Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018801 (heart failure)
72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Serum m-AST (mitochondrial isoenzyme of AST) activity in patients with acute myocardial infarction was determined quantitatively by a new immunological technique which is sensitive and easily available. All 31 patients with acute myocardial infarction showed abnormally high levels of serum m-AST (more than 5 KU/ml); the mean serum m-AST activity attained its peak (42.0 +/- 4.9 KU/ml) on the first day after the onset of infarction 5 hours later than that of serum t-AST (total AST) activity in 15 patients whose peak m- and t-AST activities were identified clearly. The individual peak m-AST activity correlated with the total CK released (r = 0.83, n = 15), indicating that the release of m-AST also reflects the infarct size. The ratio of serum m-AST/t-AST increased following myocardial infarction and showed the maximal value (average 25.7%) on the third to seventh day after onset. This ratio in the patients with acute myocardial ifarction was also greater than that in patients with liver disease or with heart failure from causes other than acute myocardial infarction. In the patients who had the additional complication of heart failure and/or cardiogenic shock the ratio was also greater than that is the patients without these hazards. These results indicate that the ratio of serum m-AST/t-AST reflects the severity of the myocardial cellular damage in acute myocardial infarction.
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PMID:Immunological determination of serum m-AST activity in patients with acute myocardial infarction. 71 64

Clinical and autopsy study of 100 cases of patients dying during the first 3 weeks of hospitalisation for myocardial infarction revealed the following causes of death: cardiac failure in 59 cases (including 40 of cardiogenic shock), rupture of the heart in 29 cases (24 of rupture of the ventricular wall, 4 of the septum and 1 of a mitral papillary muscle). 4 ventricular arrhythmias and 6 haemorrhagic or embolic complications. In 2 cases, the cause of death could not be accurately determined. In cardiogenic shock, death usually occurred early. It was later in cases of refractory left ventricular failure. Conduction disturbances were much commoner in cases of myocardial infarction complicated by fatal cardiac failure (57.6%) than in the presence of any other complication (17.1%) (p less than 0.001). The responsible infarction was often extensive and recurrent. Rupture of the heart invariably occurred during the first three days of an infarction often initial (p less than 0.001), anterior (apart from septal rupture) and small in size (p less than 0.01). Other complications play only a secondary role in mortality at the present time, in particular arrhythmias, the gravity of which has greatly decreased since the reduction of delays before hospitalisation and improvements in anti-arrhythmic therapy.
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PMID:[Clinicopathological study of the causes of mortality during the acute phase of myocardial infarction (author's transl)]. 74 57

To evaluate the relationship between myocardial infarction and angina pectoris, history of symptomatic coronary heart disease was analyzed in 146 patients who had had documented myocardial infarction. There were 126 males and 70 females of mean age 55 years (range 32 to 70 years). Infarction had occurred 6 to 63 months prior to the study (mean: 30 months). Angina pectoris occurred at some time during the clinical course of 75 patients (51%), and 71 patients (49%) had not experienced angina. In the majority of the group with angina (n = 39; 52%) the symptom had not been present before infarction, appearing initially thereafter. Angina was present both before and after infarction in 31 patients (41%). In only 5 patients (7%) was precedent angina lost after infarction. Angina was, therefore, present in 70 of 146 patients (48%) after, compared to 36 patients (25%) before, infarction and in 86% (31/36) of patients with angina before infarction it persisted following the attack. Prior angina following myocardial infarction was not related to increased activity since in the majority of patients activity level was less after than before infarction. Post-infarction cardiac failure, which developed in 9 patients who had prior angina, was not associated with abolition of angina in any of this group. It is concluded that: 1. angina is frequent after myocardial infarction, 2. when present before infarction it usually persists thereafter, 3. angina commonly appears as a new symptom after infarction when not previously present and 4. disappearance of angina after infarction is distinctly uncommon.
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PMID:Relationship of myocardial infarction to presence of angina pectoris in patients with coronary heart disease: lack of abolition of angina by infarction. 75 12

1329 patients were discharged alive after acute myocardial infarction initially treated in a CCU. In a five-year follow-up, 537 (40%) of the patients died. Routine data registered uniformly during the CCU period showed that, apart from age, the most important factors regarding long-term prognosis in general were previous ischaemic heart disease and direct or indirect signs of heart failure registered in the CCU. The possibilities to predict sudden death (130 patients died within 2 hours of onset of final symptoms during the follow-up period) were small, although a definite dominance of this mode of death was noted in patients below 60 years of age. The clinical profile of the majority of the 134 patients who died during the first half-year was distinguished by a history of prior myocardial infarction and signs of left heart failure during the CCU stay. However, in a significant number of patients dying early after discharge, none of the ordinary unfavourable prognostic signs had been registered.
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PMID:Early and sudden deaths after myocardial infarction. A report from the Swedish CCU study. 76 Apr 5

Left ventricular function was investigated at rest and during exercise by heart catheterization in 15 patients 3-5 months after acute myocardial infarction. The effect of 1 mg digoxin i.v. in ten patients was correlated to placebo (saline solution) in five patients. A significant decrease of the left ventricular enddiastolic pressure, increase of left ventricular systolic ejection fraction and a shift of the left ventricular function curve to left upwards was found after digoxin with no changes in the placebo group. This beneficial effect of acute digitalization in patients convalescing from uncomplicated myocardial infarction without clinical signs of manifest heart failure could have therapeutic implication.
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PMID:Hemodynamic effects of acute digitalization several months after acute myocardial infarction. 78 4

