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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The frequency with which pulmonary embolism remains unrecognized clinically is well known and explains the value of pulmonary scintigraphy when there is the slightest suspicion of pulmonary embolism or in cases of unexplained dyspnoea of effort after a standard cardiac and pleuro-pulmonary examination. The practical value of a regular pre-operative electrocardiogram and of anticoagulant treatment during the acute phase of myocardial infarction are emphasized. Certain precautions to be observed during the use of antivitamins K in cases of heart failure are outlined.
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PMID:[Cardiologist's approach to deep phlebitides of the leg]. 120 21

The autopsy findings and clinical features in 60 patients with fatal pulmonary embolism (PE) in University College Hospital, Ibadan, between 1985 and 1989 are analysed in the current study. Pulmonary embolism occurred in 3,8 pc of all autopsied patients during this period. There was a male to female ratio 1,4 to one and average age was 47 years. Malignant neoplasms, infections and cardiac failure were the leading predisposing factors to PE identified. The ante-mortem clinical features consisted largely of non-specific respiratory symptoms of dyspnoea, cough, chest pain and haemoptysis. Of these patients, 15,6 pc were diagnosed ante-mortem as having PE. Pulmonary infarction occurred in 13,3 pc of the cases and was commoner in females and in patients with underlying cardiac diseases. This study emphasises the need for a high clinical index of suspicion to improve the antemortem diagnosis of this potentially fatal condition and to advocate a greater use of prophylactic anti-coagulant therapy in high risk patients.
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PMID:Pulmonary embolism in Ibadan, Nigeria: five years autopsy report. 130 38

Four children, three males, with ages 5, 1, 16 and 6 years, presented with isolated tricuspid valve endocarditis. Two of them were submitted to surgical treatment. Sepsis, cardiac murmur and heart failure were present in all of them. Three presented pulmonary embolism. Echocardiography demonstrated vegetation in the tricuspid valve in all cases. Two patients, one of them submitted to surgery, died. Tricuspid valve endocarditis in children with sepsis, heart failure and pulmonary embolism is a severe condition and early surgical treatment may diminished the high mortality.
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PMID:[Tricuspid valve endocarditis in children]. 134 Jul 11

The SDH and LDH activity in ventricular myocardium was studied in early autopsies of 16 patients, which died from acute pulmonary thromboembolism, and also in 17 dogs with experimental pulmonary embolism. In general the data of histoenzymological study of experimental and sectional material were identical. We revealed some factors, which correlated with low activity of catabolic enzymes in ventricular myocardium of the patients with pulmonary embolism: small volume of embolic occlusion (the thromboembolism of lobar and segmental pulmonary arteries); the presence of prior chronic cardiopulmonary disease; the advanced age and the female sex. Preexisting cardiopulmonary disease, as well as age and sex changes of myocardial metabolism, may assist the development of heart failure by relatively small volume of embolic obstruction.
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PMID:[Clinico-experimental study of histoenzymological changes in the ventricular myocardium in pulmonary embolism]. 142 Dec 85

A review of the literature shows a very variable mortality, especially after emergency operations for abdominal aortic aneurysm (AAA) (14-70%). We therefore analyzed the mortality of our patients in different subgroups. The hospital data of 82 patients operated on for abdominal aortic aneurysm were analyzed retrospectively. 42 patients underwent emergency operations and 40 patients elective surgery. The mean age was 67.5 +/- 9.4 and 70.7 +/- 7.3 years respectively. The overall 30-day mortality in elective cases was 5% (2/40); elective patients under the age of 75 years had a mortality of 0%. 33% of the emergency cases died within 30 days. The mortality in various subgroups was as follows: "asymptomatic AAA" 5.4% (2/37), "symptomatic AAA" 10% (1/10), "retroperitoneal rupture" 34% (11/32) and "intraperitoneal rupture" 66.6% (2/3). Preoperatively 21/42 patients who underwent emergency surgery were in hypovolemic shock (systolic blood pressure < or = 90 mm Hg). The mortality of these patients was 52% (11/21) compared to 9.5% (2/21), (p < 0.01), in emergency patients without preoperative shock. The causes of death after emergency procedures were hypovolemic shock in 6, heart failure in 4, and multi-organ failure, respiratory insufficiency, unknown and pulmonary embolism in 1 each. 5/14 patients died in theatre. Two patients died after elective procedures: one 9 days postoperatively from myocardial infarction and the second 23 days after the operation from an unknown cause. Reoperation rate after elective and emergency procedures was 7.5% and 16.6% respectively. Mortality after reoperation was 40%.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Abdominal aortic aneurysm. Risks and early postoperative course]. 144 85

