| Objectives:This study was designed to observe the change of the serum apelin-36and basic fibroblast growth factor (bFGF) levels in patients with pulmonary arterial hypertension (PAH) associated with congenital heart disease (CHD) and analyze its correlation with mean pulmonary arterial pressure (mPAP) and the correlation between them, exploring the clinical implication of apelin-36and bFGF in patients with CHD-PAH.Methods:80cases of left to right shunt CHD patients who were admitted in Department of cardiovascular of Xiangya No.2Hospital from May2013to April2014and was confirmed by echocardiography,There are12males,68females, mean age32.06±11.72years old.Cardiovascular malformations included atrial septal defect (ASD) in37cases,ventricular septal defect (VSD) in24cases and patent ductus arteriosus (PDA) in19cases. Patients were divided into three groups according to mPAP:CHD without PAH group(A group,n=22, mPAP<25mmHg), CHD with mild-to-moderate PAP group(B group,n=21,25mmHg≤mPAP<45mmHg),CHD with severe PAH group(C group,n=37,mPAP>45mmHg).18normal subjects were recruited as control group.All the subject’s clinical data were collected. The concentration of serum apelin-36and bFGF were assayed with enzyme-linked immunosorbent assays. All data were analysed by SPSS version19.0.Results:1.The results showed that serum apelin-36levels were significantly decreased in patients of group B and C compared with control group (224.11±17.87vs270.79±21.00, P<0.05;168.71±27.19vs270.79±21.00, P<0.05, respectively); The serum apelin-36levels were significantly decreased in patients of group B and C compared with group A(224.11±17.87±3.18vs267.21±31.92, P<0.05;168.71±27.19vs 267.21±31.92, P<0.05, respectively); The serum apelin-36levels were significantly decreased in patients of group C compared with group B(168.71±27.19vs224.11±17.87, P<0.05);But no statistic difference of serum apelin-36levels was observed between group A and control group(267.21±31.92vs270.79±21.00, P=0.742).2.The serum bFGF levels were significantly increased in patients of group B and C compared with the patients in control group(31.04±4.64vs24.81±4.04, P<0.05;42.41±5.26vs24.81±4.04, P<0.05, respectively). The serum bFGF levels were significantly increased in patients of group B and C compared with group A(31.04±4.64vs25.07±3.78, P<0.05;42.41±5.26vs25.07±3.78, p<0.05, respectively); The serum bFGF levels were significantly increased in patients of group C compared with group B(42.41±5.26vs31.04±4.64, P<0.05);But no statistic difference of serum bFGF levels was observed between group A and control group (25.07±3.78vs24.81±4.04, P=0.712).3.The serum apelin-36levels were negatively correlated with mPAP (r=-0.674,p<0.01) in patients with CHD. the serum bFGF levels were positively correlated with mPAP(r=0.664,p<0.01)in patients with CHD. the serum apelin-36levels were negatively correlated with bFGF (r=-0.473,p<0.05) in patients with CHD.Conclusions:1.The serum apelin-36levels were significantly decreased in patients with CHD-PAH, while the serum bFGF levels were significantly increased in patients with CHD-PAH,suggesting apelin-36and bFGF involved in the pathophysiology of CHD-PAH.2. The serum apelin-36levels were moderately negatively correlated with mPAP in patients with CHD, while the serum bFGF levels were moderately positively correlated with mPAP, suggesting apelin-36and bFGF may be use as biomarkers to assess the severity of PAH in patients with CHD.3. The serum apelin-36levels were negatively correlated with bFGF, suggesting that apelin-36and bFGF may enteract with each other, contributing to the development of PAH in patients with CHD. |