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Background of coronary heart disease (coronary heart disease, CHD) is a serious harm to human health and life of cardiovascular disease, coronary heart disease (coronary heart disease, CHD) is one of the major diseases that threaten human health in developed countries, China in recent years The incidence of the disease showed a rising trend. Coronary artery disease, including unstable angina and acute coronary syndrome (acute coronary syndrome, ACS). Acute coronary syndrome is a type of severe coronary artery disease, including unstable angina (unstableangina pectoris, UAP), ST segment elevation myocardial infarction (ST elevation myocardial infarction, STEMI) and non-ST-segment elevation myocardial infarction (non-ST elevation myocardial infarction, NSTEMI). Main pathogenesis of ACS in coronary atherosclerosis (atherosclerosis, AS) lesions on the basis of vulnerable plaque (vulnerable plaque) cracks, erosion, rupture secondary to platelet in activated partial aggregation, thrombosis, and vasospasm other factors are involved, it is caused by complete or incomplete coronary occlusion. Pathological research found that the majority of ACS did not happen in the severe stenosis of the coronary artery based on, but occurs in patients with mild to moderate coronary artery stenosis, which indicates that the occurrence of ACS with no significant coronary stenosis. Coronary memory AS plaque is caused by the fundamental cause of the ACS, vulnerable plaque rupture, direct cause secondary thrombosis is caused by the ACS, the risk of plaque rupture is mainly depending on the morphology and function of the plaque and does not depend on the severity of the stenosis, the severity of coronary artery disease depends largely on the vulnerability of atherosclerotic plaque, therefore, how the early identification of vulnerable plaque predict risk of ACS size, early intervention prevent vulnerable plaque rupture, has important clinical implications. Atherosclerosis (AS) is a chronic inflammatory disease, a large number of experimental data show that the inflammatory response throughout the whole process of atherosclerosis lesions occur, development and deterioration, and to some extent determines atherosclerotic plaques block stability and natural process. Secretory phospholipase A2 for secretory phospholipase A2 (sPLA2) and artery atherosclerosis and coronary heart disease are closely related, can cause increased vulnerability of coronary atherosclerotic plaque, leading to the occurrence of ACS. Soluble OX40 ligand (soluble OX40 ligand, sOX40L) involved in the whole process of atherosclerosis and development of vulnerable plaque stability, may be involved in the development of the ACS. The aim of the present study was to be through the determination of acute myocardial infarction (acute myocardial infarction, AMI) group, UAP group, stable angina (stable angina pectoris, SAP) group and normal control group, serum secretory phospholipase A2 (sPLA2), and plasma sOX40L level combined with coronary angiography (coronary angiography, CAG) results, the assessment of coronary atherosclerotic plaque vulnerability, and to explore the relationship between serum secretory phospholipase A2 (sPLA2) and the plasma sOX40L level with ACS to find on the coronal artery vulnerable plaque sensitive biological indicators of ACS in patients with atherosclerosis risk evaluation, to guide early intervention to vulnerable plaque. The method selected cases from April 2008 to July 2008 of Cardiology, the First Affiliated Hospital of Zhengzhou University, hospitalized patients, including 67 cases of patients with CHD underwent CAG ① According to the different clinical types of CHD patients were divided into three subgroups: AMI group, 22 patients, 13 males and 9 females, average age (59.5 ± 10.7) years old; UAP group of 24 cases, including 15 males and 9 females, mean age (62.0 ± 8.1) years old; SAP Group 21 cases, including 12 males and 9 females, mean age (58.7 ± 10.4) years; control group for the same period 21 cases CAG result of normal subjects, 13 men and 8 women, mean age (57.2 ± 10.1) years old. Involving the coronary luminal diameter stenosis ≥ 50% (2) in accordance with coronary angiography coronary arteries are divided into three groups of single, double vessel and three-vessel disease group. ③ coronary Gensini score method to evaluate coronary artery stenosis. ④ morphological features of coronary plaque plaque type Ⅰ, type II and type III plaque group. Control group and coronary heart disease in patients with serum sPLA2 levels and plasma sOX40L