Author + information
- Received October 8, 1985
- Revision received March 17, 1986
- Accepted April 1, 1986
- Published online September 1, 1986.
- W. Robert Morrow, MD1,
- James C. Huhta, MD, FACC*,1,2,
- Daniel J. Murphy Jr., MD1 and
- Dan G. McNamara, MD, FACC1
- ↵*Address for reprints: James C. Huhta, MD, Pediatric Cardiology, 1-253, Texas Children's Hospital, 6621 Fannin Street, Houston, Texas 77030.
It has been speculated that neonatal coarctation results from postnatal constriction of the aortic isthmus and ductus arteriosus. However, aortic arch hypoplasia is present in some neonates with coarctation and is presumed to be due to decreased aortic arch blood flow in utero. To measure the degree of aortic arch hypoplasia and to analyze the distribution of blood flow in neonatal coarctation, quantitative morphometric analysis of the great vessels from two-dimensional echocardiograms was performed in 14 neonates with isolated coarctation and 14 normal control neonates, all less than 1 month old. Measurements of the aortic valve, pulmonary valve, ascending aorta, transverse aortic arch between the carotid and subclavian arteries, aortic isthmus, descending aorta, main pulmonary artery and brachiocephalic ves- sels were obtained to the nearest 0.5 mm. In coarctation patients the transverse arch and isthmus were significantly smaller than in control subjects (p < 0.001). In addition, pulmonary valve and main pulmonary artery diameters were significantly greater in neonates with coarctation than in normal neonates.
Transverse arch hypoplasia and increased pulmonary valve and pulmonary artery diameters are present in neonates with coarctation. This suggests decreased aortic arch flow and increased pulmonary and ductus arteriosus flow in utero, which produce a characteristic echo-cardiographic appearance of transverse arch hypoplasia with a large main pulmonary artery.
- Received October 8, 1985.
- Revision received March 17, 1986.
- Accepted April 1, 1986.
- American College of Cardiology Foundation