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Dive into the research topics where Donald C. Harrison is active.

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Featured researches published by Donald C. Harrison.


Circulation | 1974

Sensitivity and Specificity of Echocardiographic Diagnosis of Pericardial Effusion

Michael S. Horowitz; Clifford S. Schultz; Edward B. Stinson; Donald C. Harrison; Richard L. Popp

In order to evaluate the reliability and sensitivity of echocardiograms for detecting and quantitating pericardial effusion, 41 patients had echocardiograms on the day prior to cardiac operation. A fluid trap was used to aspirate the pericardium at operation. Thirty-nine of 41 patients had echocardiograms of diagnostic quality. In 25 patients, the echocardiogram was negative for pericardial effusion, with 0-16 ml identified at operation. In 13 patients, the echocardiogram was positive for pericardial effusion, with 15-775 ml aspirated at operation. A transition of patterns of relative posterior epicardial-pericardial movement was noted as the pericardial fluid volume increased. More than 15 ml was always found when a posterior echo-free space persisted throughout the cardiac cycle between a flat pericardium relative to the epicardium. In the presence of such a posterior echo-free space, a large anterior echo-free space made a moderately large pericardial effusion likely. In the absence of this diagnostic posterior echo-free space, an anterior echo-free space had no diagnostic significance, as it was found in 11 patients with less than 16 ml of pericardial effusion. A small posterior echo-free space persisting throughout the cardiac cycle between pericardial and epicardial echoes demonstrating virtually identical movements was found in two patients without any surgical evidence for pericardial effusion, but with evidence of adhesive fibrocalcific pericardial disease. A method of estimating pericardial volume is proposed, which uses the difference between the cubed diameters at the end-diastole of the pericardium and epicardium.


The New England Journal of Medicine | 1967

Effect of Lidocaine on Ventricular Arrhythmias in Patients with Coronary Heart Disease

Ralph E. Gianelly; J. von der Groeben; Alfred P. Spivack; Donald C. Harrison

LIDOCAINE (Xylocaine) has become one of the most frequently used drugs in the treatment of ventricular arrhythmias, particularly those associated with acute myocardial infarction. It has been shown...


The New England Journal of Medicine | 1962

Augmentation of the Plasma Nor-Epinephrine Response to Exercise in Patients with Congestive Heart Failure

Charles A. Chidsey; Donald C. Harrison; Eugene Braunwald

THE manner in which the cardiovascular system responds to the increased metabolic demands of muscular exercise is of considerable interest to the clinician and physiologist. It has been suggested t...


The American Journal of Medicine | 1978

Early Anthracycline Cardiotoxicity

Michael R. Bristow; Paul D. Thompson; Randolph P. Martin; Jay W. Mason; Margaret E. Billingham; Donald C. Harrison

Eight patients in whom cardiac dysfunction developed within four weeks of receiving their first or second course of daunorubicin or doxorubicin are described. Four patients presented with pericarditis; three of these four had evidence of myocardial dysfunction. Histopathologic analysis of these patients was consistent with an acute myocyte damage and secondary inflammatory process. An additional group of four patients presented with symptoms and signs of heart failure. These patients were either elderly or had evidence of previous cardiac disease. One of these patients suffered a myocardial infarction 24 hours after receiving 60 mg/m2 of daunorubicin; earlier doses in the same course had been associated with evidence of myocardial ischemia. We conclude that anthracycline antibiotics may manifest clinically significant cardiotoxicity at total cumulative doses much less than have been associated with chronic cardiomyopathy.


Circulation | 1974

Changes in Diastolic Stiffness and Tone of the Left Ventricle During Angina Pectoris

William H. Barry; Jeff Z. Brooker; Edwin L. Alderman; Donald C. Harrison

Reported elevations of left ventricular filling pressures during angina suggest increased myocardial stiffness. Both left ventricular beginning- and end-diastolic pressures and volumes were measured in seven patients before, during, and after angina induced by atrial pacing. During nine episodes of angina, mean end-diastolic pressure rose from 12 to 29 mm Hg and ejection fraction fell from 0.47 to 0.37. Logarithms of beginning and end-diastolic pressures were plotted against the corresponding volumes for each angiogram. During angina, there was a marked increase in beginning as well as end-diastolic stiffness of the ventricle. These changes, which were reversible with resolution of angina, may be due to sustained contraction or failure of relaxation of a portion of the left ventricular myocardium during angina pectoris.


Circulation | 1971

Interrelationships of Hepatic Blood Flow, Cardiac Output, and Blood Levels of Lidocaine in Man

Robert E. Stenson; Robert T. Constantino; Donald C. Harrison

Factors that regulate the arterial level of lidocaine during a constant infusion were investigated in 17 patients undergoing cardiac catheterization. Lidocaine was administered by a 50 mg bolus, followed by a constant infusion of 40 μg/kg/min until steady state conditions were achieved. Cardiac output and estimated hepatic blood flow were also determined. An inverse relationship between arterial lidocaine levels and cardiac index was observed. With a low cardiac index of 1.9 ± 0.3 liters/min/m2 the arterial level was 2.4 (±0.4 SEM) μg/ml, while with a normal cardiac index of 3.3 ± 0.8 liters/min/m2 it was 1.5 (±0.2 SEM) μ/ml.A linear relationship was also observed between estimated hepatic blood flow and cardiac index. Therefore, an inverse relationship between arterial lidocaine levels and estimated hepatic blood flow was noted. At steady-state conditions, the liver accounted for 70% (±16% SEM) of the metabolism or removal of the lidocaine administered. These studies suggest that the administration of smaller doses of lidocaine will produce effective therapeutic levels when reduced hepatic blood flow exists.


