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)

To determine whether survival of patients with beta-thalassemia major has been prolonged by management that utilizes hypertransfusion and chelation with deferoxamine, we analyzed longevity by the Kaplan-Meier product-limit method. Group 1 patients (n = 71) followed between 1960 and 1976 with a low-transfusion regimen (pretransfusion hemoglobin level 7 to 8 gm/dl) and no chelation had an estimated median age of survival of 17.4 years, whereas it was 31.0 years for group 2 subjects (n = 80), who began hypertransfusion between 1976 and 1978 (pretransfusion hemoglobin level 10.5 to 11.5 gm/dl) and chelation with deferoxamine (20 to 60 mg/kg per day) (p less than 0.0001). For 70 patients who were treated with hypertransfusion and deferoxamine, we had data to calculate the ratio of total milligrams of transfusional iron to cumulative grams of deferoxamine. The 24 patients who died had a total iron burden of greater than 1.05 gm/kg; the ratio for them exceeded 31. These patients were characterized by poor compliance with chelation or by late start of therapy, with inability to receive enough deferoxamine before death. Death was preceded by arrhythmia requiring therapy in all but one, and by cardiac failure in all. Of 41 similarly iron-loaded survivors, 33 had a ratio of less than 31; only three had an arrhythmia, and five had cardiac failure. We conclude that treatment with deferoxamine, when used in amounts proportional to iron burden, delayed cardiac complications and improved longevity.
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PMID:Prolonged survival in patients with beta-thalassemia major treated with deferoxamine. 200 28

In experiments with isolated animal hearts it has been ascertained that free hemoglobin, lactic acids, catecholamines, vasopressin and acetylcholine at the concentrations they appear in patients' blood during open heart surgeries can produce cardiodepressive effects and cause acute heart failure. Cardiac reperfusion with a solution containing 20% less sodium, potassium, calcium, magnesium and hydrogen ions leads to severe heart failure: lower osmotic capacity and/or concurrent smaller Na+ and H+ concentrations were responsible for myocardial contractility disturbances.
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PMID:[Causes of disorders of the contractile function of the heart after cardioplegia]. 204 40

Four male patients aged 32 to 42 years were followed up. The clinical picture of the disease was typical of dilated (congestive) cardiomyopathy with a subacute onset, development of pronounced heart failure; all the patients were found to have exudate pericarditis. All the men were of the same occupation; they worked at the hard alloy works at a bay of wet grinding in ethanol of metallic Co and hard alloy carbides. The content of Co in the air of the working premises exceeded the MAC and amounted to 7.8-10 mg/m3. Besides, 47 workers of the same occupation (90% of the number of persons engaged in making up powdered compositions of hard alloys) were examined in addition. 16 persons showed the signs of alcoholization, including 9 (out of 11) working at a bay of wet grinding. During the recent 20 years, no cases of respiratory occupational diseases were recorded at the bay. The cardiotoxic properties of Co manifest themselves after the preceding toxic exposures, among which the leading part is played by alcohol. Of the 4 patients, 3 developed the disease in the presence of alcoholism, in 1 patient, it was coupled with tuberculous intoxication. Marked tendency towards polycythemia and increase of the content of hemoglobin was a frequently occurring manifestation of Co action on the workers (rather than a sign of intoxication).
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PMID:[Cobalt-induced cardiomyopathy in workers engaged in the manufacture of hard alloys]. 206 57

