Association Between Markers Of Inflammation And Acute Coronary Syndromes

Objective:Inflammation biomakers play a crucial role in arteriosclerosis and plaque disrupation. Three inflammation biomaker tissue inhibitor of MMP 1 (TIMP1), matrix metalloproteinase 9 (MMP9), Neopterin, was selected concentration levels in patients with acute myocardial infarction, unstable angina, stable angina and normal control were observed, to study the relationship between the new markers and the traditional myocardial infarction biomaker, such as high sensitive C-reactive protein (Hs-CRP), creatine kinase (CK),and cardiac troponin I (CTnI), to find effective in AMI and possibility to prognosis.Methods:197 consecutive patients were chosen, and divided into 4 groups-acute myocardial infarction group(51 patients), unstable angina group (48 patients), stable angina groups (54 patients), and healthy control group(44 patients). All patients were diagnosised according to WTO and Chinese Medical Associaition guideline. The blood plasma was collected and the concentration of MMP9, TIMP1, Neopterin assayed by ELISA. Statistical analysis was performed using SPSS software methods for small samples. A P value＜0.05 was considered statistically significant.Result:(1) Clinical characteristics:There were no significant differences in age and the prevalence of hyperlipemia and diabetes mellitus in the four groups. In nomarl group, there were less men, hypertension and smoke history. (2)In AMI group, there were a higher levels in Hs-CRP, CK, CK-MB and CTnI.There were no significant differences in traditional myocardial infarction biomaker in other three groups. (3)In AMI groups, there were a higher levels in MMP9.TIMP1.MMP9/TIMP1 and neopterin.There were no significant differences in inflammation biomaker between other three groups. (4) Hs-CRP and neopterin, CK(P<0.05) were found associated. No correlation were obsereved between other inflammation biomakers and traditional myocardial infarction biomaker.Conclusion:In AMI groups, the inflammation biomakers(MMP9, TIMP1, neopterin) were significant elevated.There was a association between Hs-CRP and neopterin. Howere no association between other inflammation biomakers and traditional myocardial infarction biomaker was found in the study. Objective:Lipoprotein-associated Phospholipase A2(LP-PLA2) as denoted as platelet-activating factor acetylhydrolase (PAF-AH), is a lipoprotein-bound enzyme that possibly play a crucial role in inflammation and arteriosclerosis. The present study was designed to elucidate the relationship of LP-PLA2 and the effect on the stability of plaque and stenosis in acute coronary syndrome.Methods:197 patients were choose, and was divided into 4 groups-acute myocardial infarction group(51 patients), unstable angina group (48 patients), stable angina group (54 patients), and normal group(44 patients). All patients were to make a definite diagnosis by WTO and Chinese Medical Associaition guideline. The blood plasma was collected and assay concentration by ELISA. Statistical analysis was performed using Spss software methods for small samples. A P value<0.05 was considered statistically significant.Result:(1) Clinical characteristics:There were no significant differences in age and the prevalence of hyperlipemia and diabetes mellitus. In normal group, there were less men, hypertension and smoke history. (2) The concentration of Hs-CRP, Neopterin, TIMP1 and MMP9 was significantly higher in AMI groups compared with other groups. (3) The LP-PLA2 levels was significantly higher in unstable angina group and stable angina group compared with normal group. (4)There was a higher LP-PLA2 levels in more numbers of lesion branchs but was not significant in subgroups, because LP-PLA2 was not increased in unstable angina or AMI, we included all CAD patients in evaluation. LP-PLA2 levels was elevated significant with the numbers of lesion branchs in all patients. (5) There were not a association between the LP-PLA2 levels with other inflammation biomarkers such as Hs-CRP (r= 0.02, p= 0.06), MMP9(R=0.005, P=0.30) and TIMP1 (R=0.01, P=0.13)Conclusion:There weren't a relationship between the LP-PLA2 levels and the stability of plaque in acute coronary syndrome.there was a closed connection between the LP-PLA2 levels and the numbers of lesion branchs...