Change Of B-type Natriuretic Peptide In Patients With Cardiac Valve Replacement Perioperatively

Objectives: B-type natriuretic peptide was isolated from pig brain in 1988.It synthesized in bursts,and released from ventricular myocytes as a 76 aminoacid N-terminal fragment (N-terminal BNP) and a 32 aminoacid active hormone (BNP).BNP concentration is closely related to left ventricular pressure and volume indices . Actions of BNP includes:increase glomerular filtration and inhibit sodium reabsorption,causing natriuresis diuresis;relax vascular smooth muscule ,causing arterial and venous dilation and leading to reduced blood pressure and ventricular preload;inhibit central and peripheral sympathetic nervous system,block cardiac sympathetic nervous system ,inhibit the renin-angiotensin-aldosterone axis;diastole myocardium directly ,antihyperplasia and antifibrosis of vascular tissue .BNP is cleared by bingding to natriuretic peptide receptor and inactivated by neutral endopeptidase.BNP concentration varieties with age and gender,it is higher in male than that in female and increasing with age.BNP plays an aid role in diagnosis of congestive heart failure and hasprognostic value in congestive heart failure and acute coronary syndrome .But the data of BNP concentration changing during perioperative period and its relationship with recovery of left ventricular systolic function after operation in patients with cardiac valve replacement are rare .This study is to investigate the perioperative serum concentration of BNP in the patients with cardiac valve disease ,observe its secretion during perioperative period.Method: 20 patients who underwent valve replacement in our hospital during June 2005-December 2005 were enrolled ,patients with coronary artery heart disease or cardiac myopathy were excluded .9 patients were male and 11 female,mean age 47.9±10.0 years .14 patients were rheumatic heart disease ,3 degenerative calcified valve disease ,2 chronic infective endocarditis and 1 bicuspid aortic valve. 14 patients of 20 suffered from atrial fibrillation. Heart function II 10 , III 9 and IV 1 .Control group were healthy people without heart disease history,normal heart function,9 male and 11 female,mean age 41.8±9.2 years (p>0.05,compared with operation group). Each patient in operation group checked echocardiography before operation. Serum concentration of BNP was measured after anesthesia and 24 48 96 hours after pump off in 20 patients with cardiac valve disease,compared withthat in healthy people and analysed together with their preoperative cardiac function, echocardiography results and their postoperative condition.Patients in Operation group checked cardiography 24-36 hours after operation again.Results: Basic serum concentration of BNP in the patients with cardiac valve disease was 7.2- fold greater than that in healthy people .Its concentration significant arose after pump off(p<0.01),its level after pump off had positive correlation with basic level (r=0.64> 0.72^ 0.50, p<0.05) ,but no correlation with aortic cross time (r=-0.044^ 0.15> 0.28, p>0.05 ) .And its basic level had negative correlation with LVEF(r=-0.47,p<0.05)but no correlation with end diastolic volume or diastolic diameter of left ventricle(r=0.087> 0.077, p>0.05). 24-36 hours after operation, LVEF in patients underwent valve replacement recovered4quite well compared with preoperation period[ (59.1±7.3) % vs (62.2±10.3)%, p>0.05]. BNP level in patients with New York Heart Association functional classification system III-IV much higher than that in patients with heart function II [ (182±109)//g/ml vs ( 58.6±42.2) //g/ml,p<0.01].Basic BNP levels had no significant difference between patients with mitral or (and) aortic valve insufficiency and mitral stenosis[ (107±117) /*g/ml vs (130±105) //g/ml,p>0.05].Conclusion: Basic serum level of BNP in the patients with cardiac valve disease was much higher that in healthy patients, its secretion may be affected by several factors, such as ventricular overloading ,ventricular wall stress increased, chronic myocardial damage caused by underlying disease, hemodynamics change, atrium fibrillation and so on. BNP release was not parallel with recovery of LVEF after operation, it was not a proper indicator of recovery of LVEF shortly after valve replacement.