Robert E. Whalen

Type A behavior, hostility, and coronary atherosclerosis.

&NA; Type A behavior pattern was assessed using the structured interview and hostility level was assessed using a subscale of the Minnesota Multiphase Personality Inventory in 424 patients who underwent diagnostic coronary arteriography for suspected coronary heart disease. In contrast to non‐Type A patients, a significantly greater proportion of Type A patients had at least one artery with a clinically significant occlusion of 75% or greater. In addition, only 48% of those patients with very low scores (less than or equal to 10) on the Hostility scale exhibited a significant occlusion; in contrast, patients in all groups scoring higher than 10 on the Hostility scale showed a 70% rate of significant disease. The essential difference between low and high scorers on the Hostility scale appears to consist of an unwillingness on the part of the low scorers to endorse items reflective of the attitude that others are bad, selfish, and exploitive. Multivariate analysis showed that both Type A behavior pattern and Hostility score are independently related to presence of atherosclerosis. In this analysis, however, Hostility score emerged as more related to presence of atherosclerosis than Type A behavior pattern. These findings confirm previous observations of increased coronary atherosclerosis among Type A patients. They suggest further that an attitudinal set reflective of hostility toward people in general is over and above that accounted for by Type A behavior pattern. These findings also suggest that interventions to reduce the contribution of behavioral patterns to coronary disease risk might profitably focus especially closely on reduction of anger and hostility.

P-Wave Analysis in Valvular Heart Disease

Electrocardiographic analysis of the P waves occurring in a series of 113 normal subjects and 100 patients with specifically defined valvular lesions are reviewed. The former methods of analysis showed a marked lack of specificity. By dividing the P wave in lead V1 into initial and terminal portions, a measure designated as the P terminal force has been derived. This measure is of value in two respects: (1) it correctly separates normal subjects from those patients with left-sided valvular lesions in 92 per cent of this series and (2) once a given valve lesion is suspected clinically, this measure enables one to make an estimation of the severity of that lesion from the degree of abnormality of the P terminal force at V1. The P terminal force does not indicate the type of valvular disease present, nor does it correlate with any one specific hemodynamic measure. The abnormality does appear to be related, within each separate type of valve disease, to the specific hemodynamic abnormality of that type of val...

Cardiovascular and blood gas responses to hyperbaric oxygenation

Abstract Ten normal subjects were studied while they breathed air and 100% oxygen at 1 and 3.04 atmospheres. Oxygen inhalation at 3.04 atmospheres was associated with a significant increase in arterial and venous pO 2 and O 2 content. Hemoglobin in the venous circulation was completely saturated in 8 of 10 subjects. Oxygen inhalation at 3.04 atmospheres produced a small but significant increase in venous pCO 2 , presumably due to the loss of the buffering effect of reduced hemoglobin. Heart rate and cardiac output fell significantly with little change in stroke volume during oxygen inhalation at 3.04 atmospheres, indicating that the decrease in cardiac output was rate-dependent. There was little change in mean arterial pressure but an increase in calculated peripheral resistance during oxygen inhalation at 3.04 atmospheres. Two subjects who demonstrated signs of acute oxygen intoxication did not differ significantly from the group as a whole either in terms of blood gas values or patterns of hemodynamic response.

Effect of Ventricular Rate on the Cardiac Output in the Dog with Chronic Heart Block

The effect of heart rate on cardiac output and associated rate induced hemodynamic changes in dogs with chronic heart block is presented and discussed. At heart rates below 60/min., the stroke volume was maximum and relatively constant, and the cardiac output was largely rate-dependent. These relationships did not exist at ventricular rates above 60/min. Cinefluorographic evidence of decreased diastolic ventricular filling with increasing ventricular rates is presented. At very slow and very fast ventricular rates, the cardiac output decreased despite an increase in right atrial and right ventricular end-diastolic pressure. At slow rates the decreased output was due to rate alone, while at rapid rates it was attributed to the decreased diastolic filling period and resistance to ventricular distention, resulting in decreased diastolic filling.

Hereditary nephropathy, deafness and renal foam cells

Abstract A family with hereditary nephropathy and deafness is described. Postmortem examination of one member of the family revealed changes compatible with chronic glomerulonephritis. Large numbers of foam cells were noted in the cortex of the kidneys. The staining characteristics of these cells suggest that they contain neutral fat, mucopolysaccharides, phospholipids, cholesterol and phosphatides. Foam cells may be seen in a variety of renal lesions. A review of the records of 105 consecutive autopsy cases of chronic glomerulonephritis led to the discovery of foam cells in nine patients. Two had hereditary nephropathy and deafness; one had hereditary nephropathy alone; two had a questionable family history of renal disease; three gave no family history of renal disease; and one was thought to be an example of arabinosis. A review of the records of 105 consecutive autopsy cases of pyelonephritis uncovered six patients with renal foam cells. Only one of these had a family history of renal disease. Among this group were patients with xanthogranulomatous pyelonephritis, the de Toni-Fanconi syndrome with cystinosis, and Wegeners granulomatosis with renal abscesses. Although renal foam cells thus are not limited to cases of hereditary nephropathy, their presence should lead to a vigorous search for a family history of renal disease. The basic pathological picture in hereditary nephropathy with deafness is probably quite similar to that of chronic glomerulonephritis, but pyelonephritis may frequently be superimposed. At present there is no explanation for the pathogenesis of hereditary nephropathy or renal foam cell formation.

Demonstration of the dynamic nature of idiopathic hypertrophic subaortic stenosis.

