Rexford Kennamer
University of California, Los Angeles
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Featured researches published by Rexford Kennamer.
The American Journal of Medicine | 1954
Myron Prinzmetal; Rexford Kennamer; Morton H. Maxwell
Abstract The electrocardiogram of through-and-through infarction was studied in sixteen dogs with chronic lesions produced by coronary artery ligation. Failure to elicit injury currents at epicardial and intramural levels established the absence of viable muscle within the infarcted regions. Histologic examination confirmed that the regions were completely dead. Direct leads from the epicardium and from various intramural levels of each region yielded pure QS waves identical or almost identical with the cavity QS complex. This observation indicated that the negative cavity potential was transmitted unaltered through the infarct, causing the coronary QS wave.
Circulation Research | 1954
L. Allen Smith; Rexford Kennamer; Myron Prinzmetal
Controlled studies of ventricular excitation were performed in dogs exhibiting various Degreess of right and left bundle-branch block. Increases in the intraventricular conduction time during complete bundle-branch block are attributed to free wall as well as septal factors. Incomplete bundle-branch block may be either segmental or diffuse. In the segmental type, delayed excitation is present in only a portion of the involved ventricle. In the diffuse type, delayed excitation of the entire homolateral ventricle occurs, but some portions of the ventricle tend to be delayed to a greater extent than others. Certain segements of the ventricular myocardium appear to be supplied by fixed portions of the conducting system, without cross connections operating physiologically. The clinical implications of these observations are briefly discussed.
American Heart Journal | 1953
Rexford Kennamer; Jacob L. Bernstein; Morton H. Maxwell; Myron Prinzmetal; Clinton McK. Shaw
Abstract 1. 1. By means of a specially designed plunge electrode, intraventricular leads were recorded from multiple sites throughout the walls, papillary muscle, septum and cavities of thirty-two dogs during normal sinus rhythm. A series of experiments was performed which established (a) that the presence of the plunge electrode in the myocardium did not alter the normal course of depolarization, and (b) that the depolarization complexes registered by the plunge electrode represented essentially local potentials. 2. 2. Pure QS or rS waves were recorded throughout at least the innermost two-thirds of the intramural myocardium in both ventricles as well as from all levels of the left papillary muscle. Intraseptal leads also exhibited essentially negative deflections, although considerable positivity was noted in the center and right side of the septum. Only the epicardial surface and a thin subjacent layer of the walls yielded predominantly positive depolarization complexes. In general, negative potentials were found to predominate in roughly 80 per cent of the musculature during ventricular depolarization while about 20 per cent of the myocardium was predominantly positive. This observation indicates that the ventricular wall does not depolarize in the same manner as the auricles. 3. 3. Pure QS waves consistently were obtained throughout the left ventricular cavity as well as from all portions of the right ventricular cavity except in the immediate vicinity of the septum. Cavity leads recorded near the right septal surface occasionally displayed a small R wave derived from the initial positivity of the right septal surface. 4. 4. The velocity of the depolarization wave was measured in twenty animals by timing the onset of the downstrokes in intramural leads from multiple depths of the left ventricular wall. As determined by this method, the rate of depolarization appears to be considerably more rapid in the innermost two-thirds of the wall than in the superficial layers. 5. 5. Currents of injury, manifested by RS-T segment elevation, always occurred for a brief period following the introduction of the plunge electrode into the myocardium. The RS-T segment deviation was markedly less in subendocardial leads than in subepicardial leads, indicating that subepicardial muscle characteristically is capable of producing more intense injury currents than are the deeper layers of the myocardium. 6. 6. The observed weakness of subendocardial injury currents in experimental animals suggests that the downward RS-T segment deviation, which is seen clinically in angina pectoris, is not attributable to subendocardial anoxia as is generally believed. On the basis of the same experimental observation, a new theory concerning the cause of RS-T segment elevation following coronary occlusion is proposed which appears to reconcile apparent discrepancies among the electrocardiographic, anatomic, and pathologic findings.
