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Dive into the research topics where Richard A. Carleton is active.

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Featured researches published by Richard A. Carleton.


Circulation | 1970

Abnormal Left Ventricular Contraction in Patients with Mitral Stenosis

Stanley J. Heller; Richard A. Carleton

Twenty-five patients with pure mitral stenosis and nine normal subjects were studied by selective left ventricular cineangiocardiography. Left ventricular volumes were measured at end systole, throughout diastole, and at end diastole. Although filling curves showed that the left ventricles filled slowly in patients with mitral stenosis, normal end-diastolic volumes were attained provided diastole lasted 400 msec. Despite normal end-diastolic volumes, end-systolic volumes were significantly larger (P < 0.0005) in the patients with mitral stenosis (av=64.6 ml) than in normal subjects (30.8 ml). Correspondingly, left ventricular ejection fractions were significantly lower (P < 0.0005) in the patients with mitral stenosis (55.7%) than in the normal subjects (76.7%).Qualitative analysis of the cineangiocardiograms demonstrated that 20 patients with mitral stenosis had distortion, immobility, and rigidity of the posterobasal area of the left ventricle.It is hypothesized that a rigid “mitral complex” immobilizes the posterobasal area of the left ventricle in patients with mitral stenosis, thereby impairing left ventricular contraction, and that this impairment is an important factor in the reduced cardiac output of these patients.


American Journal of Cardiology | 1971

Change in left ventricular volume during angiocardiography

Richard A. Carleton

Abstract Seven selective left ventricular angiocardiograms that permitted measurement of end-diastolic volume for 5 consecutive cardiac cycles were analyzed. Neither end-diastolic volume nor end-systolic volume changed significantly between the first and second cycles after ventricular opacification. A progressive increase in the major and minor ventricular semiaxes occurred beginning with the third opacified cycle. Correspondingly, the average end-diastolic volume and end-systolic volume increased by 6.9 ml and 3.4 ml, respectively, between the second and third cardiac cycles. Ventricular volumes progressively increased between the third and fifth cardiac cycles in each patient. These data suggest that sodium diatrizoate has a negative inotropic effect on left ventricular myocardium by the third cardiac cycle after injection. Physiologic information from cineangiocardiography should be derived from the first 2 cardiac cycles after opacification.


Circulation Research | 1968

Measurement of Left Ventricular Diameter In the Dog by Cardiac Catheterization Validation and Physiologic Meaningfulness of an Ultrasonic Technique

Richard A. Carleton; James G. Clark

A cylindrical ultrasonic transducer on a catheter tip lodged in the cleft between the free wall of the right ventricle and the interventricular septum provides an easily measured echo from the posteroinferior left ventricular epicardial surface. The sonic path represents a diameter of the left ventricle at approximately its largest cross-sectional area. Experiments in six dogs demonstrated that measurements by ultrasound agree within ±6% with simultaneous radiographic measurements of left ventricular diameter. Procedures designed to alter left ventricular volume were employed in 14 dogs to clarify the physiologic meaningfulness of the left ventricular diameter measured by ultrasound. Both end-diastolic and end-systolic diameter increased with anoxia, with sudden injections of saline into the left ventricle, after propranolol, and after inflation of a balloon in the thoracic aorta. These diameters decreased with isoproterenol, with increased heart rate, and after inflation of a balloon in the inferior vena cava. The present technique provides accurate and physiologically meaningful estimates of left ventricular diameter. Ventricular diameter measurements obtained during cardiac catheterization should permit assessment of ventricular distensibility and of ventricular function.


Circulation | 1969

Hemodynamic performance of a transplanted human heart.

Richard A. Carleton; Stanley J. Heller; Hassan Najafi; James G. Clark

Cardiac catheterization studies, performed 3 weeks after cardiac homotransplantation, revealed nearly normal cardiac performance. Alteration in heart rate by right atrial pacing, passive elevation of the legs, and exercise modified cardiac performance predominantly by variation in ventricular filling. Isoproterenol infusion increased stroke volume above the level predicted from the ventricular end-diastolic pressure.The heart was hypersensitive to beta-adrenergic stimulation with isoproterenol as judged by a greater responsiveness of the donor sinus node than the recipient sinus node, by prolongation of ventricular filling time, and by shortening the P-R interval for any given paced heart rate. These measures permitted tests for endogenous catecholamine effects during passive leg elevation and during exercise. Only after the 3 minutes of exercise was a small beta-adrenergic effect detectable.These data demonstrate the dependence of the denervated human heart upon variation in ventricular filling as the predominant mode of regulation of cardiac performance.


