Quantitative study of infarcted myocardium in cardiogenic shock.
TL;DR: A post-mortem study of the heart was performed in 20 patients dying of cardiogenic shock finding extensive myocardial injury predominantly affecting the left ventricle and the interventricular septum.
Abstract: A post-mortem study of the heart was performed in 20 patients dying of cardiogenic shock. The extent of infarcted myocardium was defined by using a mitochondrial dehydrogenase stain nitro-BT which allowed macroscopical recognition of tissue death as early as 12 hours. Extensive myocardial injury was found to accompany cardiogenic shock predominantly affecting the left ventricle and the interventricular septum. Severe atheromatous involvement of the coronary arteries was noted.
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TL;DR: Estimation of cumulative infarct size differentiated patients with electrocardiographic changes and clinical sequelae from complications such as pericarditis from those patients with extension of infarction, indicating that enzyme elevations reflected CPK released from heart rather than skeletal muscle.
Abstract: Infarct size was assessed quantitatively in 33 patients with acute myocardial infarction with a new technic based on analysis of serial serum creatine phosphokinase (CPK) changes to determine its relationship to prognosis. We have recently measured infarct size in the conscious dog with this method which takes into account CPK distribution space, fractional disappearance rate, proportion degraded in myocardium, and proportion released into the circulation, and we have validated the method by measurement of myocardial CPK depletion in the same animals. In the present study, CPK activity (determined spectrophotometrically) and isoenzyme profiles (assayed electrophoretically) were measured in patient serum samples obtained every 2 hours. Infarct size was estimated by mathematical analysis of serial CPK changes utilizing the method previously developed in the conscious dog model. CPK isoenzyme profiles demonstrated prominent anodal bands, absent from normal serum, indicating that enzyme elevations reflected C...
737Â citations
TL;DR: In this paper, a 0.85 mm outer diameter catheter advanced through the lumen of the Judkins catheter was used to infuse Thrombolysin (streptokinase and plasmin) in 20 patients with evolving myocardial infarction who were hospitalized within 3 hours from the onset of symptoms during the day and within 2 hours at night.
554Â citations
TL;DR: The method described is useful for accurate assessment of infarct size in the conscious animal and for detection of modification of infArct size produced by pharmacologic interventions.
Abstract: This study was designed to develop a method for quantitative assessment of infarct size in the conscious animal based on serial changes of serum creatine phosphokinase (CPK) activity. From 11 experiments in which myocardial CPK was injected intravenously in conscious dogs, the average CPK distribution space and average CPK fractional disappearance rate from serum were found to be 11.4% of body weight and 0.48% min respectively. In other experiments, myocardial infarction was produced in 22 conscious dogs by constriction of a left coronary artery snare and serum CPK activity was determined at frequent intervals for 24 hr. Since myocardial CPK depletion reflects infarct size, infarct size was determined directly by analysis of myocardial CPK content in the same animals 24 hr after coronary artery occlusion. CPK released from the infarct was determined from observed changes in serum CPK activity analyzed according to a model taking into account the fraction of CPK released from an infarct and the rates of appearance and disappearance of CPK activity from serum. Infarct size was calculated on the basis of observed changes in serum CPK and compared to infarct size determined directly by analysis of myocardial CPK depletion. Agreement was close and results from all experiments fit the equation: [infarct size (g) determined from serum CPK] = 1.13 x [infarct size (g) determined from myocardial CPK] - 1.3, r = 0.96, n = 22. The method described is useful for accurate assessment of infarct size in the conscious animal and for detection of modification of infarct size produced by pharmacologic interventions.
548Â citations
TL;DR: Patients with cardiogenic shock were treated with the intra-aortic counterpulsating balloon in 10 institutions according to a common protocol, and clinical and physiologic problems were found.
Abstract: Eighty-seven patients with cardiogenic shock were treated with the intra-aortic counterpulsating balloon in 10 institutions according to a common protocol. Clinical and physiologic respons...
486Â citations
TL;DR: Cor coronary artery reperfusion 3 hr after coronary occlusion resulted in salvage of myocardial tissue by enzymatic and histologic criteria, as well as by functional assessment.
Abstract: The effects of coronary artery reperfusion 3 hr after coronary occlusion on contractile function and the development of myocardial damage at 24 hr was studied experimentally. In 14 control and 6 reperfused dogs, relationships between epicardial ST segment elevation 15 min after coronary occlusion and myocardial creatine phosphokinase activity (CPK) and histologic appearance 24 hr later were examined. The electrocardiograms were recorded from 10 to 15 sites on the left ventricular epicardium and transmural samples for CPK and histology were obtained from the same sites where epicardial electrocardiograms had been recorded. An inverse relation existed between ST segment elevation (mv) 15 min after occlusion and log CPK activity (IU/ mg of protein) 24 hr later, log CPK = - 0.06ST + 1.26. In dogs subjected to coronary artery reperfusion, there was significantly less CPK depression (log CPK = - 0.01ST + 1.31, [P < 0.01]) than that expected from the control group. In the control group 97% of specimens showing ST segment elevations over 2 mv at 15 min showed abnormal histology 24 hr later. In contrast, in the reperfused group 43% of sites exhibiting elevated ST segment at 15 min showed abnormal histology 24 hr later. In six additional dogs it was shown that the paradoxical movement of the left ventricular wall could be reversed within 1 hr of perfusion. Therefore, by enzymatic and histologic criteria, as well as by functional assessment, coronary artery reperfusion 3 hr after occlusion resulted in salvage of myocardial tissue.
