| Background: Brain natriuretic peptide (BNP) is the second compound of the natriuretic peptides family, a stress-induced cardiac peptide hormone secreted chiefly by ventricular myocytes. NT-ProBNP is N-terminal pro-brain natriuretic peptide. The purpose of this study is to examine the plasma levels of NT-ProBNP as well as atrial natriuretic peptide (ANP) in patients with chronic symptomatic heart failure (CHF) of coronary heart disease (CHD) . The present study analyzed their relationships with the New York Heart Association (NYHA) classification and left ventricular parameters on echocardiography, and their diagnostic value in symptomatic heart failure; To investigate the association between the plasma concentration of NT-ProBNP, ANP and the degree of ischemic damage after the first acute myocardial infarction (AMI).Methods: The study included 58 patients with symptomatic heart failure, age 42-82 (CHF group); 13 CHD patients without heart failure symptoms, age 45-73 (control group); 49 the first attack acute myocardial infarction patients, age 39-66 (AMI group) ; 30 healthy people, age 42-77 (normal group) . Plasma NT-ProBNP concentration was measured with enzyme irnmunoassay ; and plasma ANP, PRA, ANGII, ALD concentrations were measured with radioimmunoassay; Left ventricular parameters were studied by Doppler echocardiography. In CHF and control groups, cardiac deaths wererecorded over a mean period of 5. 4 1. 7 months follow-up. In AMI patients,Doppler echocardiography examinations were performed at 1, 3 months afterAMI.Results: The plasma levels of NT-ProBNP increased significantlyaccording to the severity of heart failure classified by NYHA (P<0. 01).There was a moderate inverse correlations between LVEF and both NT-ProBNP (Log-transformed BNP values) and ANP (r=-0. 59, r=-0. 52, P<0. 01). A cut-off value of 2. 2 provided sensitivity of 91. 37% and a specificity of 96.67% for the diagnosis of heart failure. The corresponding values for the negative and positive predictive value at this cut-point in this population were 98. 15% and 85. 29%. During the 5. 4 + 1. 7 months follow-up period, 8 patients died from a cardiac cause. The intergroup difference of plasma NT-ProBNP levels in the dead and survivors wasn' t significant (P>0. 05). Plasma NT-ProBNP, ANP concentrations increased after acute myocardial infarction (P<0. 01). The increment extent of the plasma NT-ProBNP (Log-transformed BNP values) is well related to the Left ventricular WMS performed at 7day, 1 month, 3 month after infarction ( r=0. 56 , r=0. 55 , r=0. 42, P<0. 05 ) , and the plasma NT-ProBNP (Log-transformed BNP values) was inversely associated with LVEF, FAC at 7day, 1 month, 3 month after infarction (r=-0. 48, r=-0. 49, r=-0. 47; r=-0. 52, r=-0.52, r=-0. 53, P<0. 05) .Conclusions: The plasma concentrations of NT - ProBNP were raised in patients with symptomatic heart failure, and the extent of the increment was related to the severity of heart failure. Plasma NT-ProBNP appeared to be excellent in identifying heart failure with high sensitivity and specificity. In this study, over a short-term follow-up, plasma NT-ProBNP didn' t associate with cardiac mortality of heart failure; The plasma concentrations of NT-ProBNP, ANP were raised in patients at 5-7 days after infarction. There was a good correlation with plasma NT-ProBNP and ischemic injury and systolic dysfunction of the left ventricular. Whether plasma NT~ProBNP can provide useful prognostic information after myocardial infarction is worth of further study.
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