Abstract

In the normal fetus the level of blood flow across the aortic isthmus is lower than after birth. This is reflected by a smaller diameter of the isthmus in relation to the ascending and descending aorta. We postulated the effects of various congenital heart lesions on aortic isthmus development in the fetus on the basis of assumed changes in flow patterns. These alterations have been confirmed by studies of cineangiograms in newborn infants. In congenital heart lesions with reduced pulmonary arterial outflow, the diameter of the aortic isthmus is wider than normal, presumably because it carries a greater than normal flow in the fetus. In lesions interfering with left ventricular outflow the aortic isthmus may be underdeveloped. However, in aortic atresia the isthmus is normally developed since it carries a normal flow but in a retrograde manner. We reviewed the clinical data and angiograms of 41 infants less than 3 months old who had aortic obstruction. They could be divided into 2 distinct groups. Twenty-three with aortic isthmus narrowing or interruption had a large ventricular septal defect and a high incidence of complex anomalies such as double outlet right ventricle. The remaining 18 infants with localized juxtaductal narrowing had a low incidence of associated intracardiac lesions. The appearance of the localized juxtaductal coarctation suggested that aortic obstruction may not be present during fetal life because the widely patent ductus arteriosus obviates aortic obstruction. We postulated that constriction of the ductus arteriosus after birth would produce obstruction. This was confirmed experimentally in fetal lambs with surgically simulated juxtaductal coarctation.

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