373Â citations
Cites background from "Quantitative study of infarcted myo..."
...cardiac failure is imiost likely the result of a large mvocar(lial infarction (2, 3), and therefore several experimlental apl)roaches have been exvaluated for decreasing the size of the developing infarcts by medical therapy (4-l0)....
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TL;DR: The results of treatment of 250 patients with established acute myocardial infarction in a coronary care unit in a university hospital are described in this article, where a classification of functional severity based on clinical evidence of heart failure or shock is presented.
Abstract: The results of treatment of 250 patients with established acute myocardial infarction in a coronary care unit in a university hospital are described. The criteria for diagnosis have been carefully defined. In 62 per cent of patients admitted with a tentative diagnosis of acute infarction, the initial impression was confirmed. Fifteen per cent of patients admitted to the unit were classified as having possible infarction; in this group, the mortality rate was 3 per cent. A classification of functional severity based on clinical evidence of heart failure or shock is presented. Morbidity and mortality in acute myocardial infarction are related to the functional severity of the illness. Although arrhythmia is common, the overriding importance of five life-threatening arrhythmias is emphasized. Mortality of patients in the coronary care unit was not improved in comparison to those treated under regular care until strong central direction of therapeutic programs, immediate treatment of arrhythmia in cardiac arrest, and delegation of some medical authority to trained nurses was accomplished. The change in concept of the purposes and practices of special coronary care from resuscitation to prevention of arrhythmia is emphasized. The mortality in myocardial infarction complicated by shock remains high. In the absence of shock, aggressive medical treatment in the coronary care unit reduced mortality from 26 to 7 per cent. The implications of these data in the management of patients admitted to a hospital with a diagnosis of acute myocardial infarction are discussed.
1,903Â citations
TL;DR: The purpose of this paper is to show how the methods of quantitation as applied to the lung, but the methods mentioned are capable of adaptation to almost any organ.
Abstract: Clinico-pathological correlation has always been one of the main aims of the morbid anatomist. However, although clinical physiologists have for many years expressed their results in a quantitative form, pathologists have progressed mainly, though not entirely, along a descriptive path. Descriptive pathology has reached a high degree of refinement with the study of ultra-structure by the electron microscope and the probing of cellular chemistry by histochemical methods. Little interest has been shown in the field of quantitative morphology, although a quantitative study of gross and microscopic pathology, correlated with the findings of physiopathologists, might well yield much useful information. Thompson (1917) pointed out many applications of this approach to general biology, and recently Grant (1961) has drawn attention to the importance of this type of study in cardiac pathology and has referred to the work of Linzbach (1960). This paper is concerned with the methods of quantitation as applied to the lung, but the methods mentioned are capable of adaptation to almost any organ. Pulmonary physiology is a subject which has undergone enormous advances over the past 30 years, mainly since the introduction of cardiac catheterization as a safe clinical procedure by Cournand and Ranges (1941). The relatively slow progress of pulmonary pathology is probably due to inadequate descriptions of the various aspects of emphysema and chronic lung disease. This has been remedied largely by the work on chronic bronchitis of Reid (1954) and the description of centrilobular emphysema by Leopold and Gough (1957). What is needed now is precise information concerning volumes of normal and abnormal regions of the lung, the surface area of the airtissue interface, and the number of the various units, such as alveoli and alveolar ducts, in normal and emphysematous lungs. The purpose of this paper is to show how these measurements can be
579Â citations
TL;DR: In the past two decades there have been momentous advances in the care of patients with cardiovascular ailments, yet, mortality from coronary-artery disease has remained unaffected, with 65% of deaths occurring in the initial three days and 85% during the first week of attack.
Abstract: In the past two decades there have been momentous advances in the care of patients with cardiovascular ailments. Yet, mortality from coronary-artery disease has remained unaffected. Year after year myocardial infarction and its complications exact the highest toll of any single disease. 1 In large metropolitan hospitals, the death rate from this condition 30 years ago ranged from 30% to 40% and remains unaltered today. Certain facts are forcing reevaluation of the problem. Peak mortality occurs at the very onset of myocardial infarction and then recedes almost exponentially, with 65% of deaths occurring in the initial three days and 85% during the first week of attack. Arrhythmias probably account for 40% of deaths. Of these about two thirds are due to ventricular fibrillation and one third to bradycardia, heart block, and asystole. 2 It is well established that these electrical catastrophes are usually not due to irreversible cardiac damage. On
497Â citations
Journal Article•
407Â citations
TL;DR: The design, equipment and staffing of the six-bedded coronary-care unit at the Royal-Infirmary, Edinburgh are described and a high proportion were due to causes such-as shock, asystole and severe cardiac failure, which at-present are mostly irremediable.
157Â citations