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Dive into the research topics where Joseph W. Linhart is active.

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Featured researches published by Joseph W. Linhart.


Circulation | 1969

Left Heart Hemodynamics During Angina Pectoris Induced by Atrial Pacing

Joseph W. Linhart; Frank J. Hildner; S.Serge Barold; John W. Lister; Philip Samet

In order to determine the associated hemodynamic events, angina pectoris was induced by an atrial pacing technic. In all patients developing angina pectoris, ischemic changes were noted electrocardiographically. The hemodynamic findings were variable: in some patients no changes were noted; in others, significant increases in cardiac output, left ventricular end-diastolic pressures (LVEDP), and femoral arterial and pulmonary arterial pressures occurred. These changes suggest that, initially, ischemia produces a decrease in myocardial compliance and this may also be associated with enhanced sympathetic nervous system activity. Myocardial failure may subsequently ensue, however. The administration of nitroglycerin, during angina at a fixed rapid heart rate, resulted in a reduction in LVEDP and cardiac work. Chest pain was always relieved following these hemodynamic changes, indicating a dependence upon these changes for the effectiveness of nitroglycerin.


Circulation | 1971

Myocardial Function in Coronary Artery Disease Determined by Atrial Pacing

Joseph W. Linhart

Right atrial pacing was performed in 21 patients with and 10 patients without coronary artery disease (CAD). The values for the control (C) and maximum paced (P) heart rate were similar in all patients. During pacing cardiac output did not change, and mean arterial pressure remained constant except for a slight increase during pacing-induced angina pectoris in 11 patients with CAD. Left ventricular end-diastolic pressure (LVEDP) decreased in the normal subjects (C=9 ± 1, P = 3 ± 1 sem mm Hg) and in all 10 patients with CAD who did not develop angina (C=5 ± 3, P = 5 ± 1 mm Hg). In 11 patients with CAD, developing angina, LVEDP did not decrease before pain occurred (C=9 ± 1, P = 9 ± 2 mm Hg) and increased during induced angina (P = 14 ± 3 mm Hg). Pacing ventricular function curves (VFC) relating induced changes in LVEDP and stroke work were abnormal in five of 10 patients with CAD and without induced angina when compared to the normal subjects. In patients developing angina, pacing VFC were normal in five of 10 before pain and then became abnormal in four of these five when angina occurred. Atrial pacing may be used to evaluate ventricular function and may demonstrate abnormalities in patients with CAD even in the absence of pacing-induced angina. Angina pectoris is usually associated with an overall decrease in myocardial function.


American Journal of Cardiology | 1970

Recent Advances in the Treatment of Ectopic Tachycardias by Electrical Pacing

S.Serge Barold; Joseph W. Linhart

Abstract Cardiac pacing may be useful both prophytactically and therapeutically in the management of ectopic tachycardias. Ectopic tachycardias may be prevented by atrial or ventricular pacing for a sustained period at a rate faster than the spontaneous rate but slower than the rate of the tachycardia being suppressed. Supraventricular tachycardias, except atrial fibrillation, may be terminated by atrial or ventricular pacing for a brief period in one of three ways: (1) delivery of a single stimulus or two serial stimuli in quick succession; (2) repetitive stimulation at a rate slower than the tachycardia; or (3) repetitive stimulation (atrial only) at a rate faster than the tachycardia. Atrial pacing may slow the ventricular rate of supraventricular tachycardia resistant to all forms of therapy by (1) actually increasing the atrial rate which produces functional atrioventricular block and reduces the number of transmitted impulses to the ventricle, or (2) inducing stable atrial fibrillation with a slower average rate more easily controllable by digitalis. Aside from its relative simplicity, pacing offers certain advantages over standard d-c cardioversion for the termination of tachyarrhythmias, particularly when the latter is contraindicated as in digitalis toxicity.


