Citations

The pulmonary vessels in 2 cases of cor triloculare with subaortic stenosis are compared. Each showed medial hypertrophy of the muscular arteries of the lungs. In 1 case concerning an 8 year old boy this class of vessels showed, in addition, severe intimal fibrosis. The arterioles were normal. It is emphasized that the changes in the pulmonary arteries are similar to those seen in the Eisenmenger complex, in coarctation of the aorta proximal to a patent ductus arteriosus and in the normal fetus. These conditions, though anatomically different from each other and from cor triloculare with subaortic stenosis, are functionally alike in that there is in each a common ventricular ejectile force for the pulmonary and the systemic circulations in the absence of stenosis in the major arterial pathways to the lungs. It is suggested that in cor triloculare biatriatum with subaortic stenosis, the structure of the pulmonary muscular arteries is, and that their function seems, similar to that of the fetus. The changes in the case of the malformation may be considered a carry-over from fetal life.

The speed at which the excitatory process spreads through a certain segment of the myocardial syncytium depends upon the orientation of the fibers in that segment to each other and to the point of origin of excitation. Spread down a strip of fibers of which the long axis is parallel to the long axis of the strip is rapid as compared with spread down a strip in which the fibers run at a right angle to the long axis of the strip. Endocardial activation is rapid, not because of the presence of Purkinje fibers, but because the subendocardial bands of myocardium form a network through which excitation can move rapidly along the long axis of the fibers. Spread across the septum in bundle-branch block and across the free wall of the left ventricle in the normally activated heart is slow because excitation is moving through fibers the long axis of which is prependicular to the advancing wave of excitation.

A clinicopathologic study of 51 cases of mitral stenosis with intracardiac mural thrombi is presented with particular reference to the locations of these thrombi and their relationship to the associated thromboembolic phenomena. In 27 cases the thrombi were present only in the left side of the heart, in 15 cases they were in both sides of the heart, and in 9 cases they were present only in the right atrium. Of 42 cases in which thrombi were located in the left side of the heart, in 20 the thrombi were limited to the left auricular appendage. In the remaining 22 cases in this group the thrombi in the left side of the heart were situated on the main atrial wall, in the auricular appendage and on the main atrial wall together, or in the left ventricle. Systemic arterial emboli occurred frequently regardless of the particular site in the left side of the heart at which the thrombus formed. Of 24 cases in which thrombi were situated in the right side of the heart, in 20 the thrombi were restricted to the right auricular appendage.

Two cases of mitral insufficiency are reported. In 1 case the lesion was produced by rupture of the chordae tendineae of the posterior leaflet of the mitral valve. In the other case it was produced by fibrous adhesion of the posterior leaflet of the mitral valve to the underlying left ventricular wall, which occurred during healing of subacute bacterial endocarditis. Changes occurred in the pulmonary vascular bed which are essentially identical with those found in mitral stenosis.

Persistent pericardial effusion in the absence of obvious preceding or concurrent disease presents a baffling problem. In such cases chylopericardium, cholesterol pericarditis, lupus erythematosus, malignant disease, myxedema, severe anemia, and scleroderma, must be considered. Six cases are reported with large effusions present for from 1 to 11 years. The diagnostic measures to be used, the results of histologic examination, and the effects of surgery on the clinical course are discussed.

In complete transposition of the great vessels, survival is possible only when a route of access exists by means of which venous blood may enter the lungs. This report concerns 2 patients in relatively good health in whom a high degree of mixing of venous and arterial blood occurred through an atrial septal defect. The diagnosis was established in both patients by cardiac catheterization.

Oxygen saturation of arterial and central venous blood was measured continuously during the Valsalva maneuver in patients with and without intracardiac defects. The majority of patients with atrial septal defects and patients with ventricular septal defects and high right ventricular pressure showed a sharp decrease in saturation of radial artery blood shortly after the maneuver. These changes were not recorded accurately by ear oximetry. The patients with shunts uniformly showed a rapid increase in saturation of pulmonary artery blood during the initial period of increased airway pressure. This effect was not observed in patients without shunts. These reactions may be of special diagnostic value under certain circumstances.

Congenital insufficiency of the pulmonary valve may result if the valvular cusps develop faultily or fail to develop. It is commonly associated with ventricular septal defect, with or without pulmonary stenosis. Under these conditions a continuous precordial murmur may be present. Less commonly, congenital pulmonary valvular insufficiency may appear as an isolated cardiac malformation.

Necropsy studies in cases of pulmonary hypertension of unknown cause show structural changes in the pulmonary vessels that are called irreversible. Acetylcholine chloride was infused at a rate of 2 mg. per minute into the outflow tract of the right ventricle of a 48-year-old woman who had pulmonary hypertension. The mean pulmonary artery pressure decreased from 56 to 25 mm. Hg and the pulmonary flow increased slightly. These findings are consistent with the theory that so-called idiopathic pulmonary hypertension may at some stage be maintained by vasoconstriction.

Survival following surgical correction of congenital cardiovascular defects is unlikely if pulmonary hypertension cannot be decreased significantly. Infusions of acetylcholine decreased pulmonary vascular resistance in 6 of 11 patients having pulmonary hypertension associated with atrial or ventricular septal defects. When the acetylcholine was combined with the breathing of oxygen, resistance decreased further. These findings are consistent with the theory that, at some stage, the pulmonary hypertension in cases of congenital heart disease is maintained at least in part by vasoconstriction and therefore is potentially reversible.