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The Serum Level And Clinical Significance Of MMP-2 And Cystatin C In Patients With Acute Coronary Syndrome

Posted on:2011-06-26Degree:MasterType:Thesis
Country:ChinaCandidate:J WangFull Text:PDF
GTID:2144360305975698Subject:Internal Medicine
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Background:Acute coronary syndrome (ACS) is a serious threat to human health and life. The incidence of ACS in China showed an increasing trend with high mortality. The pathology of ACS showed different degrees of coronary artery atherosclerosis and thrombosis causing luminal stenosis or occlusion, which led to myocardial ischemia, injury or necrosis. The main clinical manifestations of ACS include unstable angina pectoris, acute non-ST segment elevation myocardial infarction, acute ST segment elevation myocardial infarction and sudden cardiac death. The patho-physiology of ACS involves coronary artery endothelial dysfunction, inflammation, plaque rupture and thrombosis. Inflammation can lead to endothelial dysfunction, and run through all the course of formation and rupture of atherosclerotic plaque, and even thrombosis in the plaque area. Exploring the expression of inflammatory mediators may be helpful in early prediction and stratification of ACS risk.A large number of studies have shown that inflammation involved in the development and progress of atherosclerosis, including the degradation of extracellular matrix and remodeling of vascular wall. Serum matrix metalloproteinase-2 (MMP-2) and cysteine proteinase inhibitor C play an important role in the development of ACS. Monocytes can secrete MMP-2, and the activity of the latter is significantly increased in patients with ACS, particularly in the area of atherosclerotic plaque. Inflammatory mediators stimulate vascular smooth muscle cells to secrete cathepsin S and K, and so on. These cathepsins can promote the dissociation of elastic tissue, and are highly expressed in the injured area of artery. On the other hand, the cysteine protease inhibiltor C (Cystatin C) is less expressed in atherosclerotic plaque area than in normal area within the artery wall, indicating an negative correlation between Cystatin C and the progress of artherosclerosis. Therefore, the lack of Cystatin C and the over expression of MMP-2 may have involved the occurrence and development of ACS.Objective:To evaluate the changes of MMP-2 and Cystatin C, and their clinical significances in patients with ACS.Methods:This study consists of 40 patients with unstable angina,40 patients with acute myocardial infarction, and 30 patients without coronary artery disease as control. The serum level of Cystatin C were measured by rate scattering turbidimetry method, (blood samples were collected within 24 hours after the onset of chest pain in patients with acute myocardial infarction). Blood samples for MMP-2 were first collected and stored in refrigerator (-20℃) and measured together later via enzyme linked immunosorbent assay method. The serum level of hs-CRP were measured by monoclonal antibody enzyme immunoassay.Results:The serum MMP-2 level is significantly higher in ACS patients than in control patients without coronary heart disease (246±58.46 vs 96.09±21.96, p<0.05), and higher in patients with acute myocardial infarction than in patients with unstable angina pectoris (294.41±35.62 vs 197.79±29.43, p<0.05). On the other hand, the level of Cystatin C in patients with ACS is significantly lower than that in control group (0.70±0.11 vs 0.88±0.079, p<0.05), so does that in patients with acute myocardial infarction as compared with that in patients with unstable angina(0.63±0.088 vs 0.76±0.067, p<0.05). The serum hs-CRP level is significantly higher in ACS patients than in control patients without coronary heart disease (11.67±1.92 vs 1.23±0.72, p<0.05), and higher in patients with acute myocardial infarction than in patients with unstable angina pectoris (16.13±1.25 vs 7.21±1.14, p<0.05). Within each group, the serum level of MMP-2 was positively correlated with high sensitive C-reactive protein (hs-CRP), and the Cystatin C was negatively correlated with hs-CRP by linear correlation analysis.Conclusion:1.Both MMP-2 and Cystatin C were involved in the occurrence and development of ACS. 2.The serum level of MMP-2 was positively correlated with and the Cystatin C was negatively correlated with the progress of instability of atherosclerotic plaque.3.Serum levels of MMP-2 and Cystatin C may become the early prediction criteria and risk factors for stratification of ACS.
Keywords/Search Tags:acute coronary syndrome, matrix metalloproteinases-2, Cystatin C, acute myocardial infarction, unstable angina
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