AIM: Matrix metalloproteinases (MMPs) contribute both in the formation as well as in the destabilization of atherosclerotic plaque. In the present study we analyzed circulating levels of MMP-7 that acts on chondroitin sulphate a proteoglycan that is particularly abundant in atherosclerotic plaque and MMP-8 which acts on Type I collagen, the synthesis and degradation of which is important for stability of the plaque and correlate with the degree of severity of coronary artery disease (CAD). METHODS: Circulating levels of MMP-7 and MMP-8 and tissue inhibitors of MMP (TIMP) -1 and TIMP-2 were analysed by Enzyme Linked ImmunoSorbent Assay (ELISA7rpar;, in patients with acute myocardial infarction (AMI) at presentation (N=48), acute coronary syndrome (ACS) group (N=227rpar; (on treatment) and stable angina group (N=17) (on treatment). RESULTS: There was significant rise in MMP-8 (88.23%, P=0.001), in AMI group which decreased in ACS treated group 7lpar;15.9%, non-significant) as compared to controls. There was increasing trend of MMP-7 in AMI and ACS group and strong correlation with hsCRP. MMP-7 predominated in stable angina group. There was significant decrease in TIMP-2 in AMI group and TIMP-1 and TIMP-2 in ACS and stable angina group as compared to controls. CONCLUSION: Significant increase in MMP-8 and decrease in TIMP-2 during acute stage of AMI suggests MMP-8 and TIMP-2 are markers for vulnerable plaque independent of hsCRP for AMI. MMP-7 was found to be elevated in stable angina patients and was correlated with hsCRP at acute phase of AMI suggesting persistent at all stages of CAD.
AIM: Matrix metalloproteinases (MMPs) contribute both in the formation as well as in the destabilization of atherosclerotic plaque. In the present study we analyzed circulating levels of MMP-7 that acts on chondroitin sulphate a proteoglycan that is particularly abundant in atherosclerotic plaque and MMP-8 which acts on Type I collagen, the synthesis and degradation of which is important for stability of the plaque and correlate with the degree of severity of coronary artery disease (CAD). METHODS: Circulating levels of MMP-7 and MMP-8 and tissue inhibitors of MMP (TIMP) -1 and TIMP-2 were analysed by Enzyme Linked ImmunoSorbent Assay (ELISA7rpar;, in patients with acute myocardial infarction (AMI) at presentation (N=48), acute coronary syndrome (ACS) group (N=227rpar; (on treatment) and stable angina group (N=17) (on treatment). RESULTS: There was significant rise in MMP-8 (88.23%, P=0.001), in AMI group which decreased in ACS treated group 7lpar;15.9%, non-significant) as compared to controls. There was increasing trend of MMP-7 in AMI and ACS group and strong correlation with hsCRP. MMP-7 predominated in stable angina group. There was significant decrease in TIMP-2 in AMI group and TIMP-1 and TIMP-2 in ACS and stable angina group as compared to controls. CONCLUSION: Significant increase in MMP-8 and decrease in TIMP-2 during acute stage of AMI suggests MMP-8 and TIMP-2 are markers for vulnerable plaque independent of hsCRP for AMI. MMP-7 was found to be elevated in stable angina patients and was correlated with hsCRP at acute phase of AMI suggesting persistent at all stages of CAD.