The American Journal of Medicine | 1971

Hyperdynamic circulatory state due to intrahepatic fistula in Osler-Weber-Rendu disease

Bijan Razi; Barry M. Beller; John Ghidoni; Joseph W. Linhart; Robert C. Talley; Ernest Urban

Abstract A case of Osler-Weber-Rendu disease with extensive hepatic arteriovenous fistulation is described in detail. The patient suffers from a hyperkinetic circulation characterized by high cardiac output and diminished reserve. The availability of an open liver biopsy specimen showing arteriovenous communications performed three years ago allows anatomic correlation with recent hemodynamic and angiographic data indicating hepatic artery to hepatic vein shunting. The progressive nature of this rare disorder is emphasized.


American Journal of Cardiology | 1972

Atrial pacing in coronary artery disease, including preinfarction angina and postoperative studies

Joseph W. Linhart

Abstract Right atrial pacing studies were performed in 58 patients with coronary artery disease and in 15 normal subjects. Angina pectoris was induced in 58 percent of patients with coronary artery disease at an average heart rate of 129 ± 3 beats/min; ischemic S-T segment depression was noted in 63 percent of such patients experiencing angina pectoris and in 31 percent of those without angina. The greater the severity of coronary artery disease, the more frequent the pacing-induced angina. The main hemodynamic difference between the normal subject and the patient with coronary artery disease was the failure of the left ventricular end-diastolic pressure to decrease during pacing in the latter. Pacing ventricular function curves were abnormal in 60 percent of patients with coronary artery disease in the absence of angina pectoris and abnormal in 90 percent during induced chest pain. Pacing studies were safely performed in 8 patients with unstable angina pectoris, with angina induced by pacing in 7. No significant hemodynamic differences were noted between these patients and those with stable coronary artery disease. Significant postoperative hemodynamic abnormalities were noted in 9 patients; preoperative and postoperative studies indicated little improvement in myocardial performance after aortocoronary arteryvein bypass surgery.


Circulation | 1971

Pacing-Induced Changes in Stroke Volume in the Evaluation of Myocardial Function

Joseph W. Linhart

For characterization of left ventricular function using changes in heart rate, we performed right atrial pacing in 16 patients during right and left heart catheterizations. Hemodynamic data was obtained before pacing (B), during pacing (D), and immediately after (A) the sudden interruption of pacing, for assessment of the consequences of rapid changes in stroke volume. In 10 patients with normal left ventricular function, as heart rate (HR) changed from 81 ± 4 SEM (B) to 125 ± 6 (D) to 77 ± 5 beats/min (A), left ventricular end-diastolic pressure (LVEDP), from 8 ± 1 (B) to 3 ± 1 (D) to 9 ± 0.5 mm Hg (A), and stroke volume, from 74 ± 9 (B) to 46 ± 4 (D) to 77 ± 9 ml/beat (A), changed linearly. No change occurred in cardiac output (5.7 ± 0.5 liters/min) or in arterial pressure. In six patients with myocardial disease, HR changed similarly (from 86 ± 5 (B) to 126 ± 8 (D) to 90 ± 3 beats/min (A)), but LVEDP, cardiac output (CO), and stroke volume (SV) values were significantly different in comparison to the corresponding values for the subjects with normal function (LVEDP was 21 ± 3 (B), 8 ± 2 (D), and 25 ± 3 mm Hg (A), P = 0.001; CO was 4.1 ± 0.5 liters/min (B, D, and A), P = 0.01; SV was 48 ± 4 (B), 32 ± 5 (D), and 47 ± 4 ml/beat (A), P = 0.02). When pacing ventricular function curves were constructed relating left ventricular stroke work (SW) to LVEDP, normal patients exhibited a steep curve, while those with myopathies had flat responses. When the change (&Dgr;) in SW was related to &Dgr;LVEDP (&Dgr;SW/&Dgr;LVEDP), the value for normal subjects was 5.6 ± 1, and that for patients with myopathies, 0.6 ± .2 (P = 0.001). Atrial pacing may be used for characterization of left ventricular function, and permits a separation of normal and abnormal responses.


