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Dive into the research topics where Edward J. Hurley is active.

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Featured researches published by Edward J. Hurley.


American Journal of Surgery | 1962

Successful homotransplantation of the canine heart after anoxic preservation for seven hours

Richard R. Lower; Raymond C. Stofer; Edward J. Hurley; Eugene Dong; Roy Cohn; Norman E. Shumway

Abstract Experiments are described in which successful homotransplantation of the dog heart was carried out after seven hours of cardiac anoxia. During the period of extracorporeal preservation, the arrested heart was maintained at 2 to 4 °C. by immersion in cold saline solution. Two animals recovered after transplantation and lived for seven and eleven days, respectively, at which time death was caused by homograft rejection.


American Journal of Surgery | 1984

Blunt cardiac trauma

William Mayfield; Edward J. Hurley

The diagnosis of blunt cardiac injury is often difficult to make because of the multiple associated injuries, the lack of specific physical findings, and the lack of sensitivity and specificity of the electrocardiograms and enzyme changes. The two-dimensional echocardiogram and the monitoring of filling pressures and cardiac indexes by pulmonary artery catheterization have an advantage over the electrocardiogram, CPK isoenzymes and technetium pyrophosphate scans because both anatomic and functional data are obtained, data are rapidly available, and the tests can be used repeatedly at the bedside.


American Heart Journal | 1967

Emergency replacement of valves in endocarditis

Edward J. Hurley; Frederic L. Eldridge; Herbert N. Hultgen

Abstract This is a case report on a 24-year-old man with Streptococcus viridans endocarditis that produced rapid circulatory deterioration because of massive aortic insufficiency. In order to prevent death from cardiac failure, early operative intervention became mandatory prior to absolute assurance that the endocarditis was controlled. Prosthetic valve replacement was carried out 10 days after the institution of antibiotic therapy. In spite of the short period of therapy, sterilization of the aortic remnants was evidenced by the lack of bacterial growth in culture and the failure of the prosthesis to become infected. The result of the initial operation was a dramatic improvement in clinical and hemodynamic status. The need for a second operation was based on the return of mild symptoms of aortic insufficiency and evidence of malfunction of the prosthesis. The lack of adequate fixation of the first ball valve was due to a failure of the sutures to remain embedded in the edematous and friable aortic annulus. Sufficient healing and scar formation permitted successful replacement of the initial valve at the time of the second operation, without further morbidity. At the time of this writing, the follow-up period had been 12 months and the patient had returned to full activity without symptoms.


Journal of Surgical Research | 1962

Isotopic replacement of the totally excised canine heart.

Edward J. Hurley; Eugene Dong; Raymond C. Stofer; Norman E. Shumway

Summary A technique is presented for isotopic replacement of the canine heart resulting in a totally denervated preparation with long term survival. The salient aspects of the method of removal and replacement are stressed, and possible clinical applications are discussed. Future physiological studies upon the functioning denervated canine heart are enumerated.


American Journal of Cardiology | 1962

Primary cardiac sarcoma

Eugene Dong; Edward J. Hurley; Norman E. Shumway

Abstract A case of primary fibromyxosarcoma of the right ventricle is described. The clinical findings simulated that of pulmonic stenosis. The diagnosis was clarified by angiocardiography. Excision was made with the aid of cardiopulmonary bypass, and the right ventricular obstruction was relieved. Cardiac arrest prior to machine support led to a 25 minute period of cerebral ischemia, from which the patient recovered sufficiently to carry out household activities. Death from cardiac sarcomas appears to be secondary to the primary lesion, and adequate palliation in this case appears to be obtained.


American Journal of Surgery | 1979

Cardial myxomas: A clinical diagnostic challenge☆

Mervin B. O'Neil; Todd M. Grehl; Edward J. Hurley

Our experience consists of seven intracardiac myxomas in five patients seen over an 8 year period. It includes one patient who had three primary tumors, each anatomically distinct, occurring at 4 year intervals. The initial clinical presentation included embolic phenomena, unexplained neurologic symptoms, hemodynamic obstruction, and vague systemic illness. Preoperative diagnosis was confirmed by echocardiography or angiocardiography in all cases. At operation, only two of seven tumors were found to arise from the vicinity of the fossa ovalis; the other five arose from the atrial wall or ventricular septum. Wide resection of the tumors constituted the key to successful treatment. All patients have done well for periods of follow-up ranging from 6 months to 8 years. Awareness of cardiac myxoma is the key to diagnosis; treatment should be uniformly successful in all instances once the proper diagnosis has been made. Although recurrences are rare, all patients must be followed up closely for the development of new tumors, and a thorough investigation of all chambers must be conducted in patients with suspected recurrence.