Circulation | 1967

The Deleterious Role of Tachycardia in Mitral Stenosis

Djavad T. Arani; Richard A. Carleton

Eleven patients with mitral stenosis and atrial fibrillation were studied during artificially induced tachycardia to determine the influence of rapid ventricular rates on hemodynamic variables. Significant elevation of pulmonary artery pressure occurred, but no increase in calculated pulmonary arterial resistance was found. Pulmonary arterial wedge pressures rose in each patient with an average increase of 7 mm Hg. Cardiac output fell at the fastest rate in each patient. These changes from rapid ventricular rates appear to account for the functional deterioration often encountered in patients with mitral stenosis with the advent of atrial fibrillation.


Circulation Research | 1966

Overestimation of Left Ventricular Volume by the Indicator Dilution Technique

Richard A. Carleton; Allen F. Bowyer; John S. Graettinger

The applicability of the indicator dilution method to the measurement of left ventricular volume has been studied. When compared with angiocardiographic measurements, the dilution technique overestimates volume by an average of 52 and 91% in end diastole and end systole respectively. Studies which demonstrated more rapid indicator washout from the outflow than from the apical portion of human and canine left ventricles suggest that faulty intraventricular indicator dispersion is the major cause of the volume over-estimates yielded by the dilution method. Procedures designed to alter ventricular size by altering venous return produced parallel changes in ventricular circumference and in ventricular indicator washout volume. The indicator dilution method does not provide a measure of left ventricular volume, but may, in carefully designed studies, yield an index of changes in ventricular size.


Circulation Research | 1967

Effects of Ouabain, Atropine, and Ouabain and Atropine, on A-V Nodal Conduction in Man

Richard A. Carleton; Paul H. Miller; John S. Graettinger

The prolongation of A-V transmission time that occurs with increasing rates of right atrial pacing has been used to study the effect of ouabain and of ouabain plus atropine on A-V nodal conduction in 14 patients with normal A-V nodes. Drugs were injected into the superior vena cava or pulmonary artery over a 1- to 2-min period. Atropine in a dose of 0.02 mg/kg shortened A-V conduction time by an average of 0.112 sec; ouabain alone in a dose of 0.01 mg/kg lengthened A-V conduction time by 0.053 sec. Ouabain given after large doses of atropine did not prolong A-V conduction at any paced rate. Thus, in these resting patients with normal A-V nodal function, usual digitalizing dosages of ouabain did not have an extravagal or antiadrenergic effect on A-V nodal conduction.


Circulation | 1967

Assessment of Aortic Valvular Stenosis from the Aortic Pressure Pulse

Djavad T. Arani; Richard A. Carleton

In a search for an indirect estimate of severity, data from 40 patients with pure aortic stenosis have been analyzed. Calculated aortic valvular areas ranged from 0.5 cm2 to 2.4 cm.2 Both aortic systolic upstroke time and the rate of aortic pressure rise were significantly altered by aortic stenosis; neither permitted reliable estimates of severity of the stenosis. An estimate of arterial compliance, stroke volume divided by pulse pressure, has been used in conjunction with the first derivative of rising aortic pressure to obtain an index of aortic stenosis. This index correlates well with calculated aortic valvular area (r = 0.912) and permits estimates of the severity of aortic stenosis when the left ventricle cannot be entered.


Circulation | 1966

Evidence of Concealed Atrioventricular Conduction in Man

Richard A. Carleton; John S. Graettinger

The occurrence of 2:1 A-V block during right atrial pacing in man provided the opportunity to compare A-V conduction time with and without an intervening atrial depolarization at similar ventricular rates. The presence of the interposed atrial depolarization produced prolongation of the subsequent A-V conduction by 0.03 to 0.13 sec, and thus provided evidence of concealed conduction in the normal human heart.


Circulation | 1968

Endocardial Fibrosis Detection by Cardiac Pacing

James G. Clark; H. Gunther Bucheleres; Richard A. Carleton

Three patients with endocardial fibrosis who had their endocardial pacing thresholds measured are described. The threshold values were elevated to at least twice normal levels. By determining the endocardial pacing threshold value, a technique is available for detection of endocardial fibrosis during diagnostic cardiac catheterization.

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John S. Graettinger

University of Illinois at Chicago

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James G. Clark

University of Illinois at Chicago

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Joseph J. Muenster

University of Illinois at Chicago

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Robert W. Sessions

University of Illinois at Chicago

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Stanley J. Heller

University of Illinois at Chicago

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A. Jerald Rothenberg

University of Illinois at Chicago

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Djavad T. Arani

University of Illinois at Chicago

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Abdul H. Khan

Lemuel Shattuck Hospital

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Allen F. Bowyer

University of Illinois at Chicago

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