The evaluation of left ventricular function in patients with acute myocardial infarction has shown: 1. Limitations in the use and interpretation of central venous pressure. 2. Pulmonary artery end-diastolic pressure reflects left ventricular end-diastolic pressure in the absence of pulmonary vascular or mitral valve disease. 3. Frequent elevations of left ventricular filling pressure in mild or clinically uncomplicated infarction. 4. Anterior infarctions present greater depression of left ventricular function than inferior infarctions. 5. Initial hemodynamic measurements in cardiogenic shock can predict prognosis with medical management. 6. Left ventricular function frequently improves during the early convalescent period. 7. Hemodynamic monitoring can be useful in following changes in left ventricular function and the response to therapy. The assessment of left ventricular performance in patients with chronic heart disease has shown: 1. Resting hemodynamic measurements are often normal but abnormalities can be observed in patients with disease of the left anterior descending coronary artery, diffuse coronary involvement, and after myocardial infarction. 2. Increases in end-diastolic volume or dilatation and left ventricular mass or hypertrophy can develop in severe coronary disease and after myocardial infarction. 3. The size of abnormally contracting segment after myocardial infarction is related to abnormalities in compliance, ventricular end-diastolic pressure, end-diastolic volume, and clinical manifestations of heart failure. 4. Exercise and atrial pacing can produce clinical and hemodynamic abnormalities. 5. The ejection fraction is significantly related to the slope of the ventricular function curve. 6. Angiographic abnormalities of left ventricular wall motion can be increased with atrial pacing and reduced with nitroglycerin or epinephrine.
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PMID:Left ventricular function in acute and chronic coronary artery disease. 80 47

Two randomized series of 60 cases of myocardial infarction or menace syndrome have been treated at the acute stage, one by Heparin alone, the other by the combination Urokinase-Heparin. The average dosage was 300 mg Heparin in the first series, of 2,700,000 CTA units of Urokinase combined with 240 mg of Heparin in the second series. After the first 24 hours, equal heparinization was performed in both series up to the third week. Significantly different results were obtained in the two series. They favour Urokinase and concern: -- the disappearance time of pain, -- the course of the arrhythmias and of cardiac failure, -- the regression or limitation of the necrosis q waves and the lesion areas on the electrocardiogram. Finally the 30th-day overall mortality was 13% in the Heparin series and 3% in the myocardial infarction on the way of constitution, or which have done so for less than 24 hours.
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PMID:[Treatment by urokinase of myocardial infarction and threatened infarction. Randomised study of 120 cases]. 81 98

In 214 patients with healed myocardial infarction an assessment was made of the prognostic value of risk factors relating to early postoperative cardiac decompensation which occurred in 50 cases. A significant influence was shown by age (greater than or equal to 75 years), pre-existing heart failure and load insufficiency, hypertension (greater than or equal to 180/95 mm Hg), advanced arteriosclerosis with cerebrovascular and renovascular symptoms, infections with fever or septicemia, emergency operations, lang-lasting surgery, decrease in blood pressure during operations (greater than or equal to 70 mm Hg systolic) and postoperative anemia (less than or equal to 3.5 millions erythrocytes/cmm). The postoperative cardiac failure took a lethal course in 60%. Pathogenetically, the discrepancy between O2-requirement and O2-supply in the previously damaged myocardium is of essential importance during the postoperative stress period.
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PMID:[Risk factors and pathogenesis of postoperative cardiac decompensation (author's transl)]. 81 21

One hundred and twenty patients went through a complete cycle of physical training. Eighty seven of them were recovering from recent myocardial infarction, eighteen had angina pectoris and fifteen were recovering from operation of aorta-to-coronary by-pass. Physical training was considered to be contra-indicated in the presence of evolutive angina pectoris, obvious signs of cardiac failure and a voluminous ventricular wall aneurysm. Severity of the anginal pains and intensity of the coronary artery lesions were not contra-indications. In all the cases, there was a decrease of the number and intensity of the pains while the extent of physical performance increased. The psychological effect was remarkable. Comparison between the maximal exercise tests before and after re-education showed an improvement of the cardio-circulatory function, as evidenced by a decreased cardiac rate, of the blood pressure and of the degree of the downward displacement of the ST segment for efforts of equal intensity.
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PMID:[Physical training in patients with coronary insufficiency. 2 year report of 2 center's activities]. 81 63

Study of four personal cases and of twelve cases reported in the literature makes it possible to describe the characteristics of coronary embolism in mitral stenosis, a rare complication but indicating the presence of a left intra-atrial thrombosis: -- variable clinical picture, dominated by a syndrome combining simultaneously a picture of myocardial infarction and of peripheral arterial emboli of other localizations; -- diagnosis to be discussed within the framework of coronary syndromes in mitral heart disease: embolism requiring to be distinguished from coronary atherosclerosis combined with mitral stenosis, more rarely a functional coronary insufficiency; -- severe course and prognosis: besides the possibility of rapidly lethal cases, coronary embolism seems liable to result in weakening and diminishing of the adaptation possibilities of the left ventricle, responsible for attacks of heart failure after mitral valvulotomy.
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PMID:[Coronary emboli in mitral stenosis]. 81 66


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