BACKGROUND: Serum N-terminal pro-brain natriuretic peptide (NT-proBNP) tends to rise in acute phase Kawasaki disease (KD), but the cause of NT-proBNP elevation has not been clarified. In a previous study, cardiac function evaluated on 2-D echocardiography (2D-E) such as ejection fraction was normal, but this does not reflect subtle changes in cardiac dysfunction, and hence the association between cardiac function and NT-proBNP elevation is still controversial. The aim of this study was therefore to elucidate the influence of cardiac function on NT-proBNP elevation, by evaluating cardiac function via strain on 3-D speckle tracking imaging (3D-STI), in acute and subacute KD patients. Given that cytokines are also thought to induce NT-proBNP in acute phase KD, serum cytokines and cytokine receptors were measured at the same time. METHODS: Laboratory data and echocardiography in 52 KD patients in the acute and subacute phases were reviewed. RESULTS: Median NT-proBNP was significantly elevated in the acute phase compared with the subacute phase (356.5 pg/mL; IQR, 145-904 pg/mL vs 103.5 pg/mL; IQR, 59-150 pg/mL, P < 0.01). All cytokines were also significantly elevated in the acute phase compared with the subacute phase. Tumor necrosis factor (TNF)-α, soluble TNF receptor (sTNFR)1, and sTNFR2 concentration were all significantly higher in the acute phase. Indices of cardiac function were not significant different between phases. NT-proBNP in the acute and subacute phases correlated with sTNFR1 (r = 0.63/0.43, P < 0.01), sTNFR2 (r = 0.50/0.31, P < 0.05), and interleukin-6 (r = 0.58/0.43, P < 0.01). NT-proBNP did not correlate with global longitudinal strain (GLS) on 3D-STI. CONCLUSION: Although no correlation was seen between NT-proBNP and GLS on 3D-STI, correlations between NT-proBNP and cytokines were clear. NT-proBNP might be a marker of inflammation in KD, but is not a marker of cardiac function.
BACKGROUND: Serum N-terminal pro-brain natriuretic peptide (NT-proBNP) tends to rise in acute phase Kawasaki disease (KD), but the cause of NT-proBNP elevation has not been clarified. In a previous study, cardiac function evaluated on 2-D echocardiography (2D-E) such as ejection fraction was normal, but this does not reflect subtle changes in cardiac dysfunction, and hence the association between cardiac function and NT-proBNP elevation is still controversial. The aim of this study was therefore to elucidate the influence of cardiac function on NT-proBNP elevation, by evaluating cardiac function via strain on 3-D speckle tracking imaging (3D-STI), in acute and subacute KDpatients. Given that cytokines are also thought to induce NT-proBNP in acute phase KD, serum cytokines and cytokine receptors were measured at the same time. METHODS: Laboratory data and echocardiography in 52 KDpatients in the acute and subacute phases were reviewed. RESULTS: Median NT-proBNP was significantly elevated in the acute phase compared with the subacute phase (356.5 pg/mL; IQR, 145-904 pg/mL vs 103.5 pg/mL; IQR, 59-150 pg/mL, P < 0.01). All cytokines were also significantly elevated in the acute phase compared with the subacute phase. Tumor necrosis factor (TNF)-α, soluble TNF receptor (sTNFR)1, and sTNFR2 concentration were all significantly higher in the acute phase. Indices of cardiac function were not significant different between phases. NT-proBNP in the acute and subacute phases correlated with sTNFR1 (r = 0.63/0.43, P < 0.01), sTNFR2 (r = 0.50/0.31, P < 0.05), and interleukin-6 (r = 0.58/0.43, P < 0.01). NT-proBNP did not correlate with global longitudinal strain (GLS) on 3D-STI. CONCLUSION: Although no correlation was seen between NT-proBNP and GLS on 3D-STI, correlations between NT-proBNP and cytokines were clear. NT-proBNP might be a marker of inflammation in KD, but is not a marker of cardiac function.