Related Experiment Videos
Plasma brain natriuretic peptide concentrations in patients with Kawasaki disease
T Kawamura1, M Wago, H Kawaguchi
1Department of Pediatrics, Hiroshima City Asa Hospital, Japan. child@asa-hosp.city.hiroshima.jp
Insights
Plasma levels of brain natriuretic peptide (BNP) are elevated in acute Kawasaki disease (KD) and decrease in the convalescent phase. BNP may serve as a biomarker for cardiovascular manifestations in KD patients.
Area of Science:
- Cardiology
- Pediatric Rheumatology
- Biomarker Research
Background:
- Brain natriuretic peptide (BNP) is a cardiac hormone elevated in heart failure and myocardial infarction.
- Kawasaki disease (KD) is a vasculitis with significant cardiovascular involvement.
- Elevated plasma BNP in KD may indicate cardiovascular complications.
Purpose of the Study:
- To investigate plasma BNP concentrations in acute and convalescent phases of Kawasaki disease.
- To compare BNP levels in KD patients with those experiencing viral infections.
- To assess the potential of plasma BNP as a biomarker for cardiovascular manifestations in KD.
Main Methods:
- Measured plasma BNP in 32 acute KD, 35 convalescent KD, and 26 viral infection patients.
- Utilized two-dimensional echocardiography to assess cardiac function and coronary arteries in KD patients.
- Compared BNP levels across different disease phases and patient groups.
Main Results:
- Acute KD patients had significantly higher plasma BNP (55.0 pg/mL) than viral infection patients (6.8 pg/mL).
- Plasma BNP levels decreased significantly in the convalescent phase of KD (5.9 pg/mL).
- Higher BNP levels were observed in KD patients with pericardial effusion (80.3 pg/mL) versus those without (46.5 pg/mL).
Conclusions:
- Plasma BNP concentration is elevated during the acute phase of KD and normalizes during convalescence.
- Plasma BNP shows potential as a useful biomarker for cardiovascular manifestations in Kawasaki disease.
- Further research is needed to elucidate the mechanisms behind elevated BNP in acute KD.
Background:
Brain natriuretic peptide (BNP) is a cardiac hormone and plasma levels of it increase in patients with congestive heart failure and in those with acute myocardial infarction. Kawasaki disease (KD) is a well-known generalized vasculitis and the most prominent features of this disease are the cardiovascular manifestations, which involve the pericardium, myocardium, endocardium and coronary arteries. It was hypothesized that the plasma concentrations of BNP in patients with KD might be increased and that plasma BNP might be a useful biological marker of cardiovascular manifestations in patients with KD.
Methods:
Blood was obtained to measure and compare plasma BNP concentrations in the acute (n = 32) and convalescent (n = 35) phases of KD and in the acute phase of the patients with viral infection (n = 26), which included adenovirus, influenza, measles and herpes group virus infection. In patients with KD, two-dimensional echocardiography was performed to check for pericardial effusion and coronary arterial lesions and to measure the dimensions of the left ventricle at diastole and the shortening fraction of the left ventricle (LVSF).
Results:
The mean plasma BNP concentration in patients with KD in the acute phase was 55.0 +/- 39.5 pg/mL, but was 6.8 +/- 7.3 pg/mL in patients with viral infection. The plasma BNP concentration in patients with KD in the acute phase was significantly higher than in patients with viral infection (P < 0.0001). In 31 cases of KD, the plasma BNP concentrations were measured both in the acute and convalescent phases. The mean plasma BNP concentration in the acute phase of KD was 55.3 +/- 40.1 pg/mL and in the convalescent phase was 5.9 +/- 5.7 pg/mL. The level of plasma BNP decreased significantly in the convalescent phase (P < 0.0001). The mean BNP level in patients with KD with pericardial effusion (n = 8) in the acute phase was 80.3 +/- 43.4 pg/mL and that in patients without pericardial effusion (n = 24) was 46.5 +/- 35.1 pg/mL. The BNP level in patients with pericardial effusion was significantly higher than that of patients without pericardial effusion (P < 0.05). There was no significant correlation between the plasma concentrations of BNP in the acute phase of KD and LVSF (r = -0.161, P = 0.39, n = 31).
Conclusion:
It was shown that the plasma BNP concentration increased in the acute phase of KD and decreased to within normal range in the convalescent phase. Further examinations are needed to clarify the mechanism by which the elevated levels of plasma BNP occur in the acute phase of KD. However, plasma BNP might be a useful biological marker of the cardiovascular manifestations in patients with KD.