Clinical laboratory · 2014
The measurement of circulating matrix metalloproteinase-8 and its tissue inhibitor and their association with inflammatory mediators in patients with acute coronary syndrome.
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Allal-Elasmi Monia, Zayani Yosra, Zidi Wiem, Zaroui Amira, Feki Moncef, Mourali Sami, Mechmeche Rachid, Kaabachi Naziha
Аннотация
BACKGROUND: The aim of the present study was to investigate differences of matrix metalloproteinase-8 and tissue inhibitor of metalloproteinase-1 in the peripheral blood of patients admitted with acute coronary syndrome (ACS) and its correlation with the widely accepted markers of inflammatory activity, C-reactive protein, fibrinogen, and white blood cell number.
METHODS: 315 patients with ACS (165 unstable angina pectoris/non-ST-elevation myocardial infarction, 150 ST elevation myocardial infarction), 111 stable angina (SA) patients, and 296 control subjects were enrolled in the study. All biochemical analyses were carried out using a Hitachi 912 analyzer (Roche). Matrix metalloproteinase-8 (MMP-8) and tissue inhibitor of metalloproteinase-1 (TIMP-1) levels were determined in citrate plasma by ELISA methods. White blood cells (WBC) and fibrinogen were also determined.
RESULTS: The plasma concentrations of matrix metalloproteinase-8, tissue inhibitor of metalloproteinase-1, C-reactive protein, fibrinogen, and WBCs in patients with acute coronary syndrome were significantly higher than those in the control group (p < 0.001). Strong positive associations were observed between MMP-8 and TIMP-1 (r = 0.328, p < 0.001), MMP-8 and CRP (r = 0.171, p < 0.001), MMP-8 and Fibrinogen (r = 0.267, p < 0.001), MMP-8 and WBC (r = 0.163, p < 0.01), TIMP-1 and CRP (r = 0.219, p < 0.01), TIMP-1 and fibrinogen (r = 0.226, p < 0.01), TIMP-1 and WBC (r = 0.094, p < 0.1). Other positive correlations were observed between CRP and fibrinogen, CRP and WBC and fibrinogen and WBC in the patients with ACS.
CONCLUSIONS: Observations suggest that ACS show an increase in both remodeling and inflammation markers. In addition, the strong relationship with MMP-8 and inflammatory mediators such as CRP, fibrinogen and WBC in ACS patients suggests that MMP-8 might be an additional marker and/or consequence of inflammatory components in ACS.
METHODS: 315 patients with ACS (165 unstable angina pectoris/non-ST-elevation myocardial infarction, 150 ST elevation myocardial infarction), 111 stable angina (SA) patients, and 296 control subjects were enrolled in the study. All biochemical analyses were carried out using a Hitachi 912 analyzer (Roche). Matrix metalloproteinase-8 (MMP-8) and tissue inhibitor of metalloproteinase-1 (TIMP-1) levels were determined in citrate plasma by ELISA methods. White blood cells (WBC) and fibrinogen were also determined.
RESULTS: The plasma concentrations of matrix metalloproteinase-8, tissue inhibitor of metalloproteinase-1, C-reactive protein, fibrinogen, and WBCs in patients with acute coronary syndrome were significantly higher than those in the control group (p < 0.001). Strong positive associations were observed between MMP-8 and TIMP-1 (r = 0.328, p < 0.001), MMP-8 and CRP (r = 0.171, p < 0.001), MMP-8 and Fibrinogen (r = 0.267, p < 0.001), MMP-8 and WBC (r = 0.163, p < 0.01), TIMP-1 and CRP (r = 0.219, p < 0.01), TIMP-1 and fibrinogen (r = 0.226, p < 0.01), TIMP-1 and WBC (r = 0.094, p < 0.1). Other positive correlations were observed between CRP and fibrinogen, CRP and WBC and fibrinogen and WBC in the patients with ACS.
CONCLUSIONS: Observations suggest that ACS show an increase in both remodeling and inflammation markers. In addition, the strong relationship with MMP-8 and inflammatory mediators such as CRP, fibrinogen and WBC in ACS patients suggests that MMP-8 might be an additional marker and/or consequence of inflammatory components in ACS.