Circulation | 1955
Jean Louis Borduas; Louis Rakita; Rexford Kennamer; Myron Prinzmetal
Seven clinical cases with electrocardiographic patterns of constant or variable short P-R interval are reported. The QRS complex was either normal or aberrant. These abnormalities were reproduced experimentally in dogs by the injection of various drugs into the region of the A-V node. The theories advanced to explain these phenomena are discussed. The results indicate that accelerated A-V nodal conduction is responsible for the short P-R interval. The form of the ventricular complex may be dependent upon synchronous or asynchronous activity of the A-V node. A classification of A-V nodal dysfunction is presented.
American Heart Journal | 1956
Rexford Kennamer; Myron Prinzmetal
Abstract Despite the absence of the coronary Q wave, there appear to be instances when myocardial infarction can be diagnosed in the presence of left bundle branch block. The experimental evidence showed that with a transmural infarction or patchy infarction with extensive surface damage there occurs a marked reduction in the size of the R wave recorded in the direct lead from that region. In some instances, the reduction in the R wave may be reflected in the corresponding precordial lead. Changes in the magnitude of the R wave in the left precordial leads in left bundle branch block will frequently be detected only if control tracings are available for comparison or if multiple precordial leads are taken. Acute myocardial injury results in elevation of the S-T segment despite the presence of left bundle branch block. Thus, the diagnosis of acute myocardial infarction can be made from the finding of significant S-T segment elevation following the large, broad, positive complex of left bundle branch block. Other changes in the coronary circulation may also be reflected by alterations in the RS-T segment despite the presence of left bundle branch block. In our experience, coronary insufficiency as well as a positive two-step exercise test has resulted in changes in the S-T segment. It would appear that the popular opinion that coronary artery disease cannot be diagnosed in the presence of left bundle branch block should be modified. It is true that there is absence of the coronary Q wave in myocardial infarction, but the previously discussed changes should aid in making more conclusive the diagnosis of coronary artery disease in the presence of left bundle branch block.
The New England Journal of Medicine | 1954
Rexford Kennamer; Myron Prinzmetal
Arrhythmias Arising in Atrioventricular Node There is both experimental and clinical evidence11 that extrasystoles and tachycardia originating in the atrioventricular node often cannot be different...
Circulation | 1957
Myron Prinzmetal; Rexford Kennamer; Rashid A. Massumi
Out of a large series of patients with coronary artery disease 6 were selected with high anterior myocardial infarction. These cases are presented in detail and their special electrocardiographic characteristics are described. The difficulty in making the diagnosis of infarction by the usual leads and the need for special leads are pointed out.
American Heart Journal | 1951
John A. Osborne; Eliot Corday; Joshua Fields; Rexford Kennamer; L. Allen Smith; Myron Prinzmetal
Abstract In BOTH man and experimental animal, the fact has been established that only a fraction of the normal P-R interval represents passage of the excitation impulse across the auricular myocardium. Lewis 1 calculated that the speed of the impulse in the dogs auricle during normal sinus rhythm is approximately 1,000 mm. per second. By means of simultaneous esophageal leads, the normal impulse in the human auricle has been found to travel at a rate of at least 500 mm. per second 2 . If these determinations are accurate, the cardiac impulse traverses the auricles from the sinoauricular node to the A-V node in approximately 0.05 second, or in about one-third of the period occupied by the P-R interval in the normal electrocardiogram. The purpose of this communication is to present new data concerning the delay in conduction responsible for the remaining portion of the normal P-R interval.
American Journal of Cardiology | 1959
Rexford Kennamer; Myron Prinzmetal
Abstract Catron (JB516), a monoamine oxidase inhibitor, appears to be an antianginal agent which has the combined qualities of effectiveness and low toxicity. It is worthy of extensive trial.
American Journal of Cardiology | 1959
Myron Prinzmetal; Rexford Kennamer
Abstract 1. (1) An unusual ECG pattern of mild acute myocardial infarction is described consisting of ST segment depressions and lowering of the R waves, usually in the same leads. 2. (2) The ECG abnormalities are usually limited to a small area of the heart. 3. (3) The clinical course of patients showing these changes is mild, and the ECG usually returns to normal. 4. (4) The infarcts responsible for this ECG pattern are probably patchy and incomplete.