Citations

The major parts of the atrioventricular conduction system of the human heart were traced in 21 instances of ventricular septal defect: 19 were examples of variously located uncomplicated ventricular septal defects and two of the tetralogy of Fallot. In the presence of a ventricular septal defect, the conduction system was found to have a normal course, except when the ventricular septal defect lay in a position normally occupied by the conduction system. In each specimen with a defect posterior and inferior to the crista supraventricularis, the conduction system occupied a position posterior and inferior to the defect. In no instance did the conduction system occupy a position superior to a defect of this type. Defects located in the posterobasal portion of the muscular part of the ventricular septum sometimes were posterior to the main parts of the conduction system, so that the conduction tissue was related to the anterior edge of the defect. No example of a defect lying superior to the crista supraventricularis was studied. In our two examples of tetralogy of Fallot, the position of the conduction system was essentially similar to that occurring in the usual variety of ventricular septal defect, that is, posterior and inferior to the crista supraventricularis.

Among 13,314 necropsies following death from neoplastic and nonneoplastic diseases performed at the Mayo Clinic from 1942 through 1958, 189 cases of secondary malignant lesions of the pericardium were demonstrated, an incidence of 1.42 per cent. Carcinoma of the lung and breast, the lymphomas, and leukemia constituted the large majority of the primary malignant lesions that caused the pericardial metastasis. Fifty-five of the 189 patients were adjudged to have had some impairment of cardiac function as a consequence of the pericardial metastasis and the following conclusions concern this group. 1. In 47 patients (86 per cent), the lesions were either the immediate or a contributory cause of death. 2. The most common mechanism whereby metastatic lesions in the pericardium interfered with cardiac function was by the development of pericardial effusion. Next in frequency was effusion combined with myocardial invasion and then cardiac constriction by tumor. Combinations of these processes with malignant encroachment on the great vessels and with invasion of coronary veins were the other mechanisms noted. Involvement of coronary arteries and the cardiac nerve supply was not noted. 3. Pericardial fluid was significant in causing tamponade in 31 cases. The fluid was frankly hemorrhagic in a small minority of these cases although fibrinous pericarditis was present in 45 (82 per cent) of the group. Pleural effusion was present in 48 (92 per cent) of 52 cases and was usually bilateral. Ascites was present in 22 (50 per cent) of 44 cases; the quantity was usually rather small. 4. Only one patient had metastasis to the pericardium without metastasis to other thoracic structures; exclusive of patients with leukemia, 43 (92 per cent) of 47 patients had extrathoracic metastatic lesions. 5. Dyspnea, cough, pleural effusion, hepatomegaly, and thoracic pain were the most commonly recorded signs and symptoms that might be related to the pericardial lesions. However, more specific signs and symptoms directing attention to pericardial or cardiac involvement were not commonly recorded. 6. The diagnosis of pericardial metastatic disease was suspected or established in only 16 (29 per cent) of the 55 patients, although 34 (62 per cent) either received treatment for congestive heart failure or were given roentgen therapy to mediastinal structures. 7. Of the 27 patients whose electrocardiograms were available, 25 had T-wave abnormalities, 22 had low QRS voltage, and 15 showed sinus tachycardia. 8. Thoracic roentgenograms, made on 53 patients, supplied clues to the diagnosis of pericardial malignancy in 28.

The records of 66 necropsied cases of periarteritis nodosa in which there was no associated collagen disease were reviewed with reference specifically to the heart. Clinically, congestive heart failure and its manifestations were the most important cardiac findings. Congestive heart failure developed some time during the illness in 57 per cent of the patients, and 44 per cent died as a direct result of this cardiac condition. Myocardial infarction was diagnosed clinically in only three cases. The electrocardiogram was abnormal in 35 of 41 cases but was diagnostic of left ventricular hypertrophy in only six cases and of acute myocardial infarction in only three cases; in the other cases the changes were of a nonspecific nature. Pathologically, 41 of the 66 hearts had evidence of necrotizing arteritis of the coronary arteries; in 39 of these the arteritis had been acute, and in two it had healed. Forty-one of the 66 hearts exhibited myocardial infarcts. Evidence of acute pericarditis was found in 22 hearts; nine of these cases were attributed to uremia, one was due to transmural myocardial infarction, three could not be classified, and the remaining nine were attributed directly to the periarteritis nodosa. Forty-one of the 64 hearts that had been weighed were hypertrophied.

