Histological changes in the lung in diseases associated with pulmonary venous hypertension

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Summary

A description is given of the histological changes found in the pulmonary arteries, veins and parenchyma of 13 patients with diseases associated with pulmonary venous hypertension. The cases were considered in three groups. The first group comprised 6 patients who had anatomical malformation of the heart leading to pulmonary venous hypertension from birth; none of them had cardiac septal defects so that the associated pulmonary arterial hypertension was related solely to the elevated blood pressure in the pulmonary veins. The second group consisted of 3 patients who had mitral atresia and a common ventricle, so that the pulmonary arterial hypertension was primarily due to a direct communication between the systemic ventricle and the lesser circulation. The third group consisted of 4 patients with heart disease leading to acquired pulmonary venous hypertension.

The configuration of elastic tissue in the pulmonary trunk is of fœtal, aortic type when the hypertension in the pulmonary arteries and veins is present from birth. It is of the adult pulmonary type when the elevation of blood pressure in the pulmonary artery is acquired in adult life.

The small pulmonary arteries show various grades of hypertensive pulmonary vascular disease.

The pulmonary veins are thick-walled owing to increase in muscle tissue in the media and to intimal fibrosis. The formation of a distinct compact muscular media with internal and external lamin˦ in the wall of the vein is pathognomonic of pulmonary venous hypertension. The characteristic severe intimal fibrosis in the vein may be cellular or acellular; it is more pronounced in the adult with acquired pulmonary venous hypertension than in the child with congenital pulmonary venous hypertension.

In the lung substance, the earliest sign of pulmonary venous hypertension is capillary distension with pulmonary h˦mosiderosis. Later severe changes occur. These are the formation and subsequent organisation of œdema coagulum in the alveolar spaces and walls. Finally, the affected lung is solid with intra-alveolar fibrosis, chronic pulmonary interstitial fibrosis, and packing of the air spaces with macrophages, many of which contain h˦mosiderin.

Spicules of bone form in the alveolar spaces infrequently. The changes in the lung substance are characteristic of, but not pathognomonic of, pulmonary venous hypertension since they occur in other conditions, including pulmonary infarction.

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Dr. Heath was in receipt of a Rockefeller Travelling Fellowship in Medicine while participating in this investigation, which was supported in part by research grant No. H3531 from the National Heart Institute, National Institutes of Health, United States Public Health Service.

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