Recently, understanding of the factors that control ductus arteriosus closure after birth has advanced dramatically. In 1975, prostaglandin E1 (PGE1), an effective vasodilator of the ductus arteriosus, was administered to a neonate with congenital heart disease for the first time. As PGE1 was very useful to maintain a patent ductus arteriosus (PDA), it be came widely used in infants in whom pulmonary or systemic hood flow depends on a PDA.
This is a report of our clinical assessment of PGE1 in patients with congenital heart disease. Seventy-two infants were examined. PGE1 was effective in 61 (84.7%) infants, and they could survive until the shunt operation or total correction. In eleven (15.3%) patients PGE1 was useless, and they died before the operation.
We divided the 72 infants into three groups. The first group consisted of congenital heart disease in which all or almost all pulmonary blood flow was supplied through the PDA. This group included pulmonary atresia with intact ventricular septal defect or other combinations such as ventricular septal defect (extreme tetralogy of Fallot, double outlet right ventricle etc.), tricuspid atresia, single ventricle, transposition of great artery and so on.
The second group consisted of patients in whom all or almost all systemic blood flow was supplied through the PDA. This group included hypo-plastic left heart syndrome (aortic atresia, mitral atresia, etc), interruption of the aortic arch and severe coarctation of the aorta.
Those with transposition of the great artery formed the third group. PGE1 dilates the PDA and pulmonary vascular bed and thus increase pulmonary blood flow and interatrial mixing. PGE1 is effective to maintain the patients condition and enable balloon atrio-septostomy to be done more safely.
Of these three groups, PGE1 was most useful in the first and third groups.
