The purpose of this study was to test observations that might aid prenatal prediction
of the presence of coarctation of the aorta in newborn infants with and without other
forms of heart disease.
Previous reports have suggested that abnormal growth of the aortic arch in utero may
be identifiable as a marker for the diagnosis of coarctation.
We reviewed the prenatal echocardiograms and postnatal outcome of 20 infants (gestational
age at initial study 18 to 36 weeks) with coarctation of the aorta established postnatally,
to identify echocardiographic findings that would most facilitate the prenatal diagnosis
of coarctation. Associated cardiac lesions included double-inlet left ventricle anatomy
(n = 5), double-outlet right ventricle (n = 4), abnormal aortic valve (n = 5), unbalanced
atrioventricular canal (n = 3), and membranous ventricular septal defect (n = 1).
Chromosomal abnormalities included XO karyotype (n = 1), trisomy 18 (n = 1), and trisomy
21 (n = 1).
Hypoplasia determined by measurement of the distal aortic arch was the most frequently
observed finding among the fetuses with coarctation. In 12 of 15 fetuses with a well
visualized transverse arch at initial prenatal study, the diameter of the transverse
arch was < or = 3rd percentile for gestational age as compared with that in a normal
group of fetuses. Ten of 10 fetuses with adequate images of the isthmus had isthmus
hypoplasia at prenatal study with a diameter < or = 3rd percentile for gestational
age. On serial study in six of seven, including three fetuses with normal distal arch
measurements at initial study, the distal arch became progressively more hypoplastic
for gestational age. In three there was no growth of the transverse arch or isthmus
on serial study, and in three there was reversal of flow from antegrade to retrograde
through the distal arch.
In our study, quantitative hypoplasia of the isthmus and transverse arch was the most
consistent observation and therefore the most definitive antenatal sign of postnatal
coarctation. The potential for progression of distal arch hypoplasia necessitates
serial study in fetuses with associated cardiac and noncardiac lesions.