Abstract 1206 Poster Session IV, Tuesday, 5/4 (poster 211)

Introduction: It has been found previously that plasma atrial natriuretic peptide(ANP)levels are higher in premature newborns with a persistently patent ductus arteriosus (PDA) and that the level of ANP decreases following closure of the PDA. There have, however, been few studies examining the relationship of ANP levels to other measures of cardiac output and in particular to the magnitude of ductal shunting.

Aim: To examine the role of ANP in early cardiovascular adjustment in very premature infants.

Methods: An echocardiogram at a postnatal age of 24hr was performed on premature infants born less than 30 weeks gestational age(GA) enrolled in this prospective study of early cardiovascular adjustment. Measures of cardiovascular function which were recorded included left(LVO) and right ventricular output(RVO), the ductal and atrial shunt diameters using colour Doppler flow (previously correlated with the size of shunt), flow through the superior vena cava, and systemic blood pressure. Total body vascular resistance(TBVR) was calculated from the LVO and systemic blood pressure. At the time of echocardiography blood was taken for measurement of plasma ANP levels. ANP was measured using a standard RIA. Statistical analyses included linear regression and rank sum testing.

Results: We studied 43 infants with mean±SD BW 1017 ±234g and GA 27±1.5wk. Median [interquartile range] plasma ANP was 83 [53 - 168] umol/L. Plasma ANP levels were lower in infants with low LVO(i.e. <200ml/kg/min) compared with those who had normal or high LVO, 67.5±37umol/L v 181.7 ±31.4umol/L (P=0.002). Univariate and multivariate regression analysis showed plasma ANP levels to increase significantly with increasing LVO(p=0.0003). Univariate analysis demonstrated a weak positive correlation between plasma ANP levels and ductal diameter (p=0.049) and inverse correlation between plasma ANP and calculated TBVR(p=0.031), both of which disappeared on multivariate analysis. Plasma ANP did not correlate with the magnitude of shunting across either the ductus (p=0.62) or the atrial septum (p=0.13), or with SVC flow (p=0.36).

Conclusions: We have demonstrated a strong relationship between increased LVO and raised ANP levels. The mechanism for this relationship is likely to be atrial distention resulting from atrial volume loading. Possible reasons for increased atrial volume loading include left to right ductal shunting and increasing LVO from other causes. As ANP is a vasodilatory substance, a secondary effect of raised ANP may be a reduction in TBVR with subsequent increase in LVO. We postulate that the previously noted association between high ANP levels and a PDA may be related to increased left ventricular output occurring in response to ductal shunting rather than the presence or absence of a PDA per se.