American Heart Journal | 1971

Chest-wall stimulation: A method of demand QRS-blocking pacemaker suppression in the study of arrhythmias

Alfonso Trevino; Barry M. Beller; Robert C. Talley; Giovanni A. Pupillo; Joseph W. Linhart

Abstract Low amplitude electrical stimuli delivered to the chest wall from a portable pacemaker may be used to suppress the implanted QRS-blocking, demand-type pacemaker. This technique allows analysis of the underlying electrocardiogram. The value of this method in the study of the natural history of conduction system disease, pacemaker-conduction system interaction, and in management of patients wearing these devices is illustrated.


Circulation | 1972

Hemodynamic Consequences of Pacing-Induced Changes in Heart Rate in Valvular Aortic Stenosis

Joseph W. Linhart

Atrial pacing was performed in 10 patients with various degrees of aortic valvular stenosis (AVS) and the hemodynamics were compared to eight normal subjects. Similar maximum heart rates (135 ± 6/min) in each group resulted in no significant complications or symptoms and no changes in cardiac output or transvalvular pressure difference while stroke work (SW) and volume and left ventricular end-diastolic pressure (LVEDP) declined. A postpacing overshoot in LVEDP (control, 14 ± 2; postpacing, 25 ± 3 mm Hg; p = 0.01) which occurred in the cases of AVS probably reflects a decrease in myocardial compliance. Pacing ventricular function curves relating induced changes in SW and LVEDP were generally steeper in patients with AVS than in the normal subjects and were definitely abnormal in three of the former. Pulsus alternans induced in two patients was associated with abnormal myocardial function while the control LVEDP level was not a good indication of the functional response of the myocardium.Atrial pacing appears to be beneficial in the preoperative evaluation of the patient with AVS when exercise stress may be dangerous because of the possibilities of inducing arrhythmias, syncope, and sudden death. It permits precisely controlled evaluation for preoperative and postoperative comparison.


The Annals of Thoracic Surgery | 1971

Aortic Regurgitation Clinical, Hemodynamic, Surgical, and Angiographic Correlations

Joseph W. Linhart

Abstract A consecutive series of aortic root cineangiograms was reviewed and the degree of aortic valve insufficiency (AI) correlated with clinical, hemodynamic, and operative data. The best correlations occurred in patients with pure AI; the clinical and hemodynamic values (pulse pressure, left ventricular end-diastolic pressure, aortic diastolic pressure, left ventricular hypertrophy) were not generally as helpful in evaluating the extent of AI in patients with mitral valve disease. Aortic root cineangiography is especially important in this latter group and is extremely accurate in determining the need for aortic valve as well as mitral valve operation.


American Journal of Cardiology | 1969

Left heart hemodynamics during angina pectoris induced by atrial pacing

Joseph W. Linhart; Frank J. Hildner; S.Serge Barold; J.W. Lister; Philip Samet

In order to determine the associated hemodynamic events, angina pectoris was induced by an atrial pacing technic. In all patients developing angina pectoris, ischemic changes were noted electrocardiographically. The hemodynamic findings were variable: in some patients no changes were noted; in others, significant increases in cardiac output, left ventricular end-diastolic pressures (LVEDP), and femoral arterial and pulmonary arterial pressures occurred. These changes suggest that, initially, ischemia produces a decrease in myocardial compliance and this may also be associated with enhanced sympathetic nervous system activity. Myocardial failure may subsequently ensue, however. The administration of nitroglycerin, during angina at a fixed rapid heart rate, resulted in a reduction in LVEDP and cardiac work. Chest pain was always relieved following these hemodynamic changes, indicating a dependence upon these changes for the effectiveness of nitroglycerin.

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Barry M. Beller

University of Texas at Austin

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S.Serge Barold

University of Texas at Austin

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Bijan Razi

University of Texas at Austin

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Frank J. Hildner

University of Texas at Austin

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Giovanni A. Pupillo

University of Texas at Austin

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Philip Samet

University of Texas at Austin

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Frank J. Hildner

University of Texas at Austin

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Philip Samet

University of Texas at Austin

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