High-volume systemic-to-pulmonary ductal shunting occurs frequently in preterm infants and is indicated by diastolic flow reversal in the descending aorta (DAo). We studied the relationship between ductal diameter, diastolic DAo reversal, and left ventricular output (LVO); and superior vena caval (SVC) flow (upper body perfusion) and DAo flow (lower body perfusion) in preterm (Ͻ31 wk) infants. Echocardiographic assessments were performed at 5, 12, 24, and 48 h postnatal age (80 infants, median gestation 28 wk, 1060 g). Incidence of ductal patency fell from 100% at 5 h to 72% at 48 h; incidence of pure systemic-to-pulmonary shunting increased from 66% to 95% of infants with patent ducts. In infants with duct diameter greater than the median, 35-48% of infants had DAo flow reversal. In infants with duct diameter greater than median, DAo reversal was associated with 23-29% increases in LVO at 5-48 h, and 35% decreases in DAo flow volume at 24 -48 h, but no differences in SVC flow. In conclusion, a large duct with left-to-right shunting is common in preterm infants. Retrograde DAo flow is a marker of high-volume shunt, evidenced by increased LVO. Preterm infants with high-volume ductal shunt may have preserved upper body perfusion but reduced lower body perfusion. T he clinical significance of shunting through the patent ductus arteriosus in the premature newborn infant remains uncertain (1-4). It is clear that prolonged patency of the ductus arteriosus is seen in preterm infants with respiratory distress (5), and can be associated with significant volume of systemic-to-pulmonary shunting (6). In addition, prolonged ductal patency is associated with a variety of adverse outcomes in preterm infants (7). However, a causative association between ductal shunting and adverse outcome has not been established (8,9), and clinical trials of therapeutic intervention have not demonstrated reductions in morbidity (1). There is increasing awareness that ductal patency may not be a primary pathologic entity but rather an epiphenomenon of prematurity itself (10).Circulatory impact of ductal shunt depends on the volume of shunt and the ability of the myocardium to produce a compensatory increase in left ventricular output (LVO). It has previously been suggested that in the first postnatal days shunt volume through the ductus would be low due to the relatively balanced pulmonary and systemic arterial pressures at this time (11). However, there is now substantial evidence that pulmonary pressure in surfactant treated infants falls rapidly after birth (12,13). High-volume ductal shunt, as evidenced by reversal of blood flow during diastole in the descending aorta (DAo), has been seen as early as 7 h after birth (8), and may occur days before clinical signs appear (5).LVO has been shown to increase with increased ductal shunting in many preterm infants (14). However, it is possible that the immature myocardium has a limited ability to increase output in the first postnatal day (15). The combination of high-volume ductal shunt...