American Journal of Cardiology | 1970

Saphenous vein bypass graft for refractory angina pectoris: Physiologic evidence for enhanced blood flow to the ischemic myocardium

Ezra A. Amsterdam; Albert B. Iben; Edward J. Hurley; Edward Mansour; James L. Hughes; Antone F. Salel; Robert Zelis; Dean T. Mason

Twentieth Annual Scientific Session American College of Cardiology The Sheraton Park Hotel, Washington, D.C., February 3 to 7, 1971 Saphenous Vein Bypass Graft for Refractory Angina Pectoris: Physiologic Evidence for Enhanced Blood Flow to the lschemic Myocardium EZRA A. AMSTERDAM, MD; ALBERT IBEN, MD; EDWARD J. HURLEY, MD, FACC; EDWARD MANSOUR, MD; JAMES L. HUGHES, MD; ANTONE F. SALEL, MD; ROBERT ZELIS, MD; DEAN T. MASON, MD, FACC, Davis, California Although surgical approach to symptomatic coronary artery disease is now extensively applied in patients with severe angina pectoris, objective documentation of the efficacy of this method has been lacking. Thus, we studied 20 consecutive patients with severe angina pectoris and angiographically documented coronary artery disease who underwent aorta to right and/or left cbronary artery saphenous vein anastomoses. Detailed determinations were made of preand postoperative (6 to 10 weeks) exercise capacity and hemodynamics with use of the upright bicycle ergometer. The heart ratemean systemic intraarterial pressure product x 10-Z (RPP) was assesged as an index of myocardial oxygen consumption (MVO,). Before surgery, intravenously administered propranolol, 0.1 mg/kg, delayed the onset of exercise-provoked angina pectoris from 6.8 to 8.2 mindtes (P <O.Ol), whereas the RPP fell from 144 to 119 (P <0.02), the response characteristic of propranolol-induced reduction of MVO,. Strikingly, after surgery, angina disappeared and could not be provoked by exercise, which was limited only by leg fatigue. Rise in myocardial blood flow was indicated by increase of the RPP from 144 (preoperative angina threshold) to 179 (level of postoperative leg fatigue) (+24%, P <0.05). In addition, electrocardiographic ischemic ST-T changes of exercise cleared or improved. These early postoperative results indicate that this technique increases myocardial oxygen delivery and is superior for relief of refractory angina in surgically amenable coronary artery disease compared to beta adrenergic blockade, which acts by reducing myocardial oxygen requirements. Asynchrony of Conduction and Reentry 1 GARY J. ANDERSON, MD: KALMAN GREENSPAN, PhD, FACC; J. BANDURA, BA, Indianapolis, Indiana Disturbances of conduction may be one of the mechaVOLUME 26, DECEMBER 1970 Abstracts are listed alphabetically according to first author. nisms of arrhythmias which are due to reentry. We explored this problem in the distal branches of the canine conducting system utilizing microelectrodes and Purkinje ‘bundle preparations resembling a “T” configuration. Such a preparation permits assessment of differential conduction velocities in Purkinje branches originating from a common bundle in response to premature stimuli (S,). Equal depression of conduction in branches distal to a common bundle was observed at wide coupling intervals (S,-S,). With progressive narrowing of the SZ-S1 coupling intervals, in the range of 160 to 200 msec, asynchrony of conduction appeared. This was due to decremental conduction occurring in 1 branch. For example, at a coupling interval of 189 msec the disparity of activation was 27 msec. Decreasing the S2-S1 coupling to 188 msec induced a 37 msec disparity of activation. Thus, an additional 10 msec disparity was induced by a 1 msec decrease in S2-S1 interval. These differential conduction velocities induced disparities of endocardial activation times in excess of 50 to 75 msec. In fibers exhibiting preferentially depressed conduction, local block and reentrant excitation were observed with further decrease in the coupling interval. Furthermore, reentry was critically dependent upon the basic (S,) rate such that shortening or prolongation abolished the reentrant beats. The results of these studies indicate that asynchronous conduction may be induced by narrow coupling of premature stimuli which in turn result in reentry. Electrophysiologic Correlate of Exit Block in


Circulation | 1968

Early Functional and Ultrastructural Recovery of Canine Cadaver Hearts

Jack G. Copeland; Jon C. Kosek; Edward J. Hurley

Simulation of sudden death in a potential heart graft donor was accomplished by producing acute anoxic arrest in canine hearts that were then maintained at cadaver temperature for periods of from 15 to 60 minutes prior to reperfusion with oxygenated blood. Functional recovery of reperfused hearts measured by contractile force was more rapid for hearts that had undergone shorter periods of anoxic arrest. The rates of recovery were nearly identical within the group for 15 to 25 minutes and for 30 to 45 minutes of anoxic arrest, but not for the 60-minute anoxic arrest group in which two of four hearts made no recovery at all. Ultrastructural reactions to anoxic arrest were evident at 15 minutes and found to progress in a predictable manner as the duration of anoxia increased. Changes occurring during anoxic periods of up to 30 minutes were for the most part reversed within 1 hour of perfusion during which time characteristic nuclear, cytoplasmic, and mitochondrial “recovery patterns” were encountered. With a “pump-dog” preparation, these reperfused hearts were well kept for up to 7 hours. Anoxic arrest of 45 minutes or more produced ultrastructural changes that were less consistently reversed by reperfusion of 1 hour. The sensitivity of mitochondrial structure to anoxic arrest and reperfusion was demonstrated, and suggested that irreversible cell damage (i.e., cell death) in anoxia is due to mitochondrial failure. The techniques of perfusion and ultrastructural sampling employed in these experiments should prove useful in studying the effects of hypothermia, drug application and other measures in the preservation and restoration of isolated hearts.


