Harold E.B. Pardee

Relation of myocardial disease to abnormalities of the ventricular complex of the electrocardiogram

Abstract Sixty cases have been studied in attempting to determine a relation between the character of the ventricular complex of the electrocardiogram and the pathological findings in the ventricular myocardium. Of 13 cases with a normal ventricular complex, a normal myocardium was found in 7. In the other six there were slight morphological changes. Of 47 cases with abnormal ventricular complexes a normal myocardium was found in 9 (19 per cent). The abnormal features of the electrocardiograms in these 9 cases were similar to those found in other cases which revealed slight or moderate pathological changes in the myocardium. In the other 81 per cent of cases with abnormal ventricular complexes there were definite myocardial changes. When the electrocardiographic abnormality involved only the QRS group, the T-wave being normal, there were found only slight or moderate myocardial changes. Although there was, in general, an association of increased duration of QRS with cardiac enlargement, yet there were notable exceptions. When the T-wave was abnormal, with or without QRS abnormality, there was a great range in the extent and the degree of the myocardial changes discovered. A frequent but not constant association was seen between the coronary T-wave and focal myocardial lesions. There was a constant association between an elevated or depressed S-T interval and the finding of areas of acute myocardial degeneration, though not always with areas of infarction. The ventricular complex attributed to marked left ventricular hypertrophy affords an exception to this statement regarding the S-T interval. Right bundle-branch block occurred twice without morphological myocardial changes being discovered and three times with such changes. Left bundle-branch block occurred twice, each time associated with myocardial changes. A review of the literature showed a few comparable studies, all of which were in general agreement with these findings.

The pulse and respiratory rates during labor as a guide to the onset of cardiac failure in women with rheumatic heart disease

I N A previously reported study1 of the pulse and respiratory varial ions of 180 normal women during labor, it was observed that the pulse and respirations remained practically unchanged throughout the first stage of labor. With the advent of bearing down efforts ill the second stage of labor 4 per cent of patients showed a rise of the pulse rate to above 110 per minute with respirations of not. over 24 per minute. Such elevations were considered as established only when they persisted for at least forty-five minutes. Thirteen per cent showed a rise in t,he respiratory rate to above 24 per minute with the pulse rat.e not over 110, and 7 per cent showed a rise of both pulse and respirat,ory rates above these values. The levels of 110 and 24 were chosen arbitrarily since a large percentage of patients approached or reached these values but relatively few esceeded them. Prolonged labor and prulungetl second stage were found to predispose to such rises but no definite influence of analgesia or of the particular analgesic used could be observed. We have extended these studies to women wit,h rheumatic+ heart disease to note if their pulse and respiratory variations during labor differed in any way from those of normal women su as to give a warning of the approach of serious cardiac insuficiency~. The 200 patients studied were first seen in the ante-yartnm clinic at various stages of t,heir pregnancy. The diagnosis of the particular form of heart disease was made at this t,ime and sometimes was amended as later observations seemed t,o indicate. The patients wer(’ classified as IO their functional capacit,y (Class 1. 2. 3, or 4) according to t,he criteria uf the New York Heart Association, and as they were followed progressively in tile antepartum clinic, this diagnosis was changt~cl as indicat,ions seemed t.0 warrant. At the onset, of labor or as soon thereafter as the patient was admitted t,o the hospital, the pulse and respirations were counted every fiftc(:rr minutes between pains and charts made of this similar to those appear-~___.

Abnormal electrocardiograms in patients with syphilitic aortitis

Summary Of 50 patients of syphilitic aortitis which were studied, two-thirds had aortic insufficiency and one-third did not; about one-third had aneurysm; 5 had both aortic insufficiency and aneurysm. In general the patients with aortic insufficiency were older than those without; shortness of breath was their chief complaint, though pain in the anterior chest was frequent, and almost one-third complained of edema. All but one showed a systolic murmur at the aortic area. The electrocardiogram showed an abnormal T-wave in 85 per cent of these patients, and in 20 per cent it was of the “coronary” type. It was abnormal in only 38 per cent of those without the valve lesion, and only 1 case (7 per cent) showed a wave of the “coronary” type. Ten autopsies were obtained on these 50 cases, and from a study of the autopsy material and the electrocardiographic records it appeared that the abnormality of the T-wave is probably due to encroachment upon the lumen of the coronary orifices by the syphilitic disease in the sinuses of Valsalva. The greater frequency of the T-wave changes in the group with aortic insufficiency is due to the fact that in these patients the aortitis involves the region of the valves near which the coronary arteries originate. Changes in the T-wave of patients with syphilitic aortitis should be viewed as an indication of serious coronary involvement, but not necessarily as an indication of myocardial pathology. This observation has an extremely important bearing upon our general understanding of the causes of abnormality of the T-wave.

Electrocardiographic findings in rheumatic heart disease

and therefore would not afford criteria for the diagnosis. On the other hand, it is certainly true that there are many instances in which the electrocardiogram may give the only sign of rheumatic activity. This is more apt to be true at the end than at the beginning of an acute attack. I have seen patients in whom there were no joint symptoms and who had only electrocardiographic changes. I remember one such patient, who came into the clinic ambulatory, with fever and with electrocardiographic changes, and we did not quite know why. She then developed a pericardial rub, and the reason for the electrocardiographic changes became evident. She later developed some joint symptoms which led to a diagnosis of rheumatic fever. But that case I think is exceptional. Usually the electrocardiogram is a manifestation of the disease which is diagnosed on the basis of other findings. There are in general three types of pathological changes: (1) There is a general inflammatory reaction with edema, interstitial swelling, leukocytosis and fibrinous degeneration. (2) There is the specific type of pathological change known as the Aschoff body, which is found in the interstitial tissue surrounding the small muscle bundles and particularly in the interstitial tissue surrounding the smaller arteries. (3) And then there is an arteritis which is also a definite rheumatic manifestation and which occurs in the coronary arteries as well as in other arteries of the body. We are particularly concerned with the coronary arteries where it causes an intimal thickening and eventually a fibrosis of the vessel wall.

PANEL DISCUSSION ON HEART DISEASE

MODERATOR STONE: It is unnecessary to make extended comment before a geriatrics group as to the importance of heart disease in older subjects. It is always a problem that we have with us, and it is the purpose of this panel to bring you the views of the participants with respect to certain aspects of heart disease. Inasmuch as atherosclerosis is perhaps the most important cause of heart disease in older individuals, I am going to call upon Dr. Wilkinson to develop for us his thoughts with respect to the pathogenesis of atherosclerosis. DR. WILKINSON: The current concept that many of us have as to the development of atherosclerosis is based not only on experimental data, but on pathologic changes seen in human beings. At the risk of oversimplification, I would say that there is, first, an inherent defect in the artery, a metabolic defect that