Study On The Effect Of Nuclear Factor Kappa B In Cardiac Ventricle Remodeling After The Acute Myocardial Infarction

Objective: This research aimed to exmine the mechanism of action and relationship between nuclear factor kappaB in the ventricular remodeling after actue myocardial infarction by detecting activation of NF-κB in peripheral blood mononuclear cell (PBMCs) and the level of tumor necrosis factor–α(TNF-α), interleukin-1β(IL -1β).Methods:Fifty-eight patients with first acute myocardial infarct were collected from our hospital in 2008.12-2009.8. Every patient common datas was collected, ACEI,β-receptor inhibitors, Simvastatin and aspirin were administered in all patients. Patients with indication percutaneous transluminal coronary intervention and percutaneous transcoronary coronary angioplasty were given corresponding treatment. All these Patients: (1) grouping: After admission hospital three days and thirty days, all patients were examined echocardiogram. According to Simpson's method, we calculated the left ventricular end-diastolic volume (LVEDV) and end-diastolic volume index(LVEDVI) by rectifing surface area. We gotΔLVEDVI by counting and madeΔLVEDVI>20% as standardization for left ventricular remodeling. Fifty-eight patients with acute myocardial infarct were divided into two groups. Thirty-three (group A) patients whoseΔLVEDVI increased over twenty percent were defined as ventricular remodeling group. Twenty-five patients were defined as ventricular no remodeling group whichΔLVEDVI increased less than twenty percent. Control group (group C, 20 patients) came from normal-man in the health examination. (2) Extract PBMCs: To extract PBMCs by mathed of density gradient. After acute myocardial infarct happening three days and fourteen days, we collected all patients'peripheral vein blood 4ml and added leukocyte cell detachment to it, then centrifugated twenty minutes through level centrifugal machine centrifuge, took mononuclearcell out of the cloud and mist layer. We used acetone to fix it at glass slide and stored at -70℃. (3) NF-κB of PBMCs was detected by immunocytochemistry. According to the principle of SABC affinity immunocytochemical technique, put the antigen into peripheral blood monouclear cells and coloretured, then observed activation degree of NF-κB. (4) TNF-αand IL-1βwere detected by radio-immunity (balancing methods), all patiens were collected peripheral vein venous blood 2ml, centrifugated and took out clear supernatant liquid.Result (1) Three was no significant difference among 3 groups in the sex and age. Risk factor of acute myocardial infarction groups were higer than control groups among following factors: hypertension, diabetes, cerebrovascular disease family history, hyperlipemia and smoking history, besides, there has statistics disparity(P<0.001). There have no significant deviation and comparability between groups A and group B. such as infarction site, complication(P>0.05).(2) After myocardial infarction three days, the activation of NF-κB and density of IL-1βand TNF-αin group A and group B had significant statistical significance to compare with group C (P<0.001). These indexs in Group A were higer than in group B, but there was no statistically significance ( P>0.05).After myocardial infarction fourteen days, three indexs mentioned above in group A had significant statistical significance to compare with groupC and groupB(P<0.001). There was no statistically significant between group B and group C (P>0.05) though indexs in group B was higher than group C.(3) Through correlate analyze, activation degree of NF-κB in Group A had two signfincant relatived index : TNF-α( R=0.649,0.535, P<0.01 ), IL-1β(R=0.463, 0.447,P<0.01 ), they were both positive correlation.Conclution (1) NF-κB avtivation is increasing in left ventricular remodeling after acute myocardial infarction lasting for many days or many weeks, which could be participate in left ventricular remodeling. (2) TNF-αand IL-1βincrease after NF-κB is avtivated. NF-κB avtivation positively correlated with them in AMI. The secrete of cytokine may be upregulated through NF-κB avtivation, which is one of the important mechanism cardiac ventricle remodeling after AMI.