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Morphologic development of the pulmonary vascular bed in experimental coarctation of the aorta
Insights
Coarctation of the aorta in fetal lambs caused changes in pulmonary vessels, including increased medial width and reduced vessel number. These findings may explain right ventricular hypertrophy in newborns with this aortic defect.
Area of Science:
- Cardiovascular Research
- Fetal Surgery
- Pulmonary Vascular Disease
Background:
- Right ventricular hypertrophy is common in newborns with coarctation of the aorta, but its cause is unclear.
- Previous studies on the pulmonary vascular bed in these infants yielded variable results.
- Pulmonary vascular changes in fetal lambs with induced coarctation were investigated.
Purpose of the Study:
- To investigate alterations in the pulmonary vascular bed of fetal lambs with surgically induced coarctation of the aorta.
- To determine if these changes are linked to pulmonary hypertension or hypoxemia.
- To elucidate the mechanism behind right ventricular hypertrophy in neonatal coarctation of the aorta.
Main Methods:
- Coarctation of the aorta was surgically created in fetal lambs (103–126 days gestation).
- Fetuses were reoperated on 12–32 days later to measure systemic and pulmonary arterial blood pressures and blood gas tensions.
- Pulmonary resistance vessels and small muscular pulmonary vessels were analyzed post-mortem using morphometric techniques.
Main Results:
- Induced juxtaductal coarctations were confirmed at autopsy.
- Fifth-generation pulmonary resistance vessels showed increased medial width and medial/external diameter ratios, with decreased external diameter.
- The number of small muscular pulmonary vessels per cm² of lung tissue was significantly reduced in study animals compared to controls.
- These pulmonary vascular alterations were not associated with fetal pulmonary arterial hypertension or hypoxemia.
Conclusions:
- Induced coarctation of the aorta in fetal lambs leads to specific structural changes in the pulmonary vasculature.
- These pulmonary vascular alterations, including medial hypertrophy and reduced vessel density, are not driven by fetal hypertension or hypoxemia.
- The observed pulmonary vascular changes provide a potential explanation for the development of pulmonary hypertension and subsequent right ventricular hypertrophy in infants with coarctation of the aorta.
Abstract:
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.