| Objective: Adiponectin ( APN ) is a recently discovered adipocyte-specific protein that is coded by gene apM1 highly expressed in white adipose tissue.At present,part of physiological function of APN has been learnt.when endodermis is hurt,APN congregates on the wall of blood vessel and can inhabit the cell adhering effect on main artery endodermis,which is induced by TNF-α.This means that APN can countermine atherosclerosis. Ventriclar remodelling is the basic mechanism of CHF.It is the ever-lasting chronic activation of the nerve-incretion-inflammation medium system that promote the ventriclar remodelling and aggravate cardiac musclar damnification and deteriorating of cardiac function,which further active nerve-incretion-cytokines.Hence,a vicious circle is formed. The study of these years showed that the plasma APN levels increase in the patients with CHF and APN is likely to be involved in the pathophysiological process of CHF. Clinical plasma adiponectin and chronic congestive heart failure and less reporting on the relationship between research, a study showed that plasma adiponectin in congestive heart failure is rising, and with proportional to the severity of the heart failure.TNF-αis a cytokine secreted by monocytes/ macrophages,which has lots of biological effects including reducing the contracting power of cardiac muscle,increasing the releasing amount of oxygen free radicel,boosting the apoptosis of cardiac muscular cell. Recent experimental studies have shown that TNF-αhas deleterious cardiovascular effects. The level of TNF-αis increased in patients with congestive heart failure ( CHF ) and may play an important role in the development and progression of heart failure. To detect the levels of APN and TNF-αin patients with chronic CHF and its clinic significance.Methods: The levels of plasma adiponectin and TNF-αwere measured by enzyme-linked immuneosorbent assay(ELISA) in 100 before treatment and after treatment(about two weeks later) patients with congestive heart failure and 20 control subjects respectively.These patients included 48 male patients and 52 female ones, with average age of 62±13.6 years old, all of them were accordant with the diagnosis criterion of CHF from America Heart Disease Association.The patients came from the in-patient department of 2th hospital with the Hebei Medical University,including 54 with ischemic cardiomyopathy,46 with dilated cardiomyopathy. According to the severity of NYHA class (New York Heart Association class in 1994)Ⅱ: 18, NYHAⅢ: 46, NYHAⅣ:36. Another 20 control subjects came from out-patient department,including 9 male healthy persons and 11 female ones,with average age of 53±9.9 years old. All subjects not only had excluded body mass index(BMI)≥25kg/m2和<18.5kg/m2, but also had no other diseases such as cerebrovas cular disease, main artery disease,liver and kidney disease, metabolic disease (diabetes, hyperthyreosis) and other cardiovascular diseases. The age,sex,BMI showed no difference among these subjects.Taking ulnar venous blood 2ml on an empty stomach, infusing anticoagulation tube, using centrifugal machine, 3000/min, centrifuging 10 minutes, the plasma in Eppendorf was preserved in -80℃refrigerator. The levels of adiponectin and TNF-αin all specimens were measured after collection respectively.Results: 1. The levels of plasma adiponectin and TNF-αin Heart failure subjects compared with those in control subjectsThe levels of adiponectin in patients with CHF before treatment were significantly higher than those in control subjects, statistical significant with regard to the difference between them(P<0.01).2. The levels of plasma adiponectin and TNF-αbefore treatment compared with after treatment in Heart failure subjects After treatment, the levels of adiponectin and TNF-αwere obviously lower than those before treatment, statistical significant with regard to the difference between before treatment and after treatment(P<0.05).3. The levels of plasma adiponectin and TNF-αin patients with congestive heart failure compared among different cardiac function The increasing of plasma adiponectin and TNF-αin patients with CHF before treatment was accordant with the severity of cardiac function, the more severe, the more higher. statistical significant with regard to the difference betweenⅣandⅢ(P<0.05).4. The levels of plasma adiponectin and TNF-αin ischemic cardiomyopathy subjects compared with those in dilated cardiomyopathy subjectsThe levels of plasma adiponectin and TNF-αof CHF patients with ischemic cardiomyopathy were higher than those in dilated cardiomyopathy.The levels of plasma adiponectin of CHF patients with ischemic cardiomyopathy versus dilated cardiomyopathy P<0.05, there was statistical significance. the levels of plasma TNF-αof CHF patients with ischemic cardiomyopathy versus dilated cardiomyopathy, there was no difference.5. In patients with CHF, the levels of plasma adiponectin was not correlative with TNF-α, r=0.127,P>0.05.6. In patients with CHF, the correlation between LVEF and the levels of plasma adiponectin and TNF-αrespectivelyThe levels of plasma adiponectin was not correlative with LVEF, r=-0.029,P>0.05.The level of plasma TNF-αwas negatively correlative with LVEF, r=-0.371,P<0.05.Conclusions: 1. The levels of plasma adiponectin and TNF-αin patients with CHF increased, moreover, they were accordant with cardiac functional class. The levels decreased after treatment. 2. Before treatment, the levels of plasma adiponectin and TNF-αof CHF patients with ischemic cardiomyopathy obviously increased,and compared with dilated cardiomyopathy patients, there was significant difference(P<0.05).But in TNF-α,there was no significant difference.3. The level of plasma TNF-αwas negatively correlative with LVEF(P<0.05).These above results indicated that the levels of plasma adiponectin and TNF-αin patients with CHF obviously increased and the levels of plasma adiponectin can be used as a significant index to monitor the severity degree of CHF. The levels of plasma TNF-αwas negatively correlative with the systole. The plasma adiponectin and TNF-αare involved in the pathogenesis of CHF and further study is needed to elucidate their exact roles. |
