| Objective: Acute coronary syndrome (ACS), including unstable angina pectoris, acute myocardial infarction, and heart sudden death, is usually caused not by enlarged atherosclerotic coronary plaque which limited coronary artery blood flow, but by plaque rupture of mild-to-moderate luminal stenosis and subsequent thrombosis which lead to serious luminal decrease or complete obstruction followed by myocardial ischemia or myocardial infarction. It is found that this kind of atherosclerotic plaque is characterized by abundant lipid core, thinner fibrous cap and activate inflammation. It has become a focus to prevent and cure coronary artery disease. But how can we identify vulnerable plaques and take measures to prevent it from rupture. Nowadays, the efficient methods include intravascular ultrasound (IVUS), coronary angioscopy and thermometry. But it is limited for clinical use of all these invasive approaches. Because they are invasive and expensive. So people are looking for simple and feasible methods to identify vulnerable plaques. These methods are magnetic resonance imaging (MRI), EBCT and detection of its biochemical markers. The markers are elastinase, matrix metalloproteinases (MMPs), interlukin-8 (IL-8), C-reactive protein (CRP), MDA-modified LDL, CD40 ligand, et al. MMPs are a family of Zn2+ dependent endopeptidases capable of cleaving components of extracellular matrix. In the atheroma progression, on one hand, the smooth muscle cells, macrophages and some other kinds of cells generate extracellular matrix, on the other hand, inflammation mediated by lipids lead to degeneration of the extracellular matrix. Lipid accumulation in atheromatic plaque accelerates local inflammation, activate the smooth muscle cells and macrophages to secrete MMPs. The activated MMPs can degenerate the ECM of atherosclerotic plaque's fibrious cap, and made it thinner, vulnerable, and easily to break. It is reported that there are a lot of macrophages in atherosclerotic plaques, especially in its shoulder region, where can detect many kinds of MMPs. But there are few reports about the diagnosis of vulnerable plaques by peripheral serum level of MMPs. The purpose of this study is to investigate the relationship between the serum level of MMP-9, LDL-c and coronary atherosclerotic plaque invulnerability. To evaluate whether joint detection of serum level of MMP-9, LDL-c can be an easily going method to plaque vulnerability.Method: seventy inpatients with coronary heart disease who were admitted from August, 2003 to January, 2004 were studied. Among them there were 20 patients with angina pectoris (SAP) and 50 patients with acute coronary syndromes (ACS) that include 30 patients with acute myocardial infarction (AMI) and 20 patients with unstable angina pectoris (UAP). At the same time, 30 cases of age matched individuals with angiographic negative findings were selected as a control group. Blood samples were drawn from the peripheral vein in every patient on the second day after admission. After centrifugation, the serum samples were divided into 2 portion, one is sent to lab department to detect LDL-c, another were frozen and stored -20℃ until they were assayed. The serum level of MMP-9 was measured by quantity Sandwich enzyme immunoassay analysis technique. The serum level of LDL-c is measured by direct detect technique. Results were expressed by mean value ± SD and analyzed by statistics. A p value < 0.05 is considered statistically significant.Result: The serum level of MMP-9 was remarkably increased in patients with ACS. The difference was remarkable compared with SAP and normal control group. There is significant difference between SAP group and normal control group. The serum level of MMP-9 in AMI group was higher than that of UAP group. But there was not significant difference in the serum level of MMP-9 between AMI group and UAP group. The serum level of LDL-c was remarkably increased in patients with ACS or UAP. The difference was remarkable compared with normal control group. But there was not <...
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