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    Title: Serum MMP-9 Activity as a Diagnosing Marker for the Developing Heart Failure of Post MI Patients
    Authors: (Gwo-Ping Jong);馬作鏹(Tsochiang Ma);(Pesus Chou);(Mu-Hsin Chang);吳介信(Chieh-Hsi Wu);(Ping-Chun Li);李信達(Shin-Da Lee);(Jer-Yuh Liu);郭薇雯(Wei-Wen Kuo);黃志揚*
    Contributors: 醫學院基礎醫學研究所
    Keywords: myocardial infarction;heart failure;MMP-2;MMP-9
    Date: 2006-04
    Issue Date: 2009-08-26 16:09:36 (UTC+8)
    Abstract: Myocardial infarction (MI) is the result, in mostly cases, of the destabilization and rupture of atherosclerotic lesions. The destruction of cardiac tissue resulting from myocardial ischemia could further result in heart failure. It has been suggested that plaque instability may be mediated by matrix metalloproteinase (MMP) family. Studies have identified increased MMP-2 and MMP-9 in human platelets, and acute myocardial infarction patients with elevated MMP-2 and MMP-9 levels. However, the alteration of MMP-2 and MMP-9 from post MI left ventricle remodeling to heart failure remains to be clarified. The purpose of this study is to investigate the serum concentrations and activities of MMP-2 and MMP-9 in the developing heart failure from post MI patients. Twenty eight patients with MI without heart failure (Killip FC I) (group A; compensated) and twenty seven MI patients with heart failure (Killip II-III) (group B; decompensated) were collected to evaluate the serum levels and activities of MMP-2 and MMP-9 by ELISA and Zymography, respectively. It was observed that the both serum levels and activities of MMP-9 significantly increased (P < 0.01) in decompensated group compared to compensated group, but there was no significant difference of serum MMP-2 levels and activities between two groups. The highly elevated serum MMP-9 concentration of decompensated patients is not related with inflammatory or localized infarct area of myocardium and the real mechanisms remain to be revealed. We suggest that the increase of MMP-9 levels and activity may be used as a new marker to diagnose the development of heart failure in patients with post MI, and provide the therapeutic implications in the future.?
    Myocardial infarction (MI) is the result, in mostly cases, of the destabilization and rupture of atherosclerotic lesions. The destruction of cardiac tissue resulting from myocardial ischemia could further result in heart failure. It has been suggested that plaque instability may be mediated by matrix metalloproteinase (MMP) family. Studies have identified increased MMP-2 and MMP-9 in human platelets, and acute myocardial infarction patients with elevated MMP-2 and MMP-9 levels. However, the alteration of MMP-2 and MMP-9 from post MI left ventricle remodeling to heart failure remains to be clarified. The purpose of this study is to investigate the serum concentrations and activities of MMP-2 and MMP-9 in the developing heart failure from post MI patients. Twenty eight patients with MI without heart failure (Killip FC Ⅰ) (group A; compensated) and twenty seven MI patients with heart failure (Killip Ⅱ-Ⅲ) (group B; decompensated) were collected to evaluate the serum levels and activities of MMP-2 and MMP-9 by ELISA and Zymography, respectively. It was observed that the both serum levels and activities of MMP-9 significantly increased (P<0.01) in decompensated group compared to compensated group, but there was no significant difference of serum MMP-2 levels and activities between two groups. The highly elevated serum MMP-9 concentration of decompensated patients is not related with inflammatory or localized infarct area of myocardium and the real mechanisms remain to be revealed. We suggest that the increase of MMP-9 levels and activity may be used as a new marker to diagnose the development of heart failure in patients with post MI, and provide the therapeutic implications in the future.
    Relation: CHINESE JOURNAL OF PHYSIOLOGY 49(2)104 ~109
    Appears in Collections:[Graduate Institute of Basic Medical Science] Journal articles

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