level was measured using enzyme-linked immunosorbent assay (enzyme linkedimmunosorbent assay, ELISA), and analysis of coronary artery lesions plaque vulnerability, the degree of stenosis, number of diseased vessels, plaque morphology relationship as well as evaluating its recent prognostic value in patients with ACS. Application SPSS10.0 statistical package for statistical analysis, count data to rate Measurement data were expressed as mean ± standard deviation ((?) ± s) said the groups were compared using analysis of variance (ANOVA) rate compared using χ ~~ 2 test, Level Two factors relationship using Spearman rank correlation analysis, multiple factors using logistic regression analysis. P <0.05 was considered statistically significant. 1.AMI group, UAP group, SAP group and control group in age, gender, smoking, family history of diabetes, high blood pressure, cholesterol and other clinical data between the difference was not significant sex (P> 0.05). Serum sPLA2 concentration in AMI group, UAP group, SAP group and control group were (83.28 ± 16.52) u / ml (79.84 ± 18.29) u / ml (52.46 ± 13.56) u / ml and (54.78 ± 11.75) u / ml. The plasma sOX40L in AMI group, UAP group, SAP group and the control group in the concentration (13.29 ± 3.65) ng / ml (12.82 ± 3.90) ng / ml, (6.28 ± 2.34) ng / ml (5.97 ± 2.68) ng / ml; AMI group, UAP group serum of sPLA2, plasma sOX40L, the level is higher than the SAP group and control group, the difference was statistically significant (P <0.01), and SAP group and the control group, serum sPLA2, the plasma sOX40L level difference statistics significance (P> 0.05), while the AMI group, UAP group serum of sPLA2 plasma sOX40L difference was not statistically significant (P> 0.05). 3.AMI group UAP group, SAP group coronary Gensini score (57.80 ± 45.76), (64.13 ± 40.94), (46.26 ± 32.39), there was no significant difference between no statistically significant (P> 0.05). Serum sPLA2 levels in single, double, triple vessel disease group and the control group were (73.27 ± 13.50) u / ml (81.96 ± 16.72) u / ml (75.29 ± 18.53) u / ml ( 54.78 ± 11.75) u / ml. Concentration the plasma sOX40L in single, double, triple vessel disease group and the control group (10.40 ± 2.67) ng / ml, (12.97 ± 2.90) ng / ml, (11.04 ± 3.48) ng / ml (5.97 ± 2.68) ng / ml. Single, double, triple lesions of serum sPLA2 and plasma sOX40L of water on average significantly higher (P <0.05), however, there is no statistically significant difference between single, double, triple lesion group ( P> 0.05). II plaques in the incidence of AMI group, UAP group was significantly higher than the SAP group, Ⅰ type III plaque incidence is lower than the SAP group (P <0.01). 6. Serum sPLA2 concentration in Ⅰ, Ⅱ type, the plaque type III group and the control group (64.95 ± 17.13) u / ml (82.66 ± 18.75) u / ml, (62.78 ± 16.21) u / ml and (54.78 ± 11.75) u / ml. Concentration of plasma sOX40L in Ⅰ, Ⅱ, the plaque type III group and the control group (9.53 ± 3.59) ng / ml (14.26 ± 3.82) ng / ml, (9.87 ± 3.30) ng / ml ( 5.97 ± 2.68) ng / ml. Of serum sPLA2 and plasma sOX40L of Ⅰ, Ⅱ, Ⅲ type plaque group were higher than control (P <0.01), and type II plaque group than type Ⅰ the plaque type III group (P <0.01) . Logistic regression analysis of all selected cases, whether the occurrence of acute coronary syndrome as the dependent variable, age, sex, history of hypertension, history of diabetes, history of smoking, HDL-C, LDL-C, TC, TG, Gensini score, serum sPLA2 plasma sOX40L level covariates, logistic regression analysis, 80.2% of the overall prediction accuracy rate to all independent variables enter the equation. The results can be found: the serum sPLA2 plasma sOX40L of the level is a significant independent risk factor for acute coronary syndrome (P <0.01). Conclusion 1. Serum sPLA2, and plasma sOX40L level in AMI and UAP group was significantly higher than the SAP group and the control group, suggesting that the serum sPLA2, and plasma sOX40L level of the forecast plaque vulnerability markers. Of serum sPLA2 and plasma sOX40L of levels in between single vessel disease, double vessel disease and three-vessel disease group, the difference was not statistically significant, was no correlation between the of of serum sPLA2 and plasma sOX40L level and coronary lesion count. 2.AMI UAP patients with type Ⅱ plaque common the SAP patients Ⅰ, Ⅲ plaque common; of serum sPLA2 with plasma sOX40L of levels in type II plaque group Ⅰ, Ⅲ plaque group was significantly higher than that prompt type II plaque instability, rupture easily.
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