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)

During the period 1960 to 1978, 98 patients underwent intracardiac repair of Fallot's tetralogy after palliative operations. Preoperative symptoms were cyanosis, dyspnea, increased fatigue with squatting and hypoxic spells. The hemoglobin concentration varied from 19 to 22 g/100 ml. At correction only 65 of 95 shunts were patent and needed surgical closure. Seventeen early deaths occurred (19%), the main causes being cardiac failure and arrhythmia. One patient died 3 years after correction from pneumonia. The subjective clinical result was excellent or good in all surviving patients. At repeat heart catheterization in 26 patients a high percentage of residual ventricular septal defects and pulmonary stenosis/insufficiency was found. However, the majority of defects were of minimal haemodynamic significance, and so far did not seem to do harm to the patients' subjective function.
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PMID:Correction of Fallot's tetralogy after palliative operations. 8 99

In this case report, the patient had been delivered by Caesarean section and weighed only 4 pounds at birth. The mother was O negative, the father A positive, and the infant A positive. Initial red cell count was 2.85 million/cu mm; white cell count, 19,200/cu mm; and hemoglobin 70% of normal. At 3 months of age hemoglobin was 10% of normal. Bone marrow examination revealed marked erythroid hyperplasia. A diagnosis of Blackfan-Diamond syndrome was made. He received blood transfusions every 2 or 3 weeks for the first 4 years of his life. During his lifetime he received 433 units of packed cells for the treatment of congenital hypoplastic anemia. Vitamin-B12, folic acid, and iron were given without benefit. At 8 years of age a spelectomy was done. 20 months after surgery he recovered from pneumonococcal meningitis without sequelae. Progressive signs of hemochromatosis developed and finally progressive signs of heart failure with edema. At 24 years of age severe epigastric pain developed. An open liver biopsy disclosed multiple liver nodules which proved to be hepatoma. Severe ascites followed the surgery. Pulmonary metastases of the liver tumor developed and heart failure. He died at age 25. This patient had received no androgen. He was consistently hepatitis antigen negative. He was prepubertal at the age of 25 and had almost no endogenous androgens. Alpha-fetoglobin was present. This test may be useful as a screening test for hepatoma.
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PMID:Hepatocellular carcinoma, transfusion-induced hemochromatosis and congenital hypoplastic anemia (Blackfan-Diamond syndrome). 18 Aug 2

One hundred consecutive patients with hemoglobin concentration less than 3.5 g/dL (hematocrit reading, less than 10%) were admitted to the University of Baghdad Teaching Hospital, Iraq, during a 30-month period. Twenty-eight patients had aplastic anemia, 27 had leukemia or other hemopoietic malignancies, 16 had chronic renal failure, eight had iron-deficiency anemia, eight had hemolytic anemia, seven had thalassemia major, and six had other conditions. Twenty-three patients died within seven days of admission, mostly due to the underlying disease or complications thereof. Heart failure developed in ten patients, and five had retinal exudates and hemorrhages attributed to severe anemia. Arrhythmias and ECG abnormalities were noted in 20 of 68 patients. Blood transfusion was instituted in all but three patients, whose anemia was corrected with specific therapy without blood transfusion. The tolerance of the 100 patients to such severe anemia was remarkable.
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PMID:Severe anemia. Clinical observations in 100 patients with very low hemoglobin levels. 47 23

Sodium nitroprusside is an excellent agent for lowering blood pressure in hypertensive emergencies, for producing controlled hypotension during anesthesia, and for treating acute myocardial infarction and chronic heart failure. Toxic effects of this drug have been reported and above-normal cyanide and thiocyanate concentrations have been observed in the blood of a small proportion of subjects receiving nitroprusside. Nitrite, syanide, and thiocyanate are major decomposition products of nitroprusside, resulting from an in vitro reaction with human blood. On the basis of the conversion mechanism, we suggest that, in the cyanide/thiocyanate cycle, only cyanide is directly responsible for any acute toxicity attributed to sodium nitroprusside. In this work, the extent of cyanide production by erythrocytes in vitro was studied. The rate of detoxification of cyanide by human liver in vitro was experimentally determined and data from a search for a possible inhibitor of the nitroprusside/hemoglobin reaction are presented. Also, the possible mechanism of the nitroprusside/hemoglobin reaction is discussed.
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PMID:Some aspects of sodium nitroprusside reaction with human erythrocytes. 92 83

Sodium nitroprusside is a potent, effective, and readily reversible direct vasodilating agent. It is broken down by hemoglobin into cyanide, which is in part detoxified by liver and kidney to thiocyanate. Some cyanide, especially in nitroprusside- "resistant" individuals who need large amounts of the drug, appears to remain free to cause cyanide poisoning. Patients requiring inordinate amounts probably should not continue to receive the drug, although maximum dosage limits for long-term therapy are not established. Blood thiocyanate levels do not indicate the extent to which free cyanide is limiting oxygen utilization in essential tissue, nor do blood cyanide levels. Metabolic acidosis, elevated lactate levels, elevated lactate/pyruvate ratios, and elevated mixed venous blood oxygen content are at present the best indications of the presence of cyanide poisoning during nitroprusside administration. Nitroprusside appears useful for induction of hypotension during surgery, and for treatment of hypertensive emergencies from all causes, although continuance for more than a few days is probably unwise. The reductions of cardiac afterload and ventricular filling pressure by nitroprusside appear useful in treatment of severe myocardial failure or infarction, but studies of myocardial cyanide toxicity are needed before complete acceptance of this therapy is warranted. Initial dose rates between 0.5 and 1.5 mug/kg/min are recommended only as starting points for very careful titration. Total projected intra-operative dosage should be calculated as quickly as possible and should not exceed 3-3.5 mg/kg. It is hoped that future studies will reveal the maximum dose of nitroprusside that can safely be metabolized in a 24-hour period, and may indicate that cofactors of rhodanase such as thiosulfate, or cobalamins such as hydroxocobalamin, can be administered with nitroprusside to prevent cyanide poisoning.
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PMID:Sodium nitroprusside: pharmacology, toxicology and therapeutics. 96 81

