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)

Thyroid function was studied in 40 patients with chronic heart failure. Thyroid antibodies and microsome antibodies were negative in all cases. Serum T4, and T3 concentrations showed significant inverse correlation with cardiothoracic ratio, mean right atrial pressure, pulmonary artery systolic pressure, and peripheral venous pressure. Serum T4, T3 concentrations showed significant correlation with PaO2, serum albumin, and serum cholinesterase. Serum TSH concentrations increased with increasing cardiothoracic ratio. Histological examinations showed fibrosis and atrophy of the thyroid gland in 2 cases. These findings suggest the possible development of primary hypothyroidism as a result of chronic heart failure.
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PMID:Primary hypothyroidism in severe chronic heart failure. 296 70

In anaesthetized guinea-pigs treated with lethal doses of dimethoate, cardiac failure and serious ECG disturbances developed in the early phase of intoxication. The toxic cardiac phenomena appeared to be unrelated to the degree of cholinesterase inhibition, but showed a close correlation with myocardial dimethoate concentration. Cardiac failure and mortality were first observed at a critical pesticide level of about 110 micrograms/g, while a level of 221 micrograms/g resulted in death in all cases. The present investigation refers to the direct effect of the pesticide on the myocardium, independent of its anticholinesterase action.
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PMID:Dimethoate-induced toxic cardiac failure in the guinea pig. 402 75

In order to study nutritional assessment and nutritional support therapy for elderly patients, we conducted energy supply therapy on 15 elderly (aged over 75) patients disabled with diseases such as cerebrovascular disease, pneumonia and heart failure. After recovery from acute phase, they were divided into 3 groups, and assigned to 3 different energy supply methods for 2 weeks: Six (3 males, 3 females) could take hospital diet, but only could absorb about 50% of the energy, amounting only 1,000 to 1,400 kcal/day. Additional 246 kcal was given by peripheral parental nutrition (PPN). Five (2 males, 3 females) were unable to take nutrition orally. Therefore, they were given high caloric nutrients by total parental nutrition (TPN), giving (1,222 kcal daily for a week), then 1,666 kcal for another week. Four (1 male, 3 females) also could not take meals orally, and had to be nourished by enteral nutrition (EN) with a nutrient preparation of 1,120 kcal for one week, then with 1,600 kcal for another week. In all 3 groups, the indices of rapid turnover proteins (pre-albumin, retinol binding protein and transferrin), choline esterase and vitamin A significantly elevated after 2 weeks of therapy, though the increase of pre-albumin and RBP in TPN group was slightly below the significant level. The increase in rapid turnover proteins and choline esterase was greater in the order of EN, TPN and PPN. Vitamin C, on the other hand, decreased significantly with treatment in all the groups, while vitamin E remained unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Nutritional assessment and nutritional support therapy in elderly patients]. 836 Oct 76

The available data suggests that hypotension caused by Hg2+ administration may be produced by a reduction of cardiac contractility or by cholinergic mechanisms. The hemodynamic effects of an intravenous injection of HgCl2 (5 mg/kg) were studied in anesthetized rats (N = 12) by monitoring left and right ventricular (LV and RV) systolic and diastolic pressures for 120 min. After HgCl2 administration the LV systolic pressure decreased only after 40 min (99 +/- 3.3 to 85 +/- 8.8 mmHg at 80 min). However, RV systolic pressure increased, initially slowly but faster after 