To study the values of brain natriuretic peptide (BNP) and N-terminal pro-brain natriuretic peptide (NT-proBNP) in the evaluation of cardiac function in children with congenital heart disease (CHD).
Seventy-one children with CHD were classified to two groups: congestive heart failure (CHF) (n=23 ) and non-CHF (n=48). Thirty-five age-matched normal children were used as the control group. Plasma BNP content was measured using a microparticle enzyme immunoassay (MEIA) on the AxSYM. Plasma NT-proBNP content was measured using an automated electrochemiluminescence immunoassay on a Roche Modular Analytics E170 analyzer. Echocardiographic parameters, including left ventricular end diastolic dimension index (LVEDDI) and left ventricular ejection fraction (LVEF), were measured.
Plasma BNP and NT-proBNP contents in the CHF group were significantly higher than those in the non-CHF group (P<0.01). The non-CHF group had higher plasma BNP and NT-proBNP contents than the control group (P<0.01). LogBNP and LogNT-proBNP values were negatively correlated with the LVEF in the CHF group (r=-0.64, r=-0.67 respectively, P<0.01), and they were positively correlated with the LVEDDI (r=0.58, r=0.76 respectively, P<0.01). In the non-CHF group, LogBNP and LogNT-proBNP values were not correlated with the LVEF, but a positive correlation was found between the LogNT-proBNP value and the LVEDDI (r=0.35, P<0.05). Using plasma BNP content > or =149.8 pg/mL and NT-proBNP content > or =820.1 pg/mL as cut-off values for diagnosing CHF respectively, the sensitivities were 87.0 % and 91.3% respectively, the specificities were 91.7% and 97.9% respectively, and the areas under the ROC curves were 0.935 and 0.987 respectively.
Both BNP and NT-proBNP can be useful in assessment of cardiac function and diagnosis of CHF in children with CHD. NT-proBNP appears to be more sensitive and specific in the diagnosis of CHF than BNP.
Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics 06/2009; 11(6):429-32.
To investigate the role of heme oxygenase-1 (HO-1) and its catalyst carbon monoxide (CO) in the development of myocardial damage and the effects of zinc protoporphyrin IX (ZnPPIX), an inhibitor of HO-1 on myocardium of mice with acute viral myocarditis.
A total of 112 inbred male Balb/C mice 4 - 6 weeks of age were divided randomly into 3 groups: the control group (C group, n = 32), the viral myocarditis group (V group, n = 40) and ZnPPIX group (Z group, n = 40). The Z and V groups were inoculated intraperitoneally (i.p.) with 0.1 ml of 10(-4.36) tissue culture infectious dose 50% (TCID(50))/ml Coxsackie virus B3 (CVB(3)) to produce viral myocarditis model on day 0, C group was injected i.p. with virus-free 1640 culture culture medium 0.1 ml at the same time, then operation was done as follows: the mice of group C and group V were injected i.p. with 0.1 ml NS each day. The mice of group Z were injected i.p. with 40 micromol per kilogram of body weight ZnPPIX (HO-1 inhibitor) qod. Eight mice of each group were sacrificed on days 4, 8, 15 and 21, respectively. The blood specimens were collected by taking out the eyeballs to test for the content of carboxyhemoglobin (COHb) using spectrophotometry and cardiac troponin I (cTnI) using chemiluminescent immunoassay. The hearts tissue slides were also stained by immunohistochemistry (IHC) for HO-1 and in situ hybridization (ISH) for HO-1 mRNA. The histological and ultrastructural changes were observed under light and electron microscopes.
(1) The histopathological changes of myocardial cells: in the V and Z groups myocardial inflammatory cells infiltration reached the peak on day 8, the Z group histopathological scores were significantly lower than those in V group on day 8 (2.40 +/- 0.31 vs. 1.73 +/- 0.24, P < 0.01) and on day 15 (1.78 +/- 0.29 vs. 1.43 +/- 0.23, P < 0.05). No inflammation was present in group C. (2) The changes of serum cTnI level in both V and Z groups were significantly higher than those in C group on day 4, 8 and 15 (P < 0.01). The level in Z group was significantly lower than that in V group on day 4 [(6.074 +/- 1.475) ng/ml vs (7.911 +/- 1.225) ng/ml, P < 0.05] and day 8 [(0.821 +/- 0.294) ng/ml vs (1.480 +/- 0.454) ng/ml, P < 0.05]. (3) The changes of blood COHb level: compared with V group, in Z group the COHb level was lower on day 4 (P < 0.05) and day 15 (P < 0.01) after CVB(3) inoculation. Surprisingly, in Z group COHb level elevated suddenly on day 8 and showed conspicuously higher than that of V group (P < 0.01). (4) The result of HO-1 IHC staining: in both V and Z group myocardial cells had positive expression, while C group did not. (5) The results of HO-1 ISH were similar to those of HO-1 IHC, the A values of group Z was significantly lower than that of group V on day 4, 15 and 21(P < 0.01), but on day 8 it was higher than that of group C (P < 0.05).
HO-1 inhibitor, ZnPP not only could inhibit HO-1 overexpression but also could induce HO-1 expression temporarily and protect against myocardial injury at the early stage of acute viral myocarditis.
Zhonghua er ke za zhi. Chinese journal of pediatrics 12/2007; 45(12):893-7.
To investigate the effect of plasma homocysteic acid (HCA) reduction on serum C-reactive protein (CRP) level in children with Kawasaki disease (KD).
Seventy-six children with KD were divided into 2 equal groups for treatment with aspirin and IVIG, or with vitamin B6 and folic acid besides in addition to aspirin and IVIG. Serum CRP level was tested before and after the treatments, and plasma HCA level was also measured after the treatments.
Serum CRP level was comparable between the two groups before the treatment, but significantly reduced after vitamin B6 and folic acid treatment (7.56-/+2.94 mg/L vs 12.23-/+4.16 mg/L, P<0.05). Additional vitamin B6 and folic acid treatment significantly lowered plasma HCA level (4.56-/+1.14 micromol/L vs 7.79-/+1.79 micromol/L, P<0.05), and correlation analysis demonstrated a positive correlation between plasma HCA and serum CRP levels (r=0.697, P<0.01).
Lowering plasma HCA can decrease serum CRP in children with KD to enhance the therapeutic effect.
Nan fang yi ke da xue xue bao = Journal of Southern Medical University 11/2007; 27(11):1762-3.