[Change in plasma N-terminal pro-brain natriuretic peptide in children with Kawasaki disease and its value in clinical practice].

OBJECTIVE: Brain natriuretic peptide (BNP) is a cardiac hormone and its plasma level increases in congestive heart failure and myocarditis. An increased level of serum BNP has been reported in children in the acute stage of Kawasaki disease (KD). But the mechanism of increased level of BNP in children with KD has not been elucidated and the change in BNP in children with KD in China has not been reported. The aim of this study was to investigate the change in plasma N-terminal pro-brain natriuretic peptide (NT-pro BNP) in children with KD, examine the value of NT-pro BNP in the diagnosis of KD and explore the mechanism of the change in plasma NT-pro BNP in children with KD.

METHODS: Thirteen patients, aged from 4 months to 56 months, with KD were enrolled and nine patients with acute upper respiratory infection were used as controls. Blood sample was obtained to measure plasma NT-pro BNP concentrations in the acute (n = 13) and convalescent (n = 8) phases of KD and in the acute phase of the control patients. Plasma NT-pro BNP was measured using enzyme immunoassay. Other laboratory data including complete blood cell count, C-reactive protein, etc, were also measured in acute phase in both groups. The serum cardiac troponin I was also detected in acute phase of children with KD. All patients with KD had complete echocardiographic study, including measurement of left ventricular end diastolic diameter (LVDd), left ventricular ejection fraction (LVEF) and left ventricular inflow velocity through the mitral annulus (including E-velocity and A-velocity). Two dimensional echocardiography was performed to check for coronary lesions of patients with KD. The correlation between plasma NT-pro BNP and the above parameters was analyzed.

RESULTS: The mean plasma NT-pro BNP concentration in patients with KD in the acute phase was (691 +/- 86) ng/L, and it was (47 +/- 10) ng/L in patients of control group. The plasma NT-pro BNP in patients with KD in the acute phase was significantly higher than that of the control group (P < 0.001). In 8 cases of KD, the plasma NT-pro BNP concentrations were measured both in the acute and convalescent phase. The mean plasma NT-pro BNP concentration in the acute phase of KD was (636 +/- 89) ng/L and it was (164 +/- 35) ng/L in the convalescent phase. The level of plasma NT-pro BNP decreased significantly in the convalescent phase (P < 0.01). Through linear regression analysis, there was no significant correlation between the plasma concentrations of NT-pro BNP in acute phase of KD and LVEF, LVDd and E/A ratio, respectively. But the NT-pro BNP level correlated positively with C-reactive protein and white blood cells counts (r = 0.615, P < 0.05 and r = 0.547, P < 0.05), respectively. NT-pro BNP level correlated positively with serum cTnI, a sensitive biologic marker of cardiac injury (r = 0.611, P < 0.05).

CONCLUSION: The plasma NT-pro BNP concentration increased in the acute phase and decreased significantly in the convalescent phase of KD. The plasma NT-pro BNP might be one of the useful biological markers of KD, and the mechanism of change in plasma NT-pro BNP in KD might be associated with cardiac injury and inflammatory factors.