Richard L. Naeye

Primary Pulmonary Hypertension with Coexisting Portal Hypertension A Retrospective Study of Six Cases

Six cases are described in which there was a coexisting pulmonary arterial and portal venous hypertension. In 5 of the cases, the pulmonary vascular lesions responsible for the pulmonary hypertension resembled those seen in cases of recurrent embolization. Three of the cases had portal venous thromboses. One of these also had thrombosis of esophageal varices. These thrombi may have been the site of origin for pulmonary emboli. Other possible causes of the pulmonary vascular lesions are also discussed. In one case, there was a severe necrotizing arteritis in the pulmonary arterial tree.

Relation of Poverty and Race to Antenatal Infection

Abstract Perinatal infant mortality rates in poor families in the United States are far higher than rates in the non-poor. Analysis of 1044 consecutive autopsies on stillborn and newborn infants in...

Fetal and maternal features of antenatal bacterial infections

Of 1,044 consecutive autopsies on stillborn and newborn infants, 23 per cent demonstrated the presence of congenital pneumonia, often associated with chorioamnionitis. Negro and Puerto Rican patients had higher rates of the disorder than Caucasian infants, and ward patients a higher incidence than private and semiprivate patients. Clinical features of infection and the recovery of pathogenic bacteria from maternal reproductive and urinary tracts were significantly associated with the congenital pneumonia, the predominant organism being the same from mother and infants in half of the jointly cultured cases. The existence of nonbacterial, as well as bacterial, chorioamnionitis and pneumonia is suggested by the finding that in 37 per cent of the infants with congenital pneumonia no pathogenic organisms were identified.

The duration of maternal cigarette smoking, fetal and placental disorders

Data from a large prospective study of pregnancy were used to determine whether the number of years a mother had smoked cigarettes influenced the development of common fetal and placental disorders. Three disorders increased in frequency when mothers had smoked for more than 6 yr: placenta previa +143%, abruptio placentae +72% and large placental infarcts +37% (all P less than 0.05). Mothers current smoking habits had a smaller influence on the frequency of these disorders, and the effects of smoking were largely independent of maternal pregnancy weight gain. The placentas of smokers had microscopic evidences of underperfusion from the uterus. The placental abnormalities were influenced by both the number of years mothers had smoked and by their current smoking habits.

Prenatal Narrowing or Closure of the Foramen Ovale

In the current study cases are presented in which a prenatally narrowed or closed foramen ovale was associated with left heart chambers of normal or near-normal size. Such infants develop an increased pulmonary arterial muscle mass with hypertrophy and dilation of the right cardiac chambers during fetal life. Much of the arterial muscle mass persists after birth and may well be responsiblefor the early neonatal death of the infants. The longer asymptomatic survival of one infant suggests that therapy may be possible.

Abnormalities in infants of mothers with toxemia of pregnancy

Abstract A quantitative study has been made of organ and cellular development in 11 infants with fetal growth retardation associated with maternal toxemia of pregnancy. Body length, brain, heart, and lung weights were nearest normal values while adrenals, liver, spleen, and thymus were disproportionately small. Organs were subnormal in size largely because parenchymal cells had a subnormal amount of cytoplasm. Abnormalities were virtually identical in a second group of 11 infants retarded in their intrauterine growth by placental abnormalities. In both groups, organ abnormalities help to explain clinical problems encountered in these infants.

Children at High Altitude: Pulmonary and Renal Abnormalities

Changes in pulmonary arteries and renal glomeruli were assessed in children born and resident at high altitude (Leadville, Colorado). The hypoxia appears to arrest normal neonatal decrease of pulmonary arterial smooth muscle in some of these children. No abnormalities were found in pulmonary veins or capillaries. A quantitative study also demonstrated enlargement of renal glomeruli in the hypoxic children after the first month of life, apparently due to a proliferation of normal glomerular elements.

Pulmonary Vascular Changes with Chronic Unilateral Pulmonary Hypoxia

One main bronchus was ligated in each of twelve dogs and three calves. In eight of the animals, the bronchus reopened spontaneously with a 2 to 4 mm aperture permitting re-expansion of the associated lung. Both smooth muscle hyperplasia and hypertrophy developed in small arteries of the poorly ventilated dog lungs. In the calves, muscular hyperplasia and hypertrophy developed in small pulmonary veins of the hypoxic lungs. Since arterial pressures and pulmonary arterial oxygen saturation were presumably identical in hypoxic and control lungs, changes in vascular muscle are postulated to be the result of altered oxygen tension of the surrounding alveolar gas.

Alveolar hypoventilation and cor pulmonale secondary to damage to the respiratory center

Abstract A patient is described with alveolar hypoventilation due to organic disease of the brain in whom cor pulmonale developed. Lesions were found in the portion of the medulla where the respiratory center is thought to be located. As a consequence of alveolar hypoventilation, hypercapnia and hypoxemia developed. The hypercapnia resulted in clouding of the sensorium and further depression of the respiratory center. Vascular changes in the lungs, presumably the consequence of chronic hypoxemia, are believed to have contributed to the pulmonary hypertension and cor pulmonale.

Arteriolar Abnormalities with Chronic Systemic Hypertension A Quantitative Study

A quantitative study of arteriolar structure has been undertaken in 23 individuals with chronic hypertension and 18 normotensive controls. In the hypertensive individuals, some arterioles were found to have an increased, and others a subnormal, mass of medial smooth muscle. Both abnormalities often bear a definite relation to arteriolar sclerotic lesions, those arterioles proximal to sclerotic segments having an increased medial coat and those distal, an atrophic coat. Mean values for mass of arteriolar muscle were often normal in organs of the hypertensive patients. These anatomic features can be correlated with a variety of physiological and clinical observations in the disorder.