Proceeding from their personal 5-years experience comprising over 1500 operations with extracorporeal circulation the authors formulate their tactics of the early postoperative therapy. The attention is mainly paid to the maintenance of the optimum pulmonary gas exchange, adequate haemodynamics and stable homeostasis. An important role belongs to prolonged artificial pulmonary ventilation that was used for therapeutic purposed in 324 cases of cardiac and respiratory insufficiency and for preventive purposes--in 908 patients. The therapeutic tactics for various forms of respiratory and cardiac insufficiency and multiform cardiac rhythm disorders is presented in detail. On the example of 149 patients shows that a moderately incomplete blood replacement in the postoperative period does not result in clearsut anaemia. The authors recommend donor blood transfusions when the hemoglobin level is below 10 Gm%.
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PMID:[Principles of early postoperative management of patients after open-heart surgery]. 114 36

Chronic pulmonary thromboembolism plays an important role in cardiac failure which is a major cause of death in thalassemic patients over 20 years of age. This report is a study of autopsy lung tissue from 58 patients with beta-thalassemia/hemoglobin E disease (beta-thal/HbE), including whole lungs from five, 13 patients with hemoglobin H disease (HbH), and eight patients with beta-thalassemia major (beta-thal) including whole lung from one. Pulmonary thromboembolic lesions were found in 24 of 58 (41%) patients with beta-thal/HbE, of which 21 of 39 (54%) were splenectomized patients and 3 of 19 (16%) were nonsplenectomized patients, with the incidence increasing with age. Lung maps showed the greatest number of lesions in the lingula, right middle lobe, and anterior segments of both upper lobes. Pulmonary thromboembolic lesions were also found in one of 13 HbH patients and one of 8 beta-thal patients, both splenectomized. Eight of the 27 patients with these lesions had right ventricular and 14 biventricular hypertrophy, reflecting the deleterious effect of such lesions. Possible causative factors are discussed.
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PMID:Pulmonary thromboembolism in thalassemic patients. 129 88

Mildronat potentiates the therapeutic effect of the combined treatment of heart failure, which includes the use of nitro drugs. It also decreases the level of methemoglobin in the patients' blood and improves the phosphate balance, especially that of 2,3-diphosphoglycerate to control oxygen transport by hemoglobin, which is of paramount importance in hypoxia caused by coronary heart disease.
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PMID:[The characteristics of the action of mildronate (dihydrate 3-(2,2,2-trimethylhydrazine)propionate) on the red blood parameters in heart failure]. 145 54

Thirty-one patients with chronic severe anemia of more than 3 months' duration (hemoglobin less than 7 gm/dl) and no underlying heart disease were studied by means of M-mode, two-dimensional, and Doppler echocardiography; an equal number of normal control subjects was also studied. There are conflicting reports regarding the influence of chronic severe anemia on systolic myocardial function, but diastolic function has not been systematically assessed. It is also uncertain whether anemia alone can cause heart failure in a structurally normal heart. We therefore performed a detailed study of echocardiographic indexes of systolic and diastolic left ventricular function in these patients. We found that patients with anemia have significantly faster heart rates and lower diastolic and mean blood pressures than normal subjects. They also have a significantly elevated cardiac output and stroke volume and larger left ventricles. Left ventricular contractility, assessed by the end-systolic stress-dimension relationship, was enhanced. There was no systematic evidence of diastolic dysfunction by Doppler assessment of mitral inflow. There was also no clinical evidence of congestive heart failure. We conclude that chronic severe anemia leads to a hyperdynamic state with systolic hyperfunction and no impairment of diastolic function. Anemia does not lead to congestive heart failure in the absence of underlying heart disease.
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PMID:Noninvasive assessment of systolic and diastolic left ventricular function in patients with chronic severe anemia: a combined M-mode, two-dimensional, and Doppler echocardiographic study. 146 8

A 60-year-old man was admitted with general fatigue and jaundice of one year's duration in February, 1981. The hemoglobin (Hb) was 11.4 g/dl and reticulocytes were 1.7%. A diagnosis of chronic cold agglutinin disease (CCAD) was made from the presence of cold agglutinin (CA) 1:2,048, increased serum IgM 267 mg/dl and indirect bilirubin 1.4 mg/dl. His Hb was approximately 11 g/dl in summer and 9 g/dl in winter for the subsequent ten years without therapy. In July, 1990, he was readmitted because of exacerbation of anemia and hepatosplenomegaly. The Hb was 4.6 g/dl, indirect bilirubin 3. 1 mg/dl, CA titer 1:232,144 and reticulocytes were 20%. Serum IgM was 1,065 mg/dl, and immunoelectrophoresis showed IgM-kappa M-protein. Peripheral blood lymphoid cells expressed surface membrane immunoglobulin (SmIg) M and kappa. The bone marrow showed an increased number of lymphoid cells which also expressed SmIg M and kappa. These findings were compatible with those of the features of primary macroglobulinemia (PMG). The M-2 protocol resulted in decrease in serum IgM and CA, but he died of heart failure in February, 1991. The relationship between CCAD and PMG in relation to the pathogenesis was discussed.
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PMID:[Chronic cold agglutinin disease terminating in primary macroglobulinemia after a 10 year history]. 146 90


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