Abstract Isoproterenol infusion converted a patient with potential hypertrophic subaortic stenosis into one with all the hemodynamic features of severe hypertrophic subaortic stenosis in less than 15 minutes. This response was not observed during isoproterenol infusion in 15 patients with left ventricular hypertrophy from a variety of causes. Further study of this drug in patients with left ventricular hypertrophy of unknown etiology is indicated. Infusion of isoproterenol may serve as a provocative test to identify those patients with early or latent forms of hypertrophic subaortic stenosis. Such studies will also allow a more careful examination of the hemodynamic features of the syndrome before the signs and symptoms have become so severe as to preclude extensive investigation.

Digitalis and experimental myocardial infarction

Abstract Acetylstrophanthidin tolerance tests were carried out in a series of farm pigs in the conscious unrestrained state. Serial testing of these animals showed that the dose to produce cardiac arrhythmias, the duration of the arrhythmias, and the gastrointestinal toxic dose were predictable and stable measures. Three groups of animals were compared: a control group, a sham operated group, and a group who experienced gradual circumflex coronary occlusion and subsequent infarction. The experimental infarction was induced by an Ameroid constrictor. With this technique, it was possible to carry out serial observations of acetylstrophanthidin tolerance during the evolution of the infarction. The toxic dose, the duration and the arrhythmias, and the gastrointestinal intoxicating dose remained unchanged in the control and sham groups. In the 8 animals studied during the evolution of experimental myocardial infarction, the average intoxicating dose was reduced by approximately 1 3 , the arrhythmias lasted twice as long and the usual pattern of cardiac intoxication preceding G1 symptoms was reversed.

ELECTRICAL HAZARDS ASSOCIATED WITH CARDIAC PACEMAKING

The success1*2 of implantable cardiac pacemakers has served to focus attention on methods of maintaining an adequate heart rate before implantation can be accomplished. While drug therapy is effective in many cases, electrical stimulation of the heart has assumed an increasingly more important role-especially in the management of patients in the period immediately preceding and during the surgical implantation of a pacemaker. Because pacing with external electrodes presents certain problems, internal pacing either by an electrode catheter in the right ventricle or by previously placed myocardial electrodes is now used routinely in many centers. Electrode catheters or myocardial electrodes carry certain inherent dangers because they afford a low resistance path directly to the myocardium by circumventing the usually protective resistance provided by the skin and other body tissues. Thus the possibility of inducing ventricular fibrillation by introducing usually harmless voltages, but now dangerous currents, to a patient has become a real one. Zoll and Linenthal,3 B ~ r c h e l l , ~ and other^^.^ have emphasized these dangers. The purpose of this discussion is: ( 1 ) to document the current levels which will cause ventricular fibrillation in the experimental animal and man (2 ) , to demonstrate that many pieces of routine hospital equipment are capable of delivering dangerous currents, and ( 3 ) to suggest certain precautions designed to prevent the accidental electrocution of patients with intracardiac electrodes.

Hemodynamic Findings in 123 Patients with Acute Myocardial Infarction on Admission

Hemodynamic and clinical evaluations of 123 patients with acute myocardial infarction were performed during the first hour of admission to the hospital. In the 123 patients, the right atrial pressure was less than 10 mm Hg in 49 patients, the right atrial oxygen saturation was less than 70% in 97 patients, the arteriovenous oxygen difference was greater than 5.0 vol% in 78 patients. The arterial Po2 was less than 90 mm Hg in 101 of 107 patients who could be evaluated while breathing room air. The cardiac index was depressed below 3.0 L/min/m2 in 65 of 98 patients.The hemodynamic findings generally correlated with the clinical status of the patient; however, within each clinical class of patients there was a wide spectrum of values for each measurement evaluated. There was also considerable overlap of the values found within each clinical classification. It is concluded that hemodynamic evaluation of patients with acute myocardial infarction presents a profile of the patient which is frequently different from the profile that clinical evaluation presents. An objective hemodynamic classification of patients with acute myocardial infarction may provide a more useful index for the evaluation of the patients prognosis and for the assessment of preventative therapy.

Biplane cineangiographic determinations of left ventricular function: Pressure-volume relationships

Abstract A biplane cineangiocardiographic technique with filming speeds of 30 or 60 frames per second is described to estimate the instant-to-instant changes of left ventricular volume in man. The results of postmortem studies in 13 human hearts and in 6 patients with various forms of heart disease are presented. Ninety-seven volume observations were made in the 13 postmortem hearts over a volume range of 30 to 150 c.c. The volume calculations were based upon the assumption that the chamber could be mathematically represented by the formula for an ellipsoid. The standard error of estimate was ± 5.6 c.c. and the correlation coefficient was 0.986. The angiographic left ventricular stroke volumes in a patient without anatomic left ventricular disease were 55, 60, 54, and 50 c.c., an average of 54.7 c.c. per beat. This compared favorably with the dyedilution stroke volume of 52.2 c.c. per beat. A second patient with a ventricular septal defect and patent ductus arteriosus had consecutive angiographic stroke volumes of 79 and 82 c.c., an average of 80.5 c.c. per beat. This compared favorably to the pulmonary blood flow of 82 c.c. per beat determined by the Fick method. The remaining 4 patients had valvular insufficiency and/or stenosis. The regurgitant flow per beat ranged from 13 to 109 c.c. Pressure and volume were related for the construction of pressure volume loops and the determination of the left ventricular pressure-volume work for ejection. The hemodynamic significance and changes in the contour of the loops in the various pathophysiologic states are described. The pressure-volume work was determined from the loops and compared to the stroke work calculated from conventional laboratory techniques. The determination of the pressure-volume work was demonstrated to be more informative than the conventional calculation of stroke work. The clinical application of ventricular volume measurements will provide additional information concerning the left ventricular hemodynamics of the normal and diseased state.