Clinical Chemistry
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Clinical Chemistry 52: 1522-1527, 2006. First published June 8, 2006; 10.1373/clinchem.2006.067439
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(Clinical Chemistry. 2006;52:1522-1527.)
© 2006 American Association for Clinical Chemistry, Inc.

Lipids, Lipoproteins, and Cardiovascular Risk Factors

Increased Plasma Concentration of Matrix Metalloproteinase-7 in Patients with Coronary Artery Disease

Lennart Nilsson1,2, Lena Jonasson1, Johnny Nijm2, Anders Hamsten3 and Per Eriksson3,a

1 Department of Cardiology, Heart Center, University Hospital, Linköping, Sweden.
2 Research Center of Cardiovascular Diseases, Department of Medicine, Högland Hospital, Eksjö, Sweden.
3 Atherosclerosis Research Unit, King Gustaf V Research Institute, Department of Medicine, Karolinska Institute, Karolinska University Hospital, Stockholm, Sweden.

aAddress correspondence to this author at: King Gustaf V Research Institute, Karolinska Hospital M1, SE-171 76 Stockholm, Sweden. Fax 46-8-311298; e-mail Per.Eriksson{at}ki.se.

Background: Plaque rupture is often associated with breakdown of the extracellular matrix in the shoulder region of a plaque. We tested whether plasma concentrations of various matrix metalloproteinases (MMPs) and tissue inhibitor of metalloproteinase-1 (TIMP-1) could serve as markers for plaque instability as well as relationships between plasma MMPs and inflammatory markers.

Methods: The study group included 65 men with angiographically verified CAD (45 with stable and 20 with unstable CAD) and 28 healthy controls. Circulating MMP, TIMP-1, C-reactive protein, and cytokine concentrations were measured by ELISA. Leukocyte subtype counts in whole blood were determined, and T-cell subsets and natural killer cells were measured by flow cytometry. Differences in continuous variables between groups were tested by ANOVA with the Scheffé F-test used as a post hoc test, and correlations were analyzed by a linear regression method.

Results: The plasma concentration of MMP-7 was increased in patients with stable and unstable CAD, whereas MMP-2 and -3 concentrations were decreased. The plasma concentration of TIMP-1 was significantly increased in patients with unstable CAD. MMP-2, -3, and -7 showed no correlations with established markers of inflammation. However, MMP-2 correlated positively with the number of natural killer cells in patients with stable and unstable CAD.

Conclusion: Plasma concentrations of MMPs and TIMPs may be markers of CAD but appear to be differentially regulated.






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