1 From the Department of Pathology, University of Vermont College of Medicine, Burlington, Vermont, and Congenital Heart Disease Research and Training Center, Chicago, Illinois.
A quantitative, morphological study was undertaken on pulmonary arteries of 45 infants dying with ventricular septal defects; all but one were less than 3
© 1966 American Heart Association, Inc.
The Pulmonary Arterial Bed in Ventricular Septal Defect
Anatomic Features in Childhood
years in age at death. All but four had large septal defects and most had evidences of severe pulmonary arterial hypertension. In the first 2 postnatal months, about half of the infants had a near normal mass of pulmonary arterial smooth muscle which correlates with clinical observations of a decreasing pulmonary vascular resistance during this period. Subsequently, almost all had a greatly increased mass of muscle in small pulmonary arteries which was mainly due to hypertrophy of individual smooth muscle cells. This correlates with an increased pulmonary vascular resistance reported in infants with large defects at this age. Finally, infants older than 6 months of age with septal defects had a high incidence of pulmonary arterial thrombi, and intimal proliferative and sclerotic lesions. These latter lesions were probably at an irreversible stage in one 2-year-old and one 3-year-old infant.