The prevalence of microalbuminuria and persistent proteinuria was studied in a population of 801 diabetic patients (535 with type II and 266 with type I diabetes). Urinary albumin excretion rate (AER) was measured on morning samples by laser nephelometry. Normoalbuminuria, as defined, in the absence of contaminated urine, by an albumin: creatinine (A/C) ratio below 2, was found in 551 patients, microalbuminuria (NC greater than or equal to 2 with AER below 200 mg/l) in 190 patients and persistent proteinuria (AER greater than or equal to 200 mg/l) in 60 patients. Microalbuminuria was present in 48 (18 p. 100) IDDM patients and 142 NIDDM patients. In IDDM patients, AER increased with the duration of the disease with no apparent influence of age at the onset. The prevalence of hypertension was 25 p. 100 and 61 p. 100 in IDDM patients with microalbuminuria and macroproteinuria respectively versus 10 p. 100 in patients with normoalbuminuria. This prevalence increased in NIDDM patients from 39.3 p. 100 with normoalbuminuria to 40.8 p. 100 and 76.2 p. 100 with microalbuminuria or macroproteinuria respectively. Proliferative retinopathy in type I and type II patients with normal AER was 7.4 p. 100 and 1.2 p. 100 respectively increasing to 15.2 p. 100 and 8.9 p. 100 with microalbuminuria and 27.8 p. 100 and 23.1 p. 100 with macroproteinuria. The prevalence of coronary disease increased from 4 to 10.4 p. 100 in patients with type I diabetes and microalbuminuria. The prevalence of cardiac failure increased from 1.5 to 2.1 p. 100 in type I diabetics and from 3.2 to 7.8 p. 100 in type II diabetics in the presence of microalbuminuria. Patients with microalbuminuria had increased levels of glycosylated hemoglobin A 1C but statistical difference was only obtained for patients with type II diabetes. Routine analysis of AER in diabetics allows early detection of diabetic nephropathy and emphasizes the need for tight metabolic and blood pressure control. Hypertension can be detrimental to nephropathy but might also initiate renal lesions in NIDDM patients.
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PMID:[Microalbuminuria and diabetic nephropathy. Detection and correlation with other degenerative complications]. 214 8

We describe a patient with CML who developed hypercalcemia in his course of blast crisis. A 25-years-old man was diagnosed as CML with priapism in April 1985, and controlled with BHAC-DVP, VMP, busulfan therapy. In December 1987, he readmitted to our hospital with abdominal pain. Investigations at that time showed: white blood cell count 11600/microliters (blast cells 9%); hemoglobin 8.4 g/microliters; platelets 19.0 X 10(4)/microliters; serum calcium 13.2 mg/dl; BUN 44 mg/dl; creatinine 2.7 mg/dl. Treatment with predonine, 6-MP and vincristine was begun. But serum calcium level rose gradually up to 16.5 mg/dl. So we tried middle dose Ara-c therapy, serum calcium decreased to 6.8 mg/dl. At once he was in a chronic phase, but he relapsed and died of heart failure. Necropsy showed extensive leukemic blast-cell infiltration of the bone marrow, liver, spleen, lung, and kidney. The cause of hypercalcemia in our case was suspected of local osteolytic hypercalcemia, because multiple bone destruction was found.
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PMID:[Hypercalcemia associated with blast crisis of chronic myeloid leukemia]. 218 69

Myocardial oxidative and glycolytic reserves were evaluated in four harbor seals, Phoca vitulina richardsi, and six domestic pigs, Sus scrofa (hematocrits: 58 +/- 5 and 34 +/- 1%., respectively). Progressive hypoxia was induced by lowering arterial hemoglobin-oxygen saturation in 10% decrements, each maintained for 10-min periods, until the onset of heart failure. Myocardial oxygen consumption rate (VO2), lactate release/uptake rate (L), and triple product, an index of myocardial energetic demand, were determined at each saturation level. Onset of L began in pigs at Sao2 = 57 +/- 5% and in seals at Sao2 = 35 +/- 4%. Cumulative oxygen consumption (VO2) during hypoxia, determined from the onset of cardiac lactate release, was 435 ml O2/100 g in seals and 172 ml O2/100 g in pigs. Cumulative lactate release during the same period was 14 mM/100 g in seals and 4.6 mM/100 g in pigs. The pigs' left ventricular contractile response (dP/dtmax) was greater than that of seals throughout the time of lactate release. Total myocardial energetic sources were higher in seals than in pigs, and seals were better able to tolerate myocardial hypoxia than were pigs. In a separate experiment, two seals and six pigs were made acutely hypoxic until cessation of cardiac output (seals, 17.5 min; pigs, 7.4 min) and were then reoxygenated. Both seals recovered promptly to control levels of cardiac mechanical function, whereas none of the pigs recovered. Additionally, five pigs were beta-blocked with 0.10 mg/kg of propranolol and were subjected to acute hypoxia. Tolerance to cardiac hypoxia in beta-blocked pigs was significantly increased compared with that of control animals.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Responses of harbor seal and pig heart to progressive and acute hypoxia. 222 Nov 53

