Edwards, Jesse E.

In a pathologic collection of 722 congenital heart lesions we have observed 10 cases in which a ventricular septal defect was associated with obstruction to normal left ventricular outflow. These cases are presented in the framework of a classification relating hemodynamics to the position of the obstructing lesion and the size of the ventricular septal defect. One additional case observed clinically and at operation is also reported to make more nearly complete the classification of the anatomic arrangements in which the common denominators are ventricular septal defect and obstruction to normal ventricular outflow.

A study was made of the configuration of the elastic tissue of the pulmonary trunk in 6 cases of idiopathic pulmonary hypertension. The ages of the patients ranged from 12 to 54 years. The pattern was that of the adult pulmonary type in the 5 female patients, whereas it more closely resembled the fetal, aorta-like type in the single male patient. These data are interpreted as indicating that idiopathic pulmonary hypertension is acquired in most cases but that it may be present from birth in a minority of instances.

This study attempts to bring into focus certain details which have not been described adequately in textbooks of anatomy. This information is now of considerable significance because of its role in the genesis and surgical treatment of mitral stenosis. Variations in the size and shape of the mitral valve are described, with particular reference to the fact that valve commissures, or junctional zones between the leaflets, occur in the normal valve. Measurements of commissures, chordae tendineae and valve leaflets are presented, with a discussion of the significance of some of these measurements.

The purpose of this investigation was to study the incidence and location of systemic arterial occlusion and pulmonary embolism in a consecutive series of cases of fatal acute myocardial infarction. Another consecutive series of cases in which healed myocardial infarction was demonstrated at necropsy was similarly studied. In none of the cases included in this study had anticoagulant therapy been employed. Massive pulmonary embolism was the most frequent fatal thrombo-embolic complication found among the cases of acute myocardial infarction. Cerebral infarction was the most frequent fatal thrombo-embolic complication found among the cases of healed myocardial infarction. Cerebral infarction was the most frequent fatal systemic arterial thrombo-embolic lesion in both groups. Acute splenic and renal infarcts were frequently demonstrated but with one exception appeared to play an incidental role in the clinical course of the patients. Although systemic arterial occlusion was frequently found in association with intracardiac mural thrombi, there were many other cases in which evidence of systemic arterial occlusion was found in the absence of intracardiac mural thrombi. A positive correlation existed between the presence of pulmonary and systemic arterial occlusion and the occurrence of congestive cardiac failure.

This is a study of the location and incidence of intracardiac thrombi in acute and in healed myocardial infarction. In myocardial infarction intracardiac thrombi occur predominantly in the left ventricle. Anterior myocardial infarcts are more commonly associated with mural thrombi than posterior myocardial infarcts. Large myocardial infarcts and congestive failure are factors which predispose to the formation of left ventricular mural thrombi in myocardial infarction.

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.

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.

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.

The relative importance of organic changes and vasoconstrictive influences in the production of increased pulmonary vascular resistance in congenital heart disease is problematic. With use of a grading system previously described, a study was made of the relation between each of the grades of hypertensive pulmonary vascular disease associated with ventricular or atrial septal defects and the change of pulmonary artery blood pressure immediately following closure of the abnormal communications. The immediate reversibility of the pulmonary hypertension varies inversely with the severity of the structural changes.