| BackgroundCoronary heart disease(CHD) is a serious cardiovascular disease which threatens to human health and life. In developed countries, CHD is already one of the most important disease which affects people s morbidity and mortality. The incidence of the disease is increasingly rising in our country in recent years. CHD include stable angina pectoris (SAP) and Acute coronary syndrome (ACS). ACS is one of the severe clinical type of CHD, include unstable angina pectoris (UAP), ST-segment elevation myocardial infarction (STEMI) and non-ST-segment elevation myocardial infarction (NSTEMI). Rupture or erosion of vulnerable plaque resulting in platelet accumulation and thrombus formation that causes partial or complete obstrution in the coronary arteries is the basic pathology of ACS Rupture of vulnerable plaque and subsequent thrombus formation in coronary arteries with slight or medium size stenosis rather than in significant stenosis was shown to be the most common cause of ACS by pathological studies. Atherosclerotic plaques within the coronary arteries is the fundamental cause of ACS. The rupture of vulnerable plaque and thrombus formation is the primary cause of ACS. The risk of atherosclerotic plaque rupture depends on plaque morphology and function and not on the severity of the vascular stenosis. Coronary artery lesions depend largely on the ability of the vulnerability of atherosclerotic plaques. Therefore, identification of vulnerable plaque early and forecast the risk of ACS to provide early intervention and thus prevent the rupture of vulnerable plaque is significantly important.Atherosclerosis(AS) is a chronic inflammatory disease. At all stages in the evolution of atherosclerotic plaque, from the early development of endothelial dysfunction, to the formation of the mature atheroma and its subsequent rupture. Inflammatory events have been known to be involved. The evidence that the secretory type II phospholipase A2(sPLA2) is relative to AS and CHD, which can make plague vulnerable and lead to ACS has been demonstrated by recent studies. Many studies showed that soluble OX40 ligand(sOX40L) has emerged as a potential participant in the promotion and/or propagation of atherosclerosisis, which is related with the rupture of vulnerable plaque and may play an important role in the occurrence and development of ACS.ObjectiveThe aim of this study was to measure the serum levels of secretory type II phospholipase A2(sPLA2) and the plasma levels sOX40L. At the same time, coronary angiography (CAG) were performed in patients with acute myocardial infarction (AMI), UAP, stable angina pectoris(SAP) and normal subjects without CHD to evaluate the clinical value of serum levels of secretory type II phospholipase A2(sPLA2) and the plasma levels sOX40L in patients with ACS. The aim is to search the biomarkers that can corelate the vulnerable plaque characteristic with high sensitivity and specificity. With the help of these markers, the possible risk of patients with CHD for future ACS events can be evaluated and we can interfere with vulnerable plaque earlier.MethodsAll patients were included from the Inpatient-Department of Cardiovascular, the First Affiliated Hospital of Zhengzhou University from April 2008 to July 2008.①67 patients with CHD diagnosed by CAG were divided into three sub-groups according to clinical type(22 patients in AMI group, 13 men and 9 women, mean age (59.5±10.7) years; 24 patients in UAP group, 15men and 9 women, mean age(62.0±8.1)years; 21 patients in SAP group, 12 men and 9 women, mean age(58.7±10.4)years). 21 normal patients without CHD diagnosed by CAG were taken as the control group(13 men and 8 women, mean age(57.2±10.1)years).②The CHD group was divided into the single, double and three vessel lesions group by the numbers of vessels with stenosis of≥50% diameter.③Gensini scoring system was used to assess the severity of coronary artery stenosis.