Since 1985 all patients scheduled for coronary artery bypass grafting have been evaluated for admission to a program of predeposited blood autodonation. From a total of 816 consecutive patients, 505 were admitted to the program (group 1). The other 311 (group 2) were excluded on the basis of one or more of the following criteria: 1) emergency surgical indication, 2) hemoglobin less than 12 g/dl, or 3) uncontrolled angina or clinically manifest cardiac failure. Postoperative use of homologous blood products was required by 16% of the group 1 and 44% of the group 2 patients (p less than 0.001). Altogether 597 patients (73%) had no contact with homologous blood products. There was no intergroup difference in the incidence of postoperative complications. Non-A, non-B hepatitis developed in three group 1 and four group 2 patients. Its incidence was 0.9% among all discharged patients and 3.2% of the homologous blood recipients. The findings emphasize the safety and value of the autodonation with predeposit program in significantly reducing the requirement for homologous blood in coronary artery bypass grafting.
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PMID:Efficacy and safety of predeposit blood autodonation in 500 cases of myocardial revascularization. 229 53

The clinical background relating to edema in elderly inpatients was investigated, in terms of various items in elderly (aged greater than or equal to 65) cases with edema (n = 96) and without edema (controls, n = 95). Both groups were matched for sex, age, and underlying diseases. As compared with the control patients, the patients with edema had longer hospital stays with more disabled status, and showed less activity of daily living (ADL). The rates of bed-restricted patients, dementia patients, and patients with decubitus, muscle atrophy, or incontinence were found to be significantly higher in the patients with edema. The measurement of biochemical parameters revealed that the patients with edema had significantly lower levels of serum albumin, Na, Cl, creatinine, and uric acid, in contrast to higher levels of C-reactive protein. According to the classification of the assumed causes of edema, we divided the patients with edema into five groups; group 1 (n = 33): edema associated with immobilization, group 2 (n = 18): edema due to heart failure, group 3 (n = 15): edema on paretic limbs, group 4 (n = 6): edema due to hypoproteinemia, group 5 (n = 5): edema associated with liver cirrhosis. Both group 1 and group 4 patients had lower levels of hemoglobin and albumin, whereas group 3 patients had higher scores of ADL, higher blood pressure, and higher levels of hemoglobin and albumin. These results suggest that immobilization and restriction in bed, as well as malnutrition, were important factors in causing edema in elderly inpatients.
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PMID:[A controlled study on edema in elderly inpatients]. 238 89

Blood gaseous composition, mechanisms controlling hemoglobin affinity to oxygen and hemoglobin effects of a single captopril dose were assessed in 124 patients with chronic heart failure (CHF). CHF-associated hypoxemia was shown to be mixed, with the circulatory component prevailing. Hemoglobin affinity to oxygen is increased in CHF, stage IIA, and reduced in CHF, stages IIB-III. 2,3-diphosphoglycerate is the principal regulator of hemoglobin affinity to oxygen its blood level increasing progressively as CHF aggravates. Hemoglobin affinity to oxygen may be reduced by captopril in patients with CHF of stages I-IIA.
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PMID:[Hemoglobin affinity to oxygen and its correction with captopril in chronic cardiac insufficiency]. 250 46

The primary cause of death following i.v. injection of the basic phospholipase A2 (PLA2) from Naja nigricollis venom has been attributed to its direct cardiotoxicity. In view of our recent findings that cardiac failure caused by the basic PLA2 from Naja m. mossambica is primarily due to hyperkalemia resulting from cellular damage and possibly also from hemolysis, the cause of death due to the basic PLA2 from Naja nigricollis was re-investigated. In the anesthetized mice and rats, the PLA2 (0.3 micrograms/g, i.v.) produced a transient hypotension followed by recovery and subsequently by cardiac failure with ECG changes suggestive of hyperkalemia, such as P-R prolongation, tall T-wave, biphasic QRS-T complex, low voltage of QRS, A-V block, etc. Analysis of blood chemistry revealed marked increases in the plasma levels of K+, CPK, LDH, GOT, GPT, inorganic phosphate and hemoglobin (probably a mixture of hemoglobin and myoglobin). In the atrial preparation, however, no marked cardiotoxicity was observed except for a slight negative inotropic effect at 30 micrograms/ml. When 200 micrograms of the enzyme was injected into the coronary circulation in the Langendorff preparation, also no marked cardiotoxic effect was observed except for a decrease (about 40%) of coronary flow. From these results, it is concluded that the primary cause of death following i.v. injection of the basic PLA2 from Naja nigricollis is apparently cardiac failure due to hyperkalemia, resulting from cellular damage and possibly also from hemolysis, rather than direct cardiotoxicity.
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PMID:Is direct cardiotoxicity the primary cause of death following i.v. injection of the basic phospholipase A2 from Naja nigricollis venom? 252 Mar 58


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