American Heart Journal | 1981

Histamine provocation of clinical coronary artery spasm: Implications concerning pathogenesis of variant angina pectoris

Robert Ginsburg; Michael R. Bristow; Niki E. Kantrowitz; Donald S. Baim; Donald C. Harrison

Twelve patients with nonexertional chest pain and nonobstructive fixed coronary disease (less than 50% luminal diameter narrowing) were given histamine to investigate the potential role (coronary artery H1 receptor agonism) of the endogenous agent in producing coronary artery spasm (CAS). Histamine, at intravenous dose of 0.5 to 1.0 microgram/kg/min, provoked CAS in four patients. In six patients neither histamine nor ergonovine provoked spasm, and these patients were considered by chronic follow-up evaluation to have noncardiac etiology for their chest pain syndrome. In one patient CAS was provoked with ergonovine but not by histamine, and one ergonovine-positive patient had an equivocally positive histamine result. Pretreatment with cimetidine (H2 receptor antagonism) was necessary to avoid unpleasant side effects of histamine. Thus these observations indicate that histamine should be included among the specific agents capable of inducing CAS and provide new insight concerning the mechanism(s) causing variant angina pectoris.


Circulation | 1975

Arrhythmias in patients with mitral valve prolapse.

Roger A. Winkle; Mario G. Lopes; John W. Fitzgerald; Daniel J. Goodman; John S. Schroeder; Donald C. Harrison

Resting ECGs, exercise treadmill tests and 24-hour ambulatory ECGs were recorded and analyzed in 24 unselected patients with mitral valve prolapse. Arrhythmias were frequent. There were three distinct groups of patients, defined on the basis of total number of premature ventricular contractions (PVCs) during the 24 hours: there were no PVCs in 25%, infrequent PVCs in 25%, and frequent PVCs in 50%. Complex ventricular arrhythmias, including ventricular tachycardia in five patients, were found almost exclusively in the group with frequent PVCs. Fifteen of the 24 patients demonstrated atrial premature contractions (APCs) during the 24 hours. Complex atrial arrhythmias were found among patients with infrequent, as well as those with frequent, APCs. Supraventricular tachycardia was detected in seven of these patients. The incidence of PVCs decreased during sleep in 58% of the patients, increased in 17%, and showed no change in 25%. The incidence of APCs decreased during sleep in 67% of the patients and showed no change during sleep in 33%. A poor correlation was found between symptoms recorded in patient diaries and changes noted on 24-hour ECG recordings. The peak PVCs/15 min and peak APCs/15 min during a 24-hour period of monitoring was found to be an excellent guide to the total number of PVCs and APCs occurring during that period. This permits an accurate prediction of the total number of PVCs in 24 hours after performing an exact PVC count on only 15 minutes of ECG data. Finally, the 24-hour ambulatory ECG was more sensitive than the treadmill test and both were superior to the 12-lead ECG for detecting arrhythmias in these patients.


Annals of Internal Medicine | 1974

Coronary Artery Syndromes After Sudden Propranolol Withdrawal

Edwin L. Alderman; D. John Coltart; George E. Wettach; Donald C. Harrison

Abstract Six patients with stable exertional angina pectoris immediately developed unstable angina after cessation of propranolol therapy. The character and frequency of the pain episodes were sign...


Circulation | 1970

Ultrasonic Cardiac Echography for Determining Stroke Volume and Valvular Regurgitation

Richard L. Popp; Donald C. Harrison

The ventricular dimensions of 51 patients with heart disease were determined by ultrasonic echography during cardiac catheterization. These data were used to calculate end-diastolic and end-systolic volumes and stroke volume, using a prolate ellipse as a geometric model of the left ventricle. In 30 patients without valvular regurgitation the stroke volumes determined by the echographic method were compared with those determined simultaneously by the standard Fick method with a correlation coefficient of r = 0.966. In 21 patients with valvular regurgitation, the severity of regurgitation was estimated by comparing the forward stroke volume determined by the Fick method with the total left ventricular stroke volume determined by the echographic method. These calculations of regurgitation correlated reasonably well with the degree of valvular regurgitation estimated from angiocardiographic study. It is suggested that these echographic determinations of stroke volume are an atraumatic, safe, and acceptable method in patients without valvular regurgitation. Moreover, these preliminary studies suggest that the severity of valvular regurgitation can be estimated by utilizing ultrasound echocardiography.

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Michael R. Bristow

University of Colorado Boulder

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