④According to the morphology of coronary atherosclerotic plaque the lesions were divided into type I, type II and type III plaque group. To measure the plasma levels of sOX40L in patients with CHD and control group Enzyme linked immuoserbent assay (ELISA) was performed. The relationship of the serum levels of sPLA2 and plasma levels of sOX40L to stability of coronary artery, the severity of stenosis, stenosis number and the morphology of atherosclerotic plaque were assessed. For prediction of short-term prognosis in patients with ACS the value of plasma sOX40L was evaluated.Software of SPSS 10.0 was used to carry out all statistic work. The enumeration data were indicated by rate. Chi square test was performed for the rate of analysis between groups. The measurement data were shown by (mean±SD). Analysis of variance of univariate was performed for statistic analysis among four groups. Spearman rank correlation was used to find relationship between variables. T-test was used for correlation coefficient test. Logistic regression analysis was applied for Multi-factor analysis. Statistically significant vaule was taken as .P<0.05.Results1. There was no significant difference in sex, age, smoking history, family history, diabetes, hypertension and blood lipid between AMI, UAP, SAP and the control group(P>0.05).2. The mean level of serum sPLA2 in AMI, UAP, SAP and the control group was (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 respectively; The mean level of plasma sOX40L in AMI, UAP, SAP and the control group was (13.29±3.65)ng/ml, (12.82±3.90)ng/ml, (6.28±2.34) ng/ml and (5.97±2.68)ng/ml respectively; The plasma levels of sOX40L and the serum levels of sPLA2 were found to be higher in AMI and UAP group than that in control and SAP group with significant difference (P<0.01). There was no significant difference (P>0.05) in the mean level of plasma sOX40L and serum level of sPLA2 in SAP and the control group. The mean level of serum sPLA2 and plasma sOX40L in AMI and UAP group was not significant (P>0.05).3. In AMI, UAP and the SAP group, the Gensini score of coronary artery was (57.80±45.76), (64.13±40.94) and (46.26±32.39) respectively, and there was no significant differences among them(P>0.05).4. In single, double and triple-vessel lesions and control group the mean level of serum sPLA2 was (73.27±13.50)u/ml, (81.96±16.72)u/ml, (75.29±18.53)u/ml and (54.78±11.75)u/ml respectively. In single, double and triple-vessel lesions and control group the mean level of plasma sOX40L was (10.40±2.67)ng/ml, (12.97±2.90)ng/ml, (11.04±3.48)ng/ml, (5.97±2.68)ng/ml respectively. The mean level of serum sPLA2 and plasma sOX40L in single, double and three vessel lesions group were found to be higher than that in control group (P<0.05), but the mean level of serum sPLA2 and plasma sOX40L among single, double and three vessel lesions group were not significantly different (P>0.05).5. The incidence of type II plaque was more, and type I and typeIII plaque was less in AMI and UAP group. There was significant difference in comparison with SAP group (P<0.01).6. In type I , type II and type III plaque and control group the level of serum sPLA2 was (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 respectively. In type I, type II and type III plaque and control group the level of plasma sOX40L was (9.53±3.59)ng/ml, (14.26±3.82)ng/ml, (9.87±3.30)ng/ml, (5.97±2.68)ng/ml respectively. The level of serum sPLA2 and plasma sOX40L in type I , type II and type III plaque group were found to be higher than that in control group (P<0.01). The mean level of serum sPLA2 and plasma sOX40L in type II plaque group was higher than that in type I and type III plaque group (P<0.01).7. In patients with CHD diagnosed by CAG, whether there will be ACS as a result of variables, sex, age, smoking history, history of hypertension, diabetes, total cholesterol, triglyceride, high density lipoprotein, low density lipoprotein, sPLA2, sOX40L, Gensini score as Covariates. The Logistic regression analysis was applied with all input variables equationThe overall prediction accuracy rate was 80.2%. The results show that: the level of serum sPLA2 and plasma sOX40L is an independent significant risk factor for the impact of ACS(P<0.01).Conclusion1. The suggestion that the level of serum sPLA2 and plasma sOX40L may represent as the biomarkers of vulnerable plaque is shown by the fact that AMI group and UAP group had higher level of serum sPLA2 and plasma sOX40L.But no significant different level of serum sPLA2 and plasma sOX40L was seen among single, double and three vessel lesion group. No correlation was found between the level of serum sPLA2 and plasma sOX40L in different branch vessel lesions in the CHD.2. In patients with AMI and UAP type II plaque is more common, but type I and type III plaque are more in patients with SAP. In type II plaque group the level of serum sPLA2 and plasma sOX40L are higher in compansion to that of type I and type III plaque group which indicate that type II plaque is more likely to rupture. |
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