Korean J Intern Med.
2013 Mar;28(2):165-173. 10.3904/kjim.2013.28.2.165.
Interleukin-33, matrix metalloproteinase-9, and tissue inhibitor of matrix metalloproteinase-1 in myocardial infarction
- Affiliations
-
- 1Department of Biochemistry, Namik Kemal University Faculty of Medicine, Tekirdag, Turkey. savasguzel@yahoo.com
- 2Department of Biochemistry, Taksim Education and Research Hospital, Istanbul, Turkey.
- 3Department of Family Physcian, Namik Kemal University Faculty of Medicine, Tekirdag, Turkey.
- 4Department of Internal Medicine, Taksim Training and Research Hospital, Istanbul, Turkey.
- 5Department of Biochemistry, Diyarbakir State Hospital, Diyarbakir, Turkey.
- 6Department of Biochemistry, Istanbul Education and Research Hospital, Istanbul, Turkey.
- KMID: 1501771
- DOI: http://doi.org/10.3904/kjim.2013.28.2.165
Abstract
- BACKGROUND/AIMS
Acute coronary syndrome (ACS) is characterized by increased inflammatory processes and endothelial activation. We investigated the association between ACS and inflammatory mediators and matrix-degrading enzymes.
METHODS
We prospectively enrolled 55 consecutive patients with ACS: 25 with unstable angina (UA) and 30 with non-ST elevated myocardial infarction (NSTEMI). For comparison, 25 age- and sex-matched subjects with no significant coronary artery stenosis were included as the control group. Peripheral serum levels of interleukin (IL)-33, matrix metalloproteinase (MMP)-9, tissue inhibitor of MMP-1, and C-reactive protein (CRP) were measured on admission, and at 12, 24, 48, and 72 hours after the initial evaluation.
RESULTS
Compared to serum levels in the control group, serum levels of IL-33 decreased in the NSTEMI group (p < 0.05), and levels of MMP-9 and tissue inhibitor of matrix metalloproteinase (TIMP)-1 increased in the UA group (p < 0.01, p < 0.05, respectively) and NSTEMI group (p < 0.05, p < 0.05, respectively). IL-33 levels were significantly lower on admission than at 12 hours after the initial evaluation (p < 0.05). IL-33 levels were negatively correlated with MMP-9 levels (r = -0.461, p < 0.05) and CRP levels (r = -0.441, p < 0.05).
CONCLUSIONS
Elevated levels of MMP-9, TIMP-1, and decreased levels of IL-33 play a role in the development and progression of ACS.
MeSH Terms
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Adult
Angina, Unstable/blood/*enzymology/*immunology
Biological Markers/blood
C-Reactive Protein/metabolism
Case-Control Studies
Disease Progression
Female
Humans
Inflammation Mediators/*blood
Interleukins/*blood
Male
Matrix Metalloproteinase 9/*blood
Middle Aged
Myocardial Infarction/blood/*enzymology/*immunology
Time Factors
Tissue Inhibitor of Metalloproteinase-1/*blood
Biological Markers
Inflammation Mediators
Interleukins
Tissue Inhibitor of Metalloproteinase-1
C-Reactive Protein
Matrix Metalloproteinase 9
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