Brain natriuretic peptide can be a useful biochemical marker for myocarditis in patients with Kawasaki disease

Abstract

The mean concentration of brain natriuretic peptide in the plasma was 73.2 +/- 107.7 (mean +/- SD) pg/ml in the acute phase, and 7.9 +/- 7.5 pg/ml in the convalescent phase. We checked the electrocardiograms to find abnormal Q waves, elevation or depression of the ST segments, change in the pattern of the QRS complexes, and flattening or inversion of the T wave, all believed to be markers of myocarditis in Kawasaki disease. Those in whom the concentrations were greater than 50 pg/ml in the acute phase showed abnormal electrocardiograms more frequently than did those in whom the values were less than 50 pg/ml (21/29 vs 3/40, p < 0.0001 odds ratio 32.4). Amplitudes of the T wave in standard limb leads were measured both in the acute and convalescent phases, and the differences calculated. We regarded the sum total of these differences as representing "flattening T wave", and we named this variable as the total suppressed T wave voltage. We examined the correlation between the variable and the levels of brain natriuretic peptide in the plasma during the acute phase, demonstrating a significant correlation (r = 0.500, p < 0.0001). We conclude, therefore, that the concentration of brain natriuretic peptide measured in the plasma can be a useful biochemical marker for the myocarditis of Kawasaki disease. When the titer is over 50 pg/ml, the patient probably has an abnormal electrocardiogram and is most likely to have myocarditis.

Abnormal Tissue Doppler Images are Associated With Elevated Plasma Brain Natriuretic Peptide and Increased Oxidative Stress in Acute Kawasaki Disease

“…Kawamura et al maintain that pro-inflammatory cytokines, such as interleukin-1 and TNF-, cause myocarditis and stimulate secretion of BNP in acute KD. 17 They also reported no significant correlation between plasma BNP level and LV ejection fraction (LVEF) in acute KD. In contrast, in the present study, LVSF, VCFc, and Sw in week 1 significantly correlated with plasma BNP level.…”

“…17 The mechanism responsible for the increased plasma BNP level in acute KD is not yet known. Kawamura et al maintain that pro-inflammatory cytokines, such as interleukin-1 and TNF-, cause myocarditis and stimulate secretion of BNP in acute KD.…”

“…15,16 Although elevation of BNP has been reported in acute KD patients, 17 no relation between BNP and cardiac function has been found.…”

Diastolic function in children with Kawasaki Disease

“…Recent studies have reported left ventricular diastolic dysfunction in KD patients during the acute phase based on the inflow Doppler and tissue Doppler profiles of the left ventricle [11,12]. These reports concluded that diastolic dysfunction might contribute to the increased brain natriuretic peptide (BNP) levels seen in these patients [13]. Another study by Arnold et al reported late diastolic impairment (10.6 ± 5.1 years from the onset of KD) in segments supplied by stenotic coronary arteries without any evidence of systolic dysfunction in KD patients who had a coronary artery dilation/aneurysm defined as a coronary artery diameter N3 mm by angiogram during the acute phase of the disease [14].…”

Diagnostic and prognostic impact of brain natriuretic peptide in cardiac and noncardiac diseases

“…Elevation has been reported with diverse causes, including Chagas disease, 80 Kawasaki disease, 81 viral myocarditis, 82 Duchenne muscular dystrophy and its carrier state, 83 and myocardial cytotoxicity during chemotherapy, 84 stem cell therapy, 85 and after bone marrow transplantation. 86 A recent investigation by the Framingham Heart Study reported that plasma BNP predicted a wide range of cardiovascular events, including heart failure, atrial fibrillation, stroke, transient ischemic attack, and death.…”