-397.

[2]Zhao JL, Yang YJ, You SJ, et al. Pretreatment with fosinopril or valsartan reduces myocardial no-reflow after acute myocardial infarction and reperfusion[J]. Coron Artery Dis, 2006, 17(5):463-469.

[3]Xiaozhou H, Jie Z, Li Z, et al. Predictive value of the serum level of N-terminal pro-brain natriuretic peptide and high-sensitivity C-reactive protein in left ventricular remodeling after acute myocardial infarction[J]. J Clin Lab Anal, 2006, 20(1):19-22.

[4] Tziakas DN, Chalikias GK, Hatzinikolaou EI, et al. N-terminal pro-B-type natriuretic peptide and matrix metalloproteinases in early and late left ventricular remodeling after acute myocardial infarction[J]. Am J Cardiol, 2005, 96(1):31-34.

[5]Hayashidani S, Tsutsui H, Ikeuchi M, et al. Targeted deletion of MMP-2 attenuates early LV rupture and late remodeling after experimental myocardial infarction[J]. Am J Physiol Heart Circ Physiol, 2003, 285(3):H1229-H1235.

[6] Takai S, Yamamoto D, Jin D, et al. Inhibition of matrix metalloproteinase-9 activity by lisinopril after myocardial infarction in hamsters[J]. Eur J Pharmacol, 2007, 568(1-3):231-233.

[7] Heymans S, Luttun A, Nuyens D, et al. Inhibition of plasminogen activators or matrix metalloproteinases prevents cardiac rupture but impairs therapeutic angiogenesis and causes cardiac failure[J]. Nat Med, 1999, 5(10):1135-1142.

备注/Memo

备注/Memo:
收稿日期:2009-05-18.基金项目:包头市科技计划项目(2008192001-3) 通讯作者:赵瑞平,教授,主要从事心脏介入治疗、起搏与电生理研究Email:Ruipingzhao@163.com
更新日期/Last Update: 2010-06-22