Jorge Correia-Pinto, MD, PhD
Pediatric Surgery
Gustavo Rocha, MD
Neonatology
Hercília Guimarães, MD, PhD
Neonatology
José Carlos Areias, MD, PhD
Pediatric Cardiology
Hospital São João
4200 Porto, Portugal
To the Editor.
We read with great interest "Brain-Type Natriuretic Peptide in the Diagnosis and Management of Persistent Pulmonary Hypertension of the Newborn" by Reynolds et al.1 The authors suggest the blood level of brain-type natriuretic peptide (BNP) as a marker that can be used as an adjunct parameter to differentiate newborns with persistent pulmonary hypertension from other noncardiac causes of respiratory distress. This information might be particularly useful in deciding appropriate treatment and planning early transfer to centers with echocardiographic facilities. Although hypothesized in their discussion, the study by Reynolds et al did not investigate if cardiac anomalies resulting in ventricular stress in neonates might also induce elevated blood levels of BNP. It is worth clarifying this aspect, because these patients could require a different therapeutic approach than infants with persistent pulmonary hypertension.
It is interesting to note that we currently are performing a clinical study aimed at assessing the clinical value of BNP measurements in newborns with congenital heart disease that results in pressure overload to the right ventricle. In this setting, we already studied 7 newborns that required catheterization with therapeutic purpose (1 with pulmonary atresia with intact ventricular septum and 6 with critical pulmonary stenosis). None of them had other morphologic or chromosomal anomalies. All the newborns revealed echocardiographic signs of right ventricular pressure overload, with significant tricuspid regurgitation, right-to-left interauricular shunting, and high estimated right ventricular pressure/mean blood pressure ratio (>2:3). Measurement of BNP level was performed in venous blood samples collected from femoral vein before contrast injection. None of these newborns were submitted to cardiac catheterization without a clinical purpose, and no additional blood was required. In this preliminary study, we found a significantly high value of BNP (>2500 pg/mL) in all patients. Additionally, we found a positive and significant correlation between BNP levels and systolic right ventricular pressure (r = 0.81; P < .05) as well as to the mean right ventricular pressure (r = 0.77; P < .05).
In conclusion, our preliminary results confirm the suspicion from Reynolds et al that cardiac anomalies such as pulmonary stenosis/atresia might also result in elevated blood levels of BNP, which correlated with right ventricular pressures. We believe, therefore, that the blood level of BNP reflects ventricular stress, and its elevation should be a criterion for prompt additional evaluation but not necessarily an indication for beginning any specific therapy directed at persistent pulmonary hypertension.
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