Furthermore, the placenta plays a role in clearance of NPs and loss of this clearance system contributes to the high level [21]. This surge in BNP levels at birth may play a regulatory role in the haemodynamic changes associated citation with transition to extra-uterine life. Renal maturation, a rise in systemic vascular resistance and a fall of pulmonary pressures explain the subsequent fall in peptide levels. There is a paucity of normative values of NTpBNP in neonates (Table 1). Reference ranges quoted in the literature vary according to the timing of the test, the kits used, and the population investigated [22]. Most quoted reference ranges are for term healthy neonates and therefore do not represent the intensive care population. NTpBNP is not thought to cross the placenta and therefore any variation in neonates must be explained intrinsically [23].

Table 1 Reference ranges for NTpBNP. 4. Influence of Antenatal and Postnatal Events on NTpBNP Levels in Preterm Infants The use of NTpBNP in assessing the haemodynamic status of preterm infants is gaining interest. NTpBNP is released in equimolar amounts to BNP from the myocardium. Its levels however are higher and remain in the blood stream for longer due to differing half-life and clearance [24]. Levels of NTpBNP in the early preterm period were assessed in a study of 80 preterm infants with a median gestation of 28 [IQR 26.1�C29.5] weeks and median birth weight of 1.06 [IQR 0.87�C1.21]kg. At 12 hours of life all infants had a PDA with low velocity left to right shunting.

The median NTpBNP value for the cohort was 1273pmol/L with an interquartile range (IQR) of 664�C2798pmol/L and a range of 98�C10700pmol/L. The influence of antenatal and postnatal factors on NTpBNP levels is illustrated in Table 2. Infants with RDS had significantly higher NTpBNP values compared to controls [25]. When adjusted for RDS, gestation and birth weight had no impact on NTpBNP. The premature neonatal heart is distinguished from that of older infants by several unique characteristics. The neonatal myocardium has a higher water concentration and a greater proportion of ��stiff�� collagen resulting in a noncompliant ventricle and diastolic dysfunction resulting in relatively poor ventricular filling [26]. The preterm myocardium cannot therefore respond to stress caused by the rise in afterload following the loss of the low pressure system of the placenta.

This problem is further compounded by any potential stressors such as hypoxia, anaemia and, mechanical ventilation which reduces venous return and cause pressure on the myocardium preventing effective contraction [27]. This may explain the higher values of NTpBNP seen in preterm infants compared to term infants. GSK-3 Table 2 Influence of antenatal and factors on NTpBNP levels at 12 hours (Mann Whitney U test was used to compare medians).