Ralph C. Scott

The Correlation Between the Electrocardiographic Patterns of Ventricular Hypertrophy and the Anatomic Findings

The correlation of the electrocardiogram with anatomic evidence of ventricular hypertrophy, while laden with numerous pitfalls, still remains the best available means of determining the accuracy of the electrocardiographic diagnosis of ventricular hypertrophy. In 100 instances of isolated left ventricular hypertrophy (LVH) demonstrated at autopsy, a positive electrocardiographic diagnosis was made in 85 per cent by use of conventional criteria. However, in other studies designed to test the reliability of these criteria, it was found that a false-positive diagnosis was made in 10 to 15 per cent of the cases. The electrocardiographic diagnosis of right ventricular hypertrophy (RVH) is more difficult. In electrocardiographic studies, confirmed by autopsies, the correlation has ranged from 23 to 100 per cent, while the number of false-positive diagnoses has been as high as 33 per cent. The correct electrocardiographic diagnosis is more frequent in RVH due to congenital heart disease than to acquired heart disease. The significance of the rSR′ pattern in right precordial leads is discussed. Its occurrence in anatomic RVH and the problem of the electrocardiographic diagnosis of RVH in the presence of right bundle-branch block (RBBB) are reviewed. Combined ventricular hypertrophy (CVH) is frequently missed in the electrocardiogram, the diagnosis having been made in only 8 to 26 per cent of cases proved at autopsy. The unreliability of the electrocardiographic diagnosis of LVH in the presence of left bundle-branch block (LBBB) is documented. The precise electrophysiologic phenomena that occur in ventricular hypertrophy are still largely conjectural. The more commonly accepted hypotheses are reviewed. The lack of close correlation between ventricular wall thickness or respective ventricular muscle mass and the individual electrocardiographic patterns is emphasized. The possible explanations for some of these discrepancies are presented.

Observations on the Assessment of Cardiac Hypertrophy Utilizing a Chamber Partition Technique

Three hundred fifty-four adult human hearts were dissected utilizing a technique similar to those previously described by Müller1 and Lewis.2 A classification was synthesized on the basis of anatomic characteristics of 100 normal hearts. Presumptive evidence of either left or right ventricular overload, provided by clinical and autopsy observation, served as essential corollary data in establishing normal limits. The existence of hypertrophy was readily recognized in hearts in which one or both ventricles increased in mass sufficiently to surpass the defined upper limit. Isolated ventricular hypertrophy of mild degree was recognized as a consequence of an abnormal LV+S/RV ratio in 58 hearts in which ventricular weights were within the normal range. Factors which would be expected to result in left or right ventricular overload were demonstrable in 42 of these cases. Atrial hypertrophy correlated well with hypertrophy of the corresponding ventricle and served as an invaluable aid in recognition of mild degrees of combined ventricular hypertrophy. This classification constitutes the basis for a subsequent correlative electrocardiographic study.

Diabetes and the heart

Magnitude of the problem. The estimated prevalence of known coronary artery (atherosclerotic) disease (CAD) in the United States is 3~370,000 with an annual mortality of 675,580.’ The number with clinically silent CAD is not known, Coronary artery disease has assumed epidemic proportions although recent observations suggest some decline in age-adjusted death rates.2 The estimated prevalence of diabetes mellitus in this country is nearly 5,000,000.3 The annual reported mortality of about 38,0003 is thought to be an underestimate and it has recently been suggested that as many as 300,000 diabetic patients die each year.” Diabetes has moved recently from eighth to the fifth leading cause of death in the United States.“, 5 Importance of coronary artery disease in diabetes. Coronary artery disease accounts for more than half of the deaths in diabetic subjects (with onset after the age of 20) and is thus the most frequent and hazardous risk in the diabetic population.“, ’ Autopsy studies reveal an increased incidence (and severity) of CAD in the diabetic subject (45 to 70 per cent) when compared to the nondiabetic subject (8 to 30 per cent).’ Several features of CAD in the diabetic subject deserve special emphasis. In the younger diabetic

Prediction of coronary artery disease in a population of insulin-requiring diabetic patients: Results of an 8-year follow-up study

To identify predictors of clinical coronary artery disease, 110 insulin-requiring diabetic patients with no symptoms suggestive of cardiac disease and with a normal resting ECG underwent metabolic and noninvasive cardiovascular screening including a history and physical examination, exercise ECG, M-mode echocardiography, and chemical laboratory testing. During a median follow-up interval of 100 months, 14 of these patients had clinical evidence of coronary artery disease consisting of acute myocardial infarction, sudden cardiac death, or anginal chest pain with angiographic documentation of occlusive coronary artery disease. Baseline variables that were univariately predictive of subsequent clinical coronary disease included age, peak treadmill heart rate, and retinal neovascularization. According to multivariate analysis the peak treadmill heart rate was the single most important predictor of subsequent development of clinical coronary disease. A treadmill ECG result that was either abnormal or inconclusive because of failure to achieve 90% of predicted maximal heart rate identified each patient in whom clinical coronary artery disease developed within 50 months after entry testing. Thus the entry treadmill ECG provided prognostic information not available from the history and physical examination results, but little further prognostic information was provided after the first 50 months of follow-up, suggesting the need for serial testing.