The high rate of necropsy in deaths among permanent residents of Rochester, Minnesota, provided a unique opportunity to study the prevalence of coronary heart disease and the frequency and mode of death resulting from this disease. In this community of approximately 30,000 population, necropsy was done in 73 per cent of all resident deaths during the years 1947 through 1952. Included in this group were 691 necropsies that represented 67 per cent of the 1,026 deaths of persons 20 years of age or older. Coronary heart disease caused death in 221 patients (23 per cent of all necropsies and 32 per cent of all necropsies on adults). These 221 coronary deaths in adults represented 41 per cent of the men and 22 per cent of the women. The coronary deaths were attributed to acute coronary failure (sudden death) in 94 patients (43 per cent), acute myocardial infarction in 87 patients (39 per cent), congestive heart failure in 32 patients (14 per cent) and thromboembolism in eight patients (4 per cent). The 87 patients dying during acute myocardial infarction died of congestive heart failure (30 per cent), myocardial rupture (24 per cent), acute coronary failure (23 per cent), and thromboembolism (14 per cent), with the remaining 9 per cent dying of a combination of acute myocardial infarction and additional serious systemic disease. The greatest number of deaths from coronary heart disease occurred during the seventh decade of life in men and the eighth decade in women. At least one coronary artery exhibited from 25 to 100 per cent obstruction from atherosclerosis in 513 hearts (74 per cent of the adult necropsies). These necropsies, representing two thirds of all deaths in adults in this community, disclosed that significant coronary-artery disease was present in three of four adults and was the cause of death in four of 10 men and two of 10 women.

A quantitative analysis was made of the pulmonary arterial medial thickness and index of medial surface area (ratio of medial tissue to pulmonary parenchyma) in 50 cases of uncomplicated ventricular septal defect in fetuses, infants, and children. The ages of the subjects ranged from 26 weeks of fetal life to 12 years. The results were compared with those obtained from a control group of the same age. During the fetal and newborn period, both the thickness and the index of surface area of the media were generally within normal limits, although in an occasional case pulmonary arterial branches were considerably thinner than those in corresponding controls. The subjects between 1 week and 5 weeks of age had a medial thickness and an index of medial surface area that were lower than the average values at the time of birth. In this regard the pulmonary arterial tree in cases of ventricular septal defect corresponded with that in normal newborn infants. Soon after, however, and most clearly from 8 weeks on, the subjects with ventricular septal defect showed a pronounced rise both in medial thickness and in the index of medial surface area, indicating the presence of considerable medial hypertrophy. Although intimal proliferation was observed in two infants of 11 and 27 days of age, it was uncommon in children less than the age of 1 year. Above that age it was almost invariably present. Plexiform or glomeruluslike structures were found in seven cases. The youngest patient with these lesions was 2½ years of age.

The pulmonary vascular tree was studied in 12 cases of uncomplicated atrial septal defect in fetuses, infants, and children. The ages of these subjects ranged from 24 weeks of fetal life to 11 years. A quantitative analysis was made of the medial thickness and of the index of medial surface area (ratio of medial tissue to pulmonary parenchyma) of the pulmonary arterial branches. In contrast to subjects with ventricular septal defect in corresponding age groups, the three fetuses in this series had medial hypertrophy, as indicated by a high index of medial surface area. In the postnatal group, both the medial thickness and the index of medial surface area were also usually greater than in the controls of corresponding ages, notably in two patients, who, at the ages of 7 weeks and 4 months, died of cardiac failure. No satisfactory explanation for these unexpected findings can be offered. Slight to moderate intimal proliferation was observed in some muscular and elastic pulmonary arteries, in bronchial arteries, and in pulmonary veins in several subjects. Thickening of the intima in elastic arteries was observed in a fetus of 26 weeks' gestation. Pronounced obliterative intimal changes were found in only one subject, an 11-year-old girl with severe pulmonary hypertension.

Among 60 necropsy specimens of isolated ventricular septal defects and more than 300 cases of ventricular septal defect observed at operation, 15 cases demonstrating unusual anatomic positions of the defect were found. The ventricular defect differed from the ordinary ventricular septal defect in that it usually occupied the position of the ventricular component of the defect in persistent common atrioventricular canal. For this reason it was named ventricular septal defect of the persistent common atrioventricular canal type. Deformities of one or both atrioventricular valves were common (nine of 15 cases). No atrial septal defects of the ostium primum type were present. Anatomic studies of the conduction tissue revealed that this tissue skirted the posterior and inferior aspects of the ventricular septal defect and that, as in persistent common atrioventricular canal, the course taken by the conduction tissue was unusually long, as a result of the peculiar posteroinferior position of the lower edge of the defect. The electrocardiographic features were striking. In all cases the mean electrical axis of the QRS lay above the isoelectric point; the vector loop obtained in the frontal plane from the scalar electrocardiogram was directed counterclockwise, and its main mass was above the zero line. In addition, in all cases there were signs of right ventricular overload, and in some cases of left ventricular overload as well. Electrocardiographic findings of this pattern have been thought by some authors to be diagnostic of persistent common atrioventricular canal, but we observed that they also occurred in each of the cases of isolated ventricular septal defect of the variety described herein. We recognize that in the usual variety of ventricular septal defect this electrocardiographic pattern occurs, but it does so uncommonly. We have not studied its exact incidence. The anatomy, hemodynamics, and surgical considerations are different in cases with this defect from those with persistent common atrioventricular canal. The surgical risk in these cases has been higher than that in the usual type of ventricular septal defect. In the discussion of the electrophysiologic theories that seek to explain the unusual electrocardiographic patterns in this group of cases, a new theory is offered, based on studies of the conduction system. In our opinion, the different orientation of the advancing fronts of depolarization is the result of congenital displacement of the bundle of His in its relation to the ventricular septal defect.