The Activation Of NF-κB In Peripheral Blood Lymphocytes And Its Responses To To Treatment Of Carvedilol In Patients With Chronic Heart Failure

Objective:To evaluate the possible mechanism ofβ-blocker in the treatment of chronic heart failure(CHF)through the relationship between the activation of nuclear factor kappaB(NF-κB) and the severity of cardiac dysfunction,and the clinical effects treated with carvedilol in patients with CHF.Methods:Forty patients with CHF were recruited into the study,and divided into carvedilol therapeutic group(CG,carvedilol in addition to the conventional treatment of CHF,initial dosage of carvedilol 3.125mg,2/d,and doubled every 1-2 weeks until the maximum tolerable reached,n=14) or non-carvedilol therapeutic group(NG,treated with conventional treatment of CHF,n=26),and 20 cases of healthy persons as normal controls. The activated state of NF-κB in peripheral blood lymphocytes(PBL) was assessed by immunocytochemical localisation,and the level of high-sensitivity C reactive protein (hs-CRP),erythrocyte sedimentation rate(ESR),and echocardiogrphy were determined routinely after treated for 4.3±0.6 months respectively.Results:(1) The positive rate of NF-κB(66.95±2.81%),the concentration of hs-CRP (6.61±1.11 mg/L),and ESR(9.58±1.16 mm/h) in patients with CHF were significantly higher than normal controls(23.25±2.44%,1.34±0.20 mg/L,5.10±0.44 mm/h repectively, p＜0.01 );(2) After treated with carvedilol,the positive rate of NF-κB(from 66.95±2.81% to 55.64±3.34%,p＜0.01),hs-CRP(from 6.61±1.11 mg/L to 3.56±0.67mg/L,p＜0.01),and ESR(from 9.58±1.16 mm/h to 7.00±0.80,p＜0.05) were decreased significantly in patients of CG comparing with NG;(3) The positive rate of NF-κB was correlated with LVED(r = 0.414,p＜0.01),EF(r = 0.356p＜0.05),and heart function(NYHA class)(r = 0.584,p＜0.01), and both levels of hs-CRP and ESR were correlated with activated NF-κB.Conclusion:The activation of NF-κB system may be involved in deterioration of heart failure,the mechanism of carvedilol in treatment of CHF is related to reduce inflammatory reaction by inhibiting NF-κB activity to some extent.