During the past 15 years an increasing knowledge of the pathologic changes occurring in the pulmonary arterial tree in various types of congenital heart disease has been accumulated.Botable among investigators who led the way in this field were Dammann and Ferencz,l Edwards,2 2 and Heath and Edwards,3 who demonstrated the progression of changes occurring in the small pulmonary arteries and arterioles which are responsible for the altered pulmonary resistance and blood flow in a variety of cases. Briefly stated, certain congenital defects (e.g., large ventricular septal defect and widely patent ductus arteriosus) with elevated pulmonary artery pressures maintain a high pulmonary vascular resistance early in life by persistence of the fetal pattern of thick medial hypertrophy of the small muscular pulmonary arteries and increased vascular tone. Subsequently, intimal lesions develop which produce abrupt narrowing or occlusion of the arterioles and small arteries. In contrast, patients with certain congenital defects (e.g., atrial septal defect of ostium secundum type) have a reduced pulmonary vascular resistance permitting large blood flow through an abundant dilated vascular bed at normal or mildly elevated pulmonary blood pressures. It is not until much later in life, usually in the third or fourth decade, that intimal lesions may appear which are similar to those seen at an earlier age in the patients with high pulmonary vascular resistance persisting from early life. It is these intimal occlusive lesions which, when widespread, appear to play the major role in determining pulmonary vascular resistance and probably represent an irreversible condition.Thus, in the patients under consideration for surgical repair of congenital defects, the assessment of the nature of the pulmonary vascular changes is important.The contributions of the previously mentioned workers have revealed mostly qualitative changes rather than quantitating the total extent of the pulmonary arterial disease. The important question is: &dquo;How extensive is the pulmonary arterial disease, and are the changes reversible?&dquo; Random lung biopsies do not reveal the true extent of arterial disease for they lack a broader perspective due to the focal nature of occlusive intimal lesions.The relationship between pulmonary arteriography and the histology of the pulmonary arterial bed was first demonstrated in 1951 by Evans,4 and later by Evans and Short5 and Shorts' using post mortem angiograms of the arterial tree. These workers studied the pathology of vascular changes in congenital heart disease, as well as other cardiac conditions, by a combination of arteriograms and histology. The findings have served in the past as a base line for future studies of the pulmonary arterial tree in living patients.In 1958, Bell, Shimamura, and Guthrie8 reported a clinical method for selective filling of the small pulmonary vessels, which could be performed during the course of cardiac catheterization. This method utilized injection of a small amount of radiopaque...