Plasma levels of matrix metalloproteinase-9 and tissue inhibitor of metalloproteinase-1 are increased in the coronary circulation in pa with acute coronary syndrome

被引:242
作者
Inokubo, Y [1 ]
Hanada, H [1 ]
Ishizaka, H [1 ]
Fukushi, T [1 ]
Kamada, T [1 ]
Okumura, K [1 ]
机构
[1] Hirosaki Univ, Sch Med, Dept Internal Med 2, Hirosaki, Aomori 0368562, Japan
关键词
D O I
10.1067/mhj.2001.112238
中图分类号
R5 [内科学];
学科分类号
1002 [临床医学]; 100201 [内科学];
摘要
Background Previous studies on atherectomy specimens from patients with acute coronary syndrome (ACS) implicated the role of proteolytic enzymes. We examined whether the plasma levels of matrix metalloproteinase-9 (MMP-9) and tissue inhibitor of metalloproteinase-1 (TIMP-1) were increased in the coronary circulation in ACS. Methods and Results The plasma levels (nanograms per milliliter) of MMP-9 and TIMP-1 in the aorta (Ao) and great cardiac vein (GCV) were measured in 29 patients with ACS (20 with acute myocardial infarction [group 1] and 9 with unstable angina [group 21), 17 with stable effort angina (group 3), and 20 control subjects (group 4). Group 1 patients had occlusion in the left anterior descending artery (LAD), and groups 2 and 3 patients had culprit lesion in the LAD. In group 1 blood samples were obtained at the time of direct coronary angioplasty done within 12 hours after the onset. The Ao level of either MMP-9 or TIMP-1 did not differ among the 4 groups. The GCV-Ao differences in MMP-9 and TIMP-1 were both significantly increased in groups and 2 compared with those in group 4. Neither of them was different between groups 3 and 4. Neither the GCV-Ao difference in MMP-9 or TIMP-1 level was correlated with the maximal creatine kinase level in group 1. Conclusions Increased plasma levels of MMP-9 and TIMP-1 were detected in the coronary circulation in ACS patients, suggesting a process of active plaque rupture in ACS.
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页码:211 / 217
页数:7
相关论文
共 23 条
[1]
IDENTIFICATION OF 92-KD GELATINASE IN HUMAN CORONARY ATHEROSCLEROTIC LESIONS - ASSOCIATION OF ACTIVE ENZYME-SYNTHESIS WITH UNSTABLE ANGINA [J].
BROWN, DL ;
HIBBS, MS ;
KEARNEY, M ;
LOUSHIN, C ;
ISNER, JM .
CIRCULATION, 1995, 91 (08) :2125-2131
[2]
REGULATION OF COLLAGEN DEGRADATION IN THE RAT MYOCARDIUM AFTER INFARCTION [J].
CLEUTJENS, JPM ;
KANDALA, JC ;
GUARDA, E ;
GUNTAKA, RV ;
WEBER, KT .
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY, 1995, 27 (06) :1281-1292
[3]
THROMBOSIS AND ACUTE CORONARY-ARTERY LESIONS IN SUDDEN CARDIAC ISCHEMIC DEATH [J].
DAVIES, MJ ;
THOMAS, A .
NEW ENGLAND JOURNAL OF MEDICINE, 1984, 310 (18) :1137-1140
[4]
MATRIX METALLOPROTEINASES AND CARDIOVASCULAR-DISEASE [J].
DOLLERY, CM ;
MCEWAN, JR ;
HENNEY, AM .
CIRCULATION RESEARCH, 1995, 77 (05) :863-868
[5]
CORONARY PLAQUE DISRUPTION [J].
FALK, E ;
SHAH, PK ;
FUSTER, V .
CIRCULATION, 1995, 92 (03) :657-671
[6]
MECHANISMS OF DISEASE - THE PATHOGENESIS OF CORONARY-ARTERY DISEASE AND THE ACUTE CORONARY SYNDROMES .1. [J].
FUSTER, V ;
BADIMON, L ;
BADIMON, JJ ;
CHESEBRO, JH .
NEW ENGLAND JOURNAL OF MEDICINE, 1992, 326 (04) :242-250
[7]
GALIS ZS, 1995, ANN NY ACAD SCI, V748, P501
[8]
GALLIS ZS, 1994, J CLIN INVEST, V94, P2493
[9]
SYNOVIAL PROCOLLAGENASE ACTIVATION BY HUMAN MAST-CELL TRYPTASE DEPENDENCE UPON MATRIX METALLOPROTEINASE-3 ACTIVATION [J].
GRUBER, BL ;
MARCHESE, MJ ;
SUZUKI, K ;
SCHWARTZ, LB ;
OKADA, Y ;
NAGASE, H ;
RAMAMURTHY, NS .
JOURNAL OF CLINICAL INVESTIGATION, 1989, 84 (05) :1657-1662
[10]
LOCALIZATION OF STROMELYSIN GENE-EXPRESSION IN ATHEROSCLEROTIC PLAQUES BY INSITU HYBRIDIZATION [J].
HENNEY, AM ;
WAKELEY, PR ;
DAVIES, MJ ;
FOSTER, K ;
HEMBRY, R ;
MURPHY, G ;
HUMPHRIES, S .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1991, 88 (18) :8154-8158