Clarence M. Agress
United States Department of Veterans Affairs
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Featured researches published by Clarence M. Agress.
Circulation | 1955
Clarence M. Agress; Howard I. Jacobs; Harvey F. Glassner; Marianne Lederer; Wm. G. Clark; Felix Wróblewski; Arthur Karmen; John S. Ladue
Serum glutamic oxalacetic transaminase concentrations rise sharply after myocardial infarction produced by bead embolization of the coronary tree in the closed chest dog. The peak concentration is reached in 9 to 23 hours post injury. Rises 20 to 30 times greater than normal may be obtained and are directly correlated with the amount of infarction estimated at autopsy. Serial serum transaminase levels may provide a clinical tool to supplement the electrocardiogram in the diagnosis of acute myocardial infarction as well as provide a roughly quantitative estimate of the amount of myocardium involved.
The American Journal of Medicine | 1954
Maxwell J. Binder; James A. Ryan; Stanley Marcus; Frederick Mugler; David Strange; Clarence M. Agress
Abstract 1.There is need for uniform criteria for the classification of shock following acute myocardial infarction. 2.2. Levarterenol is the vasopressor drug of choice in patients with severe coronary shock. Compared to non-specific therapy, levarterenol is beneficial and may be life-saving in an additional 20 per cent of these patients. 3.3. Neither intravenous nor intra-arterial transfusion alone reduces the mortality rate in severe coronary shock. 4.4. The mechanism of coronary shock is obscure and present day therapy is empirical. Additional data are needed on the hemodynamic changes and mechanism of this syndrome.
Journal of Clinical Investigation | 1950
Clarence M. Agress; Marvin J. Rosenburg; Abraham Schneiderman; Edward J. Brotman
The ominous form of circulatory failure which may accompany severe myocardial infarction carries a distressing mortality of some 79%o (1). The clinician confronted with the treatment of this condition finds the pathogenesis obscure (2), the relation of primary heart failure to peripheral circulatory failure confused (3), and his therapy often futile. Recently the trend has been to use blood and plasma as is done in better understood forms of shock (4-6), in spite of the prevailing conclusion that this form of failure of the circulation is not, like hemorrhagic and traumatic shock, accompanied by a fall in blood volume (2, 3, 7, 8a). This work was therefore undertaken to determine what changes occur in the blood volume after acute myocardial infarction, since a survey of the literature showed that previous studies were few and in our opinion not conclusive. In another paper (9) the authors have presented the evidence for believing that Evans blue dye (T-1824) is a valid method for studying the cir
American Journal of Cardiology | 1959
Clarence M. Agress; Louis G. Fields
Abstract 1. (1) A brief review of the history of low frequency heart sound recording is outlined. 2. (2) A new method of heart sound analysis for all frequencies is presented but with emphasis on low frequency components. 3. (3) Illustrations are given indicating the use which may be made of this technique in future study of low frequency sound.
Circulation Research | 1954
Clarence M. Agress; Howard I. Jacobs; Maxwell J. Binder; William G. Clark; Leo Kaplan; Marianne Lederer; Harvey F. Glassner
The possibility of using intravenous proteolytic agents in the treatment of acute myocardial infarction has been studied. The coronary arteries of closed-chest dogs were embolized with small repetitive doses of fibrin clots until definite electrocardiographic evidence of myocardial injury which persisted for at least two hours was observed. The treated animals were given up to six intravenous infusions of 250,000 Armour units of trypsin in 250 ml. saline over a period of eight days, and the survivors were sacrificed on the ninth day. The control animals received no trypsin. These studies showed that trypsin caused dissolution of the host thrombus which formed around the fibrin clots, without damage to the infarcted tissue; that the coronary vessels were recanalized; that the extent of infarction was decreased; and that the electrocardiographic changes were improved and the mortality was reduced.
American Journal of Cardiology | 1964
Clarence M. Agress; Stanley Wegner; Daniel J. Bleifer; Alfred Lindsey; John Van Houten; Kenneth Schroyer; Harley M. Estrin
Abstract The historical development of precordial vibration recording technics has been reviewed and the basic electronic principles outlined. Animal experiments were performed, in which left ventricular pressure curves were obtained simultaneously with precordial vibration tracings. An analog computer was utilized to derive a tracing resembling the vibrocardiogram from the pressure curve; a Krohn-Hite filter was used to obtain an apexcardiogram, a phonocardiogram and an accelerogram from the vibrocardiogram. It was demonstrated that a record closely resembling the left ventricular pressure tracing can be obtained by integration of the vibrocardiogram. The basic relationship of the precordial vibratory tracings to pressure changes within the left ventricle was demonstrated.
American Heart Journal | 1949
Marvin J. Rosenburg; Clarence M. Agress
Abstract 1. 1. Correlation of the electrical pattern of the precordial electrocardiogram with the anatomic projections of the corresponding precordial electrodes was performed. This was done in forty-four autopsied subjects by the insertion of wires into the ventricular myocardium at each of the six precordial positions of the electrocardiogram. A comparison of the anatomic position of the septum with the electrical position of the transitional zone was then made, and some conclusions drawn regarding the meaning of the transitional zone. 2. 2. The standard six precordial leads are well selected in that they span the anterior surface of the heart from precordial Position 1, which overlies the right auricle, to Position 6, which overlies the anterolateral portion of the left ventricle. 3. 3. The anatomic position of the septum is well correlated with the position of the electrical transitional zone in normal hearts and in those with predominant left ventricular hypertrophy. 4. 4. The shift in the position of the septum and, therefore, of the transitional zone is not of sufficient magnitude to identify specific ventricular hypertrophy. 5. 5. Left ventricular hypertrophy produces a sharp transitional zone. This is believed to be due to the plane of the septum being perpendicular to the anterior chest wall. 6. 6. Right ventricular hypertrophy often shows no transitional zone in the span of the standard six precordial electrodes. This is believed to be due to the transverse plane of the septum, produced by the fact that the anterior position of the right ventricle and the posterior position of the left ventricle cause the plane of the septum to be parallel to the anterior chest wall.
American Journal of Physiology | 1952
Clarence M. Agress; Marvin J. Rosenberg; Howard I. Jacobs; Maxwell J. Binder; Abraham Schneiderman; William G. Clark
The American Journal of Medicine | 1953
Clarence M. Agress; Marvin J. Rosenburg; Howard I. Jacobs; Maxwell J. Binder; Abraham Schneiderman; William G. Clark
American Journal of Cardiology | 1959
Clarence M. Agress