Ellis L. Rolett

Wall stress in the normal and hypertrophied human left ventricle

Abstract By the use of angiocardiographic technics, normal ranges for end-diastolic and peak systolic wall stresses have been defined in 6 subjects without left ventricular disease. In 41 other patients with various forms of heart disease the anatomic and functional adaptations of the left ventricle have been evaluated in terms of wall stress. Peak systolic stress appears to be better than end-diastolic stress as an index of the appropriateness of the responses. The data suggest that chronic valvular disease, representing a stimulus extrinsic to the myocardium, optimally results in a degree of hypertrophy appropriate to normalize peak systolic stress. In contrast, intrinsic muscle disease may result in a degree of hypertrophy inappropriate (either excessive or inadequate) in terms of peak stress. Normal peak stress does not preclude impaired cardiac performance, as in mitral stenosis, but elevated peak stress is characteristic of decompensated states.

Hemodynamic Studies during Angina Pectoris

Sixteen patients developed angina pectoris during cardiac catheterization.During an anginal attack, left ventricular end-diastolic pressure did not uniformly rise. When it did occur, it seemed to be more closely related to acute left ventricular hypertension.During a stress-induced anginal attack, the rise, if any, in systolic ejection rate of the left ventricle, was markedly decreased below that achieved in normal subjects or in subjects with coronary artery disease without angina. The impaired augmentation in systolic ejection rate was associated with subnormal increases in cardiac output as well as in stroke volume during the anginal state. Average heart rate and systolic ejection period were no different from the nonanginal patients.Myocardial excess lactate was found in the vast majority of cases during an anginal episode, and actual myocardial lactate production was seen in one half of the patients during angina.The abnormalities in left ventricular function may be related to abnormalities in oxygen supply to the myocardium.

Comparison of Calculations of Left Ventricular Wall Stress in Man from Thin-Walled and Thick-Walled Ellipsoidal Models

Using angiocardiographic data from 50 human subjects, a comparison was made of calculations of circumferential wall stress in the left ventricle based on the thin-walled ellipsoidal model of Sandler and Dodge and the thick-walled ellipsoidal model of Wong and Rautaharju. The Sandler and Dodge formula consistently overestimated mean stress as determined from the Wong and Rautaharju model. The degree of overestimation in terms of percent error usually varied between 5% and 15% and overall averaged about 10% at endsystole as well as at end-diastole. Analysis of the various factors influencing the discrepancy between calculations indicated that the expected increase in error associated with an increase in wall thickness during systole tended to be mitigated by a concomitant change in chamber geometry, specifically, an increase in the ratio of major to minor semiaxis. This study, then, offers an estimate of the error introduced by employing the Sandler and Dodge or similar thin-walled ellipsoidal models for computation of mean circumferential stress.

Reversible obstruction of the ventricular outflow tract.

Abstract Obstruction of the left ventricular outflow tract with characteristics of subaortic muscular hypertrophy has been produced in a human subject and 2 of 8 dogs by infusion of isoproterenol. In 2 other dogs with outflow tract gradients in the “control” state, infusion of blood relieved the obstruction. The possible role of adrenergic stress in producing the clinical disease and the relationship of both to the hyperkinetic heart syndrome are discussed.

EFFECTS OF NOREPINEPHRINE ON THE CORONARY CIRCULATION IN MAN.

The effect of norepinephrine infusion on the coronary circulation has been studied in 21 subjects. In doses ranging from 2 to 17 &mgr;g. base per minute norepinephrine caused a pari passu rise in perfusing pressure and coronary flow of 16 per cent above the control state. Despite an increase in cardiac oxygen consumption, coronary vascular resistance was unchanged, suggesting no vasodilatation in the coronary bed. On the contrary, oxygen extraction across the heart increased, implying that oxygen needs were inadequately met by rise in flow. An increase in vascular tone induced by norepinephrine is inferred from the unchanged coronary resistance at a higher perfusion pressure.Responses of the normal and failing left ventricle groups were qualitatively the same as for the group as a whole. The failure group showed greater tendency to meet oxygen needs by increased extraction than did the normal hearts.Although these observations are not strictly applicable to the role and effects of norepinephrine in states of clinical shock, nonetheless it seems likely that norepinephrine induces a suboptimal rise in coronary flow that may set the stage for ultimate myocardial ischemia, particularly when coronary perfusion pressure is inadequate.

Pressure-Volume Correlates of Left Ventricular Oxygen Consumption in the Hypervolemic Dog

Volume changes in the intact functioning canine left ventricle were induced by whole blood infusion and were measured by the thermodilution technic. Multiple regression analyses were performed to detect significant correlations between hemodynamic variables and left ventricular oxygen consumption. Hemodynamic variables, in addition to the pressure-time integral, ventricular volume, and ventricular work, included estimates of myocardial stress, force, and shortening. The most significant individual correlates of oxygen consumption were the pressure-time integral (r=0.91) and ventricular end systolic volume (r=0.81), whereas the interaction of volume with pressure-time, thus approximating wall stress and force, was the most significant variable overall (r=0.93). A number of multiple linear regression models were tested for the prediction of ventricular oxygen consumption. The equation (model E) with the greatest multiple regression coefficient (R=0.947) included heart rate, pressure-time per beat, pressure-time per minute, end systolic volume, and (end systolic volume)2/3 as independent variables. A less elaborate regression equation including only pressure-time per minute and end systolic volume as independent variables was, however, nearly as accurate as model E in the prediction of oxygen consumption. The addition of estimates of left ventricular work and shortening to these regression models did not further improve the ability to predict oxygen consumption accurately. The relationships between these hemodynamic variables and ventricular oxygen consumption were not altered by pericardiotomy or catecholamine depletion. In the hypervolumic heart acute ventricular dilatation did not occur following pericardiotomy. The results of this study confirm the postulate that an increase in ventricular volume, as well as pressure, will be accompanied by an increase in ventricular oxygen consumption. This in turn implies a relationship between the wall stress or force generated by the myocardium and the energy requirement of contraction.

