Postnatal development of obstruction in coarctation of the aorta: role of the ductus arteriosus.

The sequence of events leading to the development of acute obstruction in two infants with coarctation has been defined by clinical, hemodynamic, and angiographic studies. One infant had normally related great arteries and an isolated coarctation, while the other infant had transposition with a hypoplastic right ventricle, a ventricular septal deffect, narrowing of the aortic isthmus, and a localized site of coarctation. In each instance, a posterior aortic shelf--the basic pathologic lesion in coarctation--could be observed angiographically. Signs of aortic obstruction were absent, however, as long as the ductus arteriosus was widely patent. Following ductal obliteration, femoral pulsations diminished, a peak systolic pressure difference was recorded between the ascending and descending aorta, and a discrete area of juxtaductal coarctation was seen. The basic malformation (posterior aortic curtain) would appear to exist in utero, possibly as an aortic branch point. This lesion is nonobstructive as long as blood can traverse the aortic isthmus through the aortic end of the ductus into the descending aorta. Postnatally, as the ductus arteriosus undergoes constriction at its aortic insertion, signs of acute aortic obstruction may b =ecome apparent. Normal femoral arterial pulsations during the newborn examination do not definitively exclude coarctation. Pediatricians should recheck at 2 weeks of age if the infant is asymptomatic or sooner if there are signs of cardiac failure to establish the presence or absence of this defect.