Asthma bronchiale (a.b.) is defined as paroxysmal or permanent, partly or completely reversible dyspnoea due to a bronchospasm resulting from pathological hyperreactivity of the bronchial system. In the pathogenesis participate allergic, immuno-infiltrative and genetic factors, irritating substances (environment) and infectious. The allergic constituent acts via sensitization and allergization of the mast cell, to its degranulation with release of mediators (histamine, serotonin, leukotrienes, thromboxane, PAF) with subsequent bronchoconstriction and production of viscous mucus. As to adrenergic factors, a block of beta-adrenergic receptors and reduced adrenal function is involved. As to non-adrenergic factors an increased sensitivity of the parasympathetic--vagus is involved which conditions bronchoconstriction and hyperkrinia. From the clinical aspect extrinsic (atopic) and intrinsic (cryptogenic) asthma bronchiale can be differentiated. The former is encountered more frequently in childhood and adolescence, in subjects with a positive family-history, high IgE and positive skin tests and a known allergen. The latter type of a.b. is found in adolescence, in subjects with a negative family-history, with eosinophilia; it is conditioned by infection (e.g. chronic bronchitis), strain, cold and takes a dangerous course (aspirin). As to the course, attacks of a.b. are involved with a symptom-free interval (extrinsic a.) easily controlled by treatment. Then there is the chronic form with a variable course and the necessity of permanent treatment. Status asthmaticus is in recent years with increasing frequency the cause of death and thus calls for maximal treatment. It is the third most serious form of a.b. Assessment of arterial blood gases is very important as a check of treatment as well as from the prognostic aspect (cross-over intubation). From the differential diagnostic aspect we must consider the asthmoid component in chronic bronchitis, pulmonary embolism, left-sided cardiac failure, tracheal or bronchial compression by an aortal aneurysm, tumour. The differential diagnosis is not always easy.
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PMID:[Bronchial asthma. Pathogenesis and clinical aspects]. 145 62

We conducted a retrospective analysis on 311 patients with clinical diagnosis of pulmonary embolism (PE) in a period of 3 years. 163 patients were excluded based on clinical-laboratorial criteria. The remaining 146 patients had a median age of 69 years (range: 30-91 years). 54% of the patients were male. We found dyspnea (94%), abnormal cardiopulmonary observation (89%), risk factors for venous thromboembolism (74%), tachycardia (53%), cyanosis (49%), and neck vein distension (45%) to be the most frequent findings. 64% of the patients had heart failure, 32% had myocardial ischemia, 13% had cancer, and 11% had myocardial infarction. Lactic dehydrogenase (LDH) was higher than two-fold in 54% of the patients. There was severe hypoxemia in 55% of the cases and hypocapnia in 43% of the cases. Creatinine phosphokinase (CPK) was elevated in 16% of the cases. Electrocardiography was suggestive of PE in 37% of the cases. Echocardiography showed right heart dysfunction in 30% of the cases, 92% of the patients were treated with heparin, 37 patients (25%) died, 54% of which during the first 4 days after admittance. Trying to define an index of mortality in PE we evaluated all patients by discriminant analysis coming up with 14 items with good discriminative power. By approximation of their odds-ratios we determined how many points would correspond to each item in the total sum.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Pulmonary embolism--mortality risk]. 147 67

The damage of ventricular myocardial cells during acute experimental massive pulmonary embolism (MPE) was studied by light, polarization and electron microscopy on anaesthetized dogs. In cases, when MPE was followed by heart failure, the deep ir reversible damage of myofibrils took place, and the relative volume of myofibrils decreased in both ventricles. The damage of right ventricular myocardium, which works against increased postload during MPE, may be reason of right ventricular insufficiency.
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PMID:[Lesions of ventricular cardiomyocytes in experimental massive pulmonary embolism]. 147 75

During the acute phase of myocardial infarction, the generation of thrombin is reflected in the sudden rise of fibrinopeptide A (FPA) and the thrombin-antithrombin III (TAT) complex in blood. We have systematically determined the FPA and TAT plasma concentrations over a period of 14 days after acute myocardial infarction in 100 patients. Mean levels of both thrombin markers were the highest on admission, remained elevated over the following few days, and then gradually declined after day 5. Still, by the end of the first week two thirds of the patients had distinctly elevated TAT and FPA levels, and by the end of the second week such an abnormality was present in half of them. Continuous intravenous heparin infusion at a dose of 20,000 units/day, administered for 1 week to patients who had either received (n = 21) or not received (n = 17) streptokinase, led to a significant depression (p less than 0.05) of thrombin markers over the first 48 hours, an effect that did not persist over the subsequent days of treatment. In patients not assigned to heparin treatment, those in heart failure had significantly (p less than 0.05) higher mean TAT and FPA values on days 3, 5, and 7 compared with patients in whom heart failure was absent. Infarct extension, pulmonary embolism, and death were also associated with a rise in one or both thrombin markers, often preceding the onset of clinical symptoms. Thrombinogenesis was not accompanied by changes in mean plasma concentrations of prothrombin, antithrombin III, or alpha 2-macroglobulin.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Persistent generation of thrombin after acute myocardial infarction. 157 16

Four years after an HIV infection and without any preceding illness characteristic of AIDS, a 24-year-old woman developed dyspnoea on exertion and peripheral oedema. She had for several years been an intravenous drug addict and contracted hepatitis A and B. There were no symptoms of the HIV infection. Clinical, radiological and echocardiographic examination demonstrated right ventricular failure caused by pulmonary hypertension not due to pulmonary embolism or another known aetiology. The patient died suddenly 9 months after the diagnosis from heart failure. Autopsy established primary pulmonary hypertension with pathognomonic plexogenic pulmonary arterial disease which had led to cor pulmonale with overload myocarditis. Although there had been no clinical signs of renal failure, there was histological evidence of mesangioproliferative glomerulonephritis and non-destructive interstitial nephritis. This case demonstrates that, in addition to the typical AIDS-associated diseases, other rarer syndromes may, in uncertain ways but connected with the HIV infection, decide the prognosis of such patients.
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PMID:[Primary pulmonary hypertension and mesangioproliferative glomerulonephritis in HIV infection]. 158 15


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