Left ventricular end-diastolic pressure in chronic heart disease

Abstract In patients with chronic heart disease discrepancies have been demonstrated between left ventricular end-diastolic pressure and end-diastolic volume. In the present study we compared the end-diastolic pressure with chamber size, mass, contractility, wall forces and pressure volume work, and examined the determinants of left ventricular stroke volume and stroke work. We studied forty-seven patients (six with normal hemodynamics, seven with mitral stenosis, eighteen with compensated volume overload, three with decompensated volume overload, six with pressure overload, three with idiopathic myocardial hypertrophy and four with primary myocardial disease). No relationship was found between end-diastolic pressure and end-diastolic volume, mass, wall forces, ejection fraction and stroke work. End-diastolic stress in the patients with volume overload frequently was within 2 S.D. (standard deviations) of the normal. Only in the groups with pressure overload did end-diastolic pressure correlate with peak systolic stress. In the normal subjects and those with compensated volume overload end-diastolic volume correlated significantly with left ventricular stroke volume and stroke work. Increased end-diastolic volumes were consistently accompanied by increased left ventricular masses in all groups with chronic heart disease. Deviations from the normal resting stroke volume can result from changes in preload, contractility and afterload, and these variables can be expressed as end-diastolic wall stress, ejection fraction and peak systolic wall stress. In chronic heart disease ventricular distensibility varies from patient to patient as well as in the course of the disease and such diastolic pressure-volume relationships differ from those encountered during acute hemodynamic alterations. Under chronic conditions ventricular dilatation rarely occurs without hypertrophy, and in pressure overload ventricular hypertrophy without chamber enlargement may be encountered. In either chronic pressure or chronic volume overload without myocardial failure, left ventricular mass is more consistently related to stroke work than either end-diastolic pressure or volume alone. Therefore, in chronic heart disease in the resting state, end-diastolic pressure, volume, mass, contractility, wall stress and distensibility must be considered in the function of the left ventricle, and any principle which utilizes a single variable may not consistently predict ventricular stroke volume or stroke work.

Resuscitation from ventricular fibrillation complicating acute coronary occlusion: Report of a case

Abstract Ventricular fibrillation is a frequent complication during the twenty-four hours after acute coronary occlusion. This arrhythmia invariably results in death. A method for defibrillation of the ventricle has been developed and the successful employment of this in man has been reported in recent years. The procedure includes thoracotomy and rhythmic compression of the heart in association with artificial respiration. It must be instituted within a time limit of approximately four minutes after the onset of ventricular fibrillation. Adequate myocardial oxygenation is a requirement for success and is dependent equally upon effective artificial respiration and effective cardiac compression. The ventricle is then defibrillated by means of electric shock applied directly to the heart. What is believed to be the ninth reported case of successful open chest cardiac resuscitation in acute coronary occlusion complicated by ventricular fibrillation is recorded here. External electric defibrillation through the intact chest wall without cardiac massage is useful mainly when ventricular fibrillation occurs in a setting of complete heart block. The newly developed technic of closed chest cardiac compression may extend the usefulness of external electric shock to cases of ventricular fibrillation secondary to acute coronary occlusion. It should be emphasized that the development of ventricular fibrillation does not itself signify an irreversibly damaged heart but may instead be a chance occurrence in a relatively healthy heart. This constitutes a potentially salvagable condition. The employment of cardiac resuscitation by the physician is encouraged when acute coronary occlusion is complicated by ventricular fibrillation.

Arnold M. Katz: 1932-2016.

Cardiology lost a luminary on January 25, 2016. Arnold M. Katz died after a 14-year battle with non-Hodgkin lymphoma. At the time of his death, he was honorary professor of medicine and physiology at the Geisel School of Medicine at Dartmouth. Arnie was the justifiably proud son of a remarkable father, Louis N. Katz, an early president of the American Heart Association. Arnie attended the University of Chicago as an undergraduate and received his medical degree cum laude from Harvard Medical School in 1956. During summers, he worked in his father’s laboratory at Michael Reece Hospital on coronary blood flow and left ventricular volume, leading to first-authored papers in the American Journal of Physiology and Circulation Research before he finished medical school. After a year of medical internship at the Massachusetts General Hospital, Arnie served as a research associate in the laboratory of future Nobel Laureate Christian Anfinsen at the National Institutes of Health. A resulting 1959 publication on peptide separation in the Journal of Biological Chemistry remains frequently cited >50 years later.1 Arnie resumed his clinical training as a medical resident at the Massachusetts General Hospital and assistant registrar at the National Heart Hospital in London with Dr Paul Wood. This was followed by a research fellowship at UCLA with Wilfred Mommaerts. As an American Heart Association Established Investigator, Arnie was first appointed to the medical faculty at Columbia University and then the University of Chicago. In 1969, he became the first Philip J. and Harriet L. Goodhart Professor of Medicine (Cardiology) at Mount Sinai School …