PMID- 15056834
OWN - NLM
STAT- MEDLINE
DCOM- 20041021
LR  - 20190819
IS  - 1346-9843 (Print)
IS  - 1346-9843 (Linking)
VI  - 68
IP  - 4
DP  - 2004 Apr
TI  - Increased circulating matrix metalloproteinase-2 in patients with hypertrophic 
      cardiomyopathy with systolic dysfunction.
PG  - 355-60
AB  - BACKGROUND: Some patients with hypertrophic cardiomyopathy (HCM) develop left 
      ventricular (LV) wall thinning associated with LV dilatation and systolic 
      dysfunction. Recently, matrix metalloproteinases (MMPs) and tissue inhibitors of 
      MMPs (TIMPs) were reported to be involved in ventricular remodeling, however, 
      little is known about MMPs and TIMPs in patients with HCM. METHODS AND RESULTS: 
      Enzyme-linked immunoassays were used to measure the plasma concentrations of 
      MMP-2, MMP-3, MMP-9, TIMP-1, and TIMP-2 in 11 patients with HCM accompanied by 
      systolic dysfunction (fractional shortening (FS) <25%, group A), 17 patients with 
      HCM who had preserved systolic function (FS> or =25%, group B), and 50 
      age-matched clinically healthy control subjects (mean age: 57 years). The 
      concentration of MMP-2 in group A was significantly higher than in group B and 
      the control subjects (1,124 +/- 84, 792 +/- 49, 809 +/- 26 ng/ml, respectively), 
      whereas there was no significant difference between group B and the control 
      subjects. MMP-2 concentrations significantly increased as the New York Heart 
      Association functional class increased in patients with HCM. TIMP-2 was also 
      significantly higher in group A patients than in group B and the control subjects 
      (45.3 +/- 4.7, 34.6 +/- 2.2, 33.7 +/- 1.8 ng/ml, respectively), but there was no 
      difference between group B and control subjects. TIMP-1 was significantly higher 
      in HCM patients than in control subjects. MMP-3 and MMP-9 concentrations did not 
      differ among the 3 groups. Both MMP-2 and TIMP-2 correlated significantly with FS 
      and LV dimension, negatively and positively, respectively. CONCLUSIONS: These 
      results suggest that changes in the release and activity of MMP-2 and TIMP-2 may 
      be associated with the mechanisms responsible for cardiac remodeling in patients 
      with HCM.
FAU - Noji, Yoshihiro
AU  - Noji Y
AD  - Molecular Genetics of Cardiovascular Disorders, Division of Cardiovascular 
      Medicine, Graduate School of Medical Science, Kanazawa University, Japan.
FAU - Shimizu, Masami
AU  - Shimizu M
FAU - Ino, Hidekazu
AU  - Ino H
FAU - Higashikata, Toshinori
AU  - Higashikata T
FAU - Yamaguchi, Masato
AU  - Yamaguchi M
FAU - Nohara, Atsushi
AU  - Nohara A
FAU - Horita, Takahiro
AU  - Horita T
FAU - Shimizu, Kuniyoshi
AU  - Shimizu K
FAU - Ito, Yuji
AU  - Ito Y
FAU - Matsuda, Takeshi
AU  - Matsuda T
FAU - Namura, Masanobu
AU  - Namura M
FAU - Mabuchi, Hiroshi
AU  - Mabuchi H
LA  - eng
PT  - Journal Article
PL  - Japan
TA  - Circ J
JT  - Circulation journal : official journal of the Japanese Circulation Society
JID - 101137683
RN  - 0 (Tissue Inhibitor of Metalloproteinase-1)
RN  - 127497-59-0 (Tissue Inhibitor of Metalloproteinase-2)
RN  - EC 3.4.24.24 (Matrix Metalloproteinase 2)
SB  - IM
MH  - Cardiomyopathy, Hypertrophic/*blood/complications/physiopathology
MH  - Disease Progression
MH  - Electrocardiography
MH  - Enzyme-Linked Immunosorbent Assay
MH  - Female
MH  - Heart Failure/etiology
MH  - Humans
MH  - Male
MH  - Matrix Metalloproteinase 2/*blood/physiology
MH  - Middle Aged
MH  - Sensitivity and Specificity
MH  - Systole
MH  - Tissue Inhibitor of Metalloproteinase-1/blood
MH  - Tissue Inhibitor of Metalloproteinase-2/*blood/physiology
MH  - Ventricular Remodeling/*physiology
EDAT- 2004/04/02 05:00
MHDA- 2004/10/22 09:00
CRDT- 2004/04/02 05:00
PHST- 2004/04/02 05:00 [pubmed]
PHST- 2004/10/22 09:00 [medline]
PHST- 2004/04/02 05:00 [entrez]
AID - 10.1253/circj.68.355 [doi]
PST - ppublish
SO  - Circ J. 2004 Apr;68(4):355-60. doi: 10.1253/circj.68.355.