An Update on Patent Ductus Arteriosus and What is Coming Next

Abstract

Patent ductus arteriosus is the most common cardiovascular condition in preterm infants. There is a significant uncertainty about when and how to close ductus arteriosus in preterm infants due to a high spontaneous closure rate even in very immature preterm infants. Diagnosis and management of patent ductus arteriosus remain a challenge for both neonatologists and pediatric cardiologists. Researchers have tried to define a balance between an expectant approach and active treatment in selected infants. This review aimed to focus on the pathophysiology and management of patent ductus arteriosus and to make suggestions about approaches that might eliminate the association of morbidities with patent ductus arteriosus.

Oxygen for the Newborn: Friend or Foe?

“…PDA consists of a persistence of the fetal communication between the descending aorta and the left pulmonary artery. After birth ductus arteriosus usually closes in the first days of life and closure is due both to a decrease of circulating prostaglandin E2, a vasodilator synthetized by the placenta during fetal life, and an increase of circulating oxygen after breathing [ 78 ]. Ductus arteriosus (DA) is therefore affected by changes in pO2 as intrauterine hypoxia maintains the patency of the ductus and hyperoxia at birth facilitates its closure.…”

“…PDA is more frequently seen in preterm infants, particularly those born at <30 weeks’ gestation [ 78 ], probably due to the different role played by isoprostanes (IsoPs), a biomarker of oxidative stress, in preterm or term newborns [ 79 ]. Oxygen exposure increases IsoPs levels in newborn mouse lungs causing constriction of the isolated DA by activating the thromboxane (TxA2) receptor, however, IsoPs induce vasodilation of preterm isolated DA following the interaction with prostaglandin E2 receptor 4 (EP4).…”