Effect of ligation of patent ductus arteriosus on left ventricular performance and its determinants in premature neonates

The purpose of this study was to determine in preterm newborn infants the effects of ductal ligation on ventricular performance and its determinants: preload, afterload and contractility. Neonatal ventricular performance is highly sensitive to afterload. Therefore, the increase in systemic vascular resistance associated with ligation of a patent ductus arteriosus might worsen ventricular performance in the preterm infant. All 14 premature infants undergoing patent ductus arteriosus ligation in a 1-year period at our institution underwent echocardiography at three times: before, immediately after and 24 h after ligation. Indexes studied included ventricular performance (fractional area change), preload (left ventricular enddiastolic dimension), afterload (end-systolic wall stress) and contractility (the difference between the measured and predicted velocity of circumferential fiber shortening). Blood pressure was measured; systemic resistance was calculated. These data were compared with those of 14 preterm infants without patent ductus arteriosus. The infants with patent ductus arteriosus had higher values for ventricular performance (mean ± SD fractional area change 60 ± 9% vs. 52 ± 11%, p < 0.05) and lower values for wall stress (22 ± 6 vs. 44 ± 17 g/cm2, p < 0.05) before ligation than did the control group. At 24 h after ligation, ventricular performance was not significantly changed (fractional area change 60 ± 9% to 57 ± 12%). There were significant increases in blood pressure and systemic vascular resistance but no changes in wall stress or contractility. Ventricular performance is higher in premature infants with than in those without patent ductus arteriosus because afterload is lower in the former group. Although ductal ligation increases blood pressure and systemic resistance, wall stress and ventricular performance are maintained. Our results suggest that the premature newborn maintains ventricular performance during stress, at least in part, by manipulating afterload.