The anatomy of chronic cor pulmonale secondary to intrinsic lung disease

Summary Knowledge about the relationship of right ventricular hypertrophy to intrinsic lung disease depends upon detailed quantitative assessment of both organs. There is considerable overlap in the thickness measurement of normal and abnormal right ventricles measured in the anterior wall of the pulmonary conus. A measurement of 6 mm. or greater in this area is a reliable guide to the existence but not the severity of RVH. The mass of the free wall of the right ventricle in relation to that of the left ventricle and interventricular septum (LV+S/RV) provides a tool with considerable merit in the recognition and quantitation of chronic cor pulmonale. Pulmonary hypertension secondary to intrinsic lung disease is induced by a variety of anatomic and functional alterations determined and conditioned by the nature of the pulmonary disease. Assignment of a primary role to one or another factor does not yet seem justified, particularly in a complex disorder such as pulmonary emphysema. Here, although physiologic data are abundant, quantitative morphologic study of the lung has not yet received wide usage. Three principal mechanisms contribute to increased PVR secondary to intrinsic lung disease. Hypoxia, resulting from impaired ventilation or impairment of diffusion, may induce a functional and partially reversible increase in PVR through a mechanism as yet undetermined. Through distortion and obliteration of small blood vessels, parenchymal destruction produces an irreversible increase in PVR which may be either latent appearing only during stress, or manifest at rest. Finally, secondary hypertensive vascular changes may so restrict the vascular bed that perfusion is decreased to a degree incompatible with life. Abnormal vascular communications have been demonstrated in a variety of situations, but their hemodynamic significance is uncertain. Thus far, histologic examination of the lungs in chronic emphysema has shown only minor evidence of either hypoxic or secondary hypertensive vascular changes. On the other hand, there is evidence, as yet only partially evaluated, that restriction of the vascular bed by parenchymal changes combines with loss of respiratory surface to form the basis for pulmonary hypertension in panlobular emphysema. In contrast, the severity of the ventilatory disturbance may be more important than loss of either vascular bed or respiratory surface in central lobular emphysema. Development of new methods for postmortem measurement of the pulmonary vascular bed in relation to disturbance of respiratory volume and surface area may help resolve these issues not only in chronic emphysema, but also in the broad spectrum of intrinsic pulmonary disease with which significant pulmonary hypertension may be associated.

Visualization of the Coronary Arteries during Life

By retrograde catheterization of the carotid or the brachial arteries small polyethylene or woven catheters have been inserted into the ascending aorta in 10 individuals. Diodrast or Neo-Iopax solution was forcibly injected and serial roentgenograms were rapidly taken. The coronary arteries or branches were demonstrated in 5 of the subjects. Similar studies were made in 5 dogs with normal hearts, and also in 10 dogs in whom a coronary artery had previously been obstructed. In certain of the normal animals not only the larger, but also smaller branches were clearly shown and the absence of filling in obstructed vessels was demonstrated.

Current concepts of ventricular activation in the normal heart, in left bundle branch block, and in left bundle branch block with myocardial infarction

Abstract The current concepts of ventricular activation based upon recent studies in the normal heart have been reviewed. These concepts include the activation of the left and right septal surfaces, the septal mass, and the free right and left ventricular walls. The roles of the bundle branches and the Purkinje system are emphasized. The alterations in ventricular activation that occur as a result of complete left bundle branch block (LBBB) are summarized. The evidence for and against a physiologic “barrier” between the right and left septal masses is presented. The vector representation of depolarization of the septum and free ventricular walls in the normal heart and in LBBB is briefly summarized. Some of the newer concepts of ventricular activation in LBBB and myocardial infarction are reviewed.

Pressor and Depressor Responses to Tilting in Hypertensive Patients

The responses of intra-arterial blood pressure to passive head-up and head-down tilting are described for 50 patients with well established hypertension and compared to results obtained in subjects with normal cardiovascular systems. This study indicates that abnormal depressor and pressor responses are present in many patients with hypertension, that depressor reflexes are independent of pressor reflexes, that marked variations of depressor and of pressor reflex activity occur between hypertensive patients, but that the combination of depressor-pressor responses in a given patient usually remains constant.