| BackgroundCoronary heart disease(CHD) has been the leading cause of death of all diseases threatening people's heath all over the world. Acute coronary syndrome(ACS), including unstable angina pectors(UAP), non-ST segment elevation myocardial infarction(NSTEMI), ST segment elevation myocardial infarction(NSTEMI) and sudden death(SD), is the most severe clinical manifestation of CHD. Atherosclersis (AS) is the common pathology basement CHD.Studies indicated that AS is a chronic inflammation disease. Along with investigative graduallary penetrate deeply, some Chemokines and cytokines were detected unceasingly. For the past few years, the view that AS is inflammation was drawn again, which think AS consistent with the generally rule of inflammation appearance. Moreover the view is more and more accepted by broader scholar.Recent studies found that most patients with ACS are not caused by critical stenosis of coronary artery, but by rupture of the vulnerable plaque and subsequent thrombus formation in the coronary arteries in which there are only slight or medium stenosis. The occurrence of ACS is not associated with the severity of coronary artery stenosis. Process plaque from stable form to unstable form can induce severity clinical events occurrence, inflammation have critical effect in this course, the rupture or erosion of plaques coexist almost inflammation, inflammation in vulnerable paque is always up-regulation. Immune cells have a dominant position in early atherosclerotic lesions, their effector molecules accelerate the injury and inflammation-activated trigger ACS. Rupture of vulnerable plaque and subsequent thrombus formation in the coronary artery are considered to be responsible for the pathogenesis of ACS.Latest studies indicated that OX40 ligand(OX40L) can cripple the stability of plaque, trigger plaque rupture and participate in the occurrence of sudden cardiac events; MIF can inhibit macrophage migration and promote macrophage infiltration, hyperplasia at inflammation local, which plays an important role in multiple stages of the occurrence and development atherosclerosis. It has a close relationship with the occurrence and development of ACS.ObjectiveThis study measured the plasma concerntrations of soluble OX40 ligand (sOX40L) and macrophage migration inhibitory factor(MIF), at the same time, coronary angiography(CAG) were conducted in patients with CHD and normal control subjects without CHD to investigate the correlation between sOX40L, MIF levels and coronary lesions in patients with coronary heart disease.MethodsAll subjects came from the Inpatient-Department of Cardiology, the first affiliated hospital of Zhengzhou University from June 2008 to October 2008. 68 patients with CHD were divided into three sub-groups according to the clinic type: AMI group(14 people), UAP group(37 people), SAP group(17 people), 20 healthy subjects without CHD takes as normal control group. The CHD group was divided into the single, double and three vessel lesions group by the numbers of vessels with stenosis of≥50% diameter. The severity scale of coronary artery stenosis was quantitatively assessed according to CAG by Gensini scoring system. Enzyme Linked Immuoserbent Assay(ELISA) was used to measure the plasma levels of sOX40L and MIF. All statistical work was carried out with software of SPSS 10.0.Results1. The mean level of sOX40L in the control group, SAP group, UAP group, AMI group was 7.60±0.79 ng/ml, 8.23±1.09 ng/ml, 11.66±2.02 ng/ml, 12.92±1.72 ng/ml respectively, the mean level of MIF in the control group, SAP group, UAP group, AMI group were 96.20±18.85 pg/ml, 107.35±23.65 pg/ml, 142.97±19.51 pg/ml, 155.36±28.21 pg/ml respectively. The plasma levels of sOX40L and MIF were higher in AMI and UAP group than that in SAP and control group with significant difference (P<0.05). The plasma levels of sOX40L and MIF in SAP and the control was no significance (P > 0.05).2. In control group, single, double and triple-vessel lesion group, the mean level of plasma sOX40L was 7.60±0.79 ng/ml, 10.29±2.58 ng/ml, 11.31±1.88 ng/ml and 11.92±3.20 ng/ml, respectively, the mean level of MIF was 96.20±18.85 pg/ml,128.58±32.67 pg/ml, 138.25±15.10 pg/ml and 146.06±33.16 pg/ml, respectively. The plasma sOX40L and MIF in single, double and three vessel lesion group were higher than that in control group(P<0.05), but the plasma levels of sOX40L and MIF among single, double and three vessel lesion group were not significant difference (P > 0.05).3. The Gensini score of coronary artery in AMI, UAP and SAP group were 48.25±5.48, 61.51±5.10 and 60.36±6.85 respectively, there were no significant differences among them (P > 0.05).4. Correlation analysis4.1 A significant positive correlation was found between the plasma levels of sOX40L and MIF in AMI, UAP group(r=0. 624, P<0.05; r=0. 637, P<0.05), no correlation between the plasma levels of sOX40L and MIF in SAP group, control group.4.2 No correlation between the plasma levels of sOX40L, MIF and Gensini scoring in AMI, UAP and SAP group.Conclusion 1. The plasma levels of sOX40L, MIF are sensitive diagnostic marker for CHD. But they are not sensitive predicting marker for severity of coronary vessel lesions.2. We can improve the sensitivity of the identification of vulnerable plaques by the detection of plasma levels of sOX40L and MIF at the same time and take active actions to stabilize vulnerable plaques and decrease the occurrence of cardiac events. |
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