Circulation, Vol 60, 349-354, Copyright © 1979 by American Heart Association
DL Levin, LJ Mills and M Parkey
Although electrocardiographic evidence of right ventricular hypertrophy is
considered common in newborn infants with coarctation of the aorta, the
reason for this finding is not well established. Investigations of the
pulmonary vascular bed of these infants have resulted in variable findings,
probably due to the differences in morphometric techniques, coexisting
cardiac defects, and variable postnatal age at time of death. To study more
carefully the pulmonary vascular bed, we produced coarctation of the aorta
in fetal lambs at 103--126 days gestation. Twelve to 32 days later the
fetuses were reoperated on and systemic and pulmonary arterial blood
pressures, and arterial blood gas tensions were determined to be normal. At
autopsy, juxtaductal coarctations extended a mean of 2.8 mm into the aortic
lumen and occupied 9.5 mm of the aortic circumference. The fifth-generation
pulmonary resistance vessels had increased medial width (p less than 0.01),
decreased external diameter (p less than 0.001), and increased medial
width/external diameter ratios (p less than 0.001) compared with vessels
from control fetuses. The number of small muscular pulmonary vessels/cm2
lung tissue was significantly reduced (p less than 0.01) in the study
animals compared with the control animals. These alterations of the
pulmonary vascular bed were not due to fetal pulmonary arterial
hypertension or fetal hypoxemia. These pulmonary vascular changes may
explain the occurrence of pulmonary hypertension and right ventricular
hypertrophy in newborn infants with coarctation of the aorta.
ARTICLES
Morphologic development of the pulmonary vascular bed in experimental coarctation of the aorta
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