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Journal of Molecular Biomarkers & Diagnosis
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Research Article

The Effect of Smoking on Diagnostic Value of Serum Matrix Metalloproteinase-8 in Acute Coronary Syndrome

Laura Lahdentausta1*, Timo Sorsa1,2, Pirkko J Pussinen1,2 and Erkki Pesonen3,4

1Institute of Dentistry, University of Helsinki, Finland

2Department of Oral and Maxillofacial Diseases, Helsinki University Central Hospital, Helsinki, Finland

3Skåne University, Sweden

4Department of Paediatrics, Division of Paediatric Cardiology, Skåne University Hospital, Lund

*Corresponding Author:
Laura Lahdentausta
Institute of Dentistry
University of Helsinki, Finland
E-mail: [email protected]

Received date: February 14, 2013; Accepted date: March 20, 2013; Published date: March 23, 2013

Citation: Lahdentausta L, Sorsa T, Pussinen PJ, Pesonen E (2013) The Effect of Smoking on Diagnostic Value of Serum Matrix Metalloproteinase-8 in Acute Coronary Syndrome. J Mol Biomark Diagn S4:002. doi:10.4172/2155-9929.S4-002

Copyright: © 2013 Lahdentausta L, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited


Background: Smoking has been perceived to increase the levels of carcinogenic and inflammatory mediators thereby promoting presumably malignant and proinflammatory tissue destruction via activating proteolytic enzymes such as matrix metalloproteinases (MMPs) and their regulators. We studied the effect of smoking on the diagnostic ability of serum MMP-8-IFMA and TIMP-1-ELISA analysis to recognize patients with acute coronary syndrome (ACS).

Methods: The case-control population (n=605) comprised 291 patients with diagnosed acute myocardial infarction (AMI) or unstable angina pectoris (UAP) and 314 healthy control individuals. The case and the control group included 55 and 66 smoking subjects, respectively.

Results: Smoking increased the MMP-8, but not the TIMP-1, concentration in both the control and the AMI group. MMP-8 concentration, and consequently MMP-8/TIMP-1, distinguished the cases from the controls accurately in the ROC analysis, but smoking decreased the AUCs in every category. The MMP-8 concentration produced an AUC (95% CI, p-value) for ACS of 0.771 (0.723-0.818, p<0.001) and 0.684 (0.581-0.787, p=0.001) for non-smokers and smokers, respectively. Similarly, the multivariate logistic regression model indicated that smoking decreased the association of MMP-8 with ACS. The OR (95% CI, p-value) of MMP-8 for ACS was 8.1 (per ng/ml log-transformed unit increase, 5.0-13.1, p<0.001) and 2.8 (1.1-7.0, p=0.025) for non-smokers and smokers, respectively.

Conclusions: One of the most important risk factors for ACS, smoking, decreases the diagnostic ability of MMP- 8 concentration and MMP-8/TIMP-1 ratio. This must be taken account if these serum determinations are used as biomarkers of the risk for cardiovascular diseases.


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