American Journal of Cardiology | 1970

Cardiocirculatory effects of glucagon in patients with congestive heart failure and cardiogenic shock

Ezra A. Amsterdam; Robert Zelis; James F. Spann; Edward J. Hurley; Dean T. Mason

Cardiocirculatory Effects of Glucagon in Patients with Congestive Heart Failure and Cardiogenic Shock EZRA A. AMSTERDAM, MD/ROBERT ZELIS, MD/JAMES F. SPANN, Jr., MD, FACC EDWARD J. HURLEY, MD, FACC and DEAN T. MASON, MD, FACC Davis, California Although the powerful inotropic property of glucagon is well established in isolated heart muscle and experimentd animals, the efficacy of the agent in patients with severe cardiac malfunction has not been determined. The purpose of this study was to define the cardiocirculatory effects of glucagon in patients with congestive heart failure or cardiogenie shock. Accordingly, the hemodynamic actions of intravenously administered glucagon (50 k there was a small but significant (P < 0.05) rise in heart rate (93 to 99). In the 5 patients of both groups whose cardiac output rose, the maximal increase was 14%. In the 3 patients with cardiogenic shock whose blood pressure increased, the increases were 5, 11 and 30%, respectively. These data suggest that glucagon, as administered in these studies, produces inconsistent hemodynamic improvement in patients with congestive heart failure and cardiogenic shock ahd that when favorable changes occur, they are usually of small magnitude. Signs and Symptoms of the Different Causes of Endocarditis Dr. FELIX ANSCHOTZ Dafmstadt, West Germany Knowledge of the causative inflammable process of the heart valves is important to understanding of the origin, progress, prognosis and treatment of the valvular disease. It is impossible to describe valvular heart disease with the aid of hemodynamic studies alone. The origin of the endocarditis is the central problem because of the consequences in therapy and prophylaxis. The differential diagnosis of endocarditis is described by our own studies in which the signs and symptoms are related in each case to the autopsy findings (137 cases of rheumatic heaxt disease, 85 cases of subacute bacterial endocarditis, 44 cases of acute bacterial endocarditis and 40 cases of rafe causes of endocarditis) . It is easier to recognize carditis in acute rheumatic fever than in cases of chronic valvular disease in which the inflammation doubtless influences the progress of the valvular damage. In these cases other possible explanations of inflammation must be considered. Subacute bacterial endocarditis, too, will be easy to recognize, particularly if the bacterial culture is positive. Often abacterial endocarditis may be hard to diagnose because of its indistinct symptoms. The central problem is to find the strains, which is difficult because many patients have already been given antibiotics. In some cases it is impossible to diagnose the cause of the endocarditis definitely even with the help of the most modern clinical studies. Hemodynamic Effects of Glucagon in Patients with Fixed-Rate Pacemakers WILLIAM W. ASHLEY, MD/DAVID M KAMINSKY, MD/JANET I. LIPSKI, MD ARTHUR C. WEISENSEEL, Jr., MD/EPHRAIM DONOSO, MD, FACC and CHARLES K. FRIEDBERG, MD, FACC New York, New York The effects of glucagon (50 clg/kg) on cardiac output (dye dilution) and brachial arterial pressure were studied in 7 patients, aged 57 to 73, with fixed-rate pacemakers. Mean cardiac index at rest increased 0.8 + 0.07 liters/ min per m2 (9% confidence interval) without significant change in braehial arterial pressures. Exercise performed by 5 patients, without glucagon, increased the cardiac index. During the same amount of exercise with glucagon, there was no aignifioant further increase in cardiac index (0.5 + 0.06 liters/min per m*). One additional patient with congestive heart failure did not show an increased cardiac index with glucagon at rest or during exercise. Isoproterenol administered to 2 patients increased cardiac index by 1.91 and 1.90 liters/min per ma compared to 1.02 and 0.75, respectively, with glucagon. Six of 8 patients experienced nausea and lightheadedness, and in 2 patients ventricular premature systoles developed after administration of glucagon. Mean serum potassium in 9 patients decreased from 82 The Amodem JoounMl of CARDlOLOaY


Circulation | 1965

RESULTS OF TOTAL SURGICAL CORRECTION FOR FALLOT'S TETRALOGY.

Norman E. Shumway; Richard R. Lower; Edward J. Hurley; R. Cree Pillsbury

Forty-four consecutive patients have been operated upon for total correction of Fallots anomaly since the opening of the Stanford Medical Center. There were no hospital or operative deaths. The combination of uniformly reversible cardiac arrest, meticulous placement of sutures for closure of the ventricular septal defect, and a flexible plan for enlarging the outflow tract has markedly reduced the operative risk for total surgical correction of Fallots tetralogy.

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Dean T. Mason

University of California

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Robert Zelis

Penn State Milton S. Hershey Medical Center

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Richard R. Miller

Baylor College of Medicine

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Todd M. Grehl

University of California

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