Peripheral blood levels of matrix metalloproteases-2 and -9 are elevated in patients with acute coronary syndromes

被引:611
作者
Kai, HK
Ikeda, H
Yasukawa, H
Kai, M
Seki, Y
Kuwahara, F
Ueno, T
Sugi, K
Imaizumi, T
机构
[1] Kurume Univ, Sch Med, Dept Internal Med 3, Kurume, Fukuoka 8300011, Japan
[2] Kurume Univ, Sch Med, Inst Cardiovasc Res, Kurume, Fukuoka 8300011, Japan
[3] Fukuoka Univ, Fac Pharmaceut Sci, Dept Pharmaceut, Fukuoka 81401, Japan
[4] Sugi Hosp, Div Cardiol, Ohmuta, Japan
关键词
D O I
10.1016/S0735-1097(98)00250-2
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Objectives. This study was sought to investigate whether peripheral blood levels of matrix metalloproteases (MMPs) are affected in patients with acute coronary syndromes (ACS). Background. Synthesis of MMPs has been reported in coronary atherosclerotic lesions in patients with unstable angina (UA), suggesting a pathogenic role of MMPs in the development of ACS. Methods. Using sandwich enzyme immunoassay, serum MMP-2 and plasma MMP-9 were measured in 33 patients with ACS (22 with acute myocardial infarction [AMI], 11 with UA), 17 with stable effort angina (EA) and 17 normal control subjects. Results. Serum MMP-2 in patients with UA and AMI on day 0 was two times greater than that in control subjects, and patients with EA showed higher MMP-2 levels than those in control subjects. Plasma MMP-9 in patients with UA and AMI on day 0 was elevated by threefold and twofold versus that in control subjects, respectively. In patients with UA and AMI who underwent medical treatment (n = 11 and 13, respectively), MMP-2 elevation was sustained until day 7. In patients with UA, MMP-9 elevation on day 0 was followed by a gradual decrease toward the control range up to day 7. Some patients with AMI showed a transient MMP-9 elevation with a peak on day 3, whereas in others, MMP-9 levels were significantly elevated on day 0 and remained higher than those in control subjects up to day 3. Conclusions. Serial changes in serum MMP-2 and plasma MMP-9 were documented in patients with ACS. These findings provide an insight into the molecular mechanism of plaque destabilization. (C) 1998 by the American College of Cardiology.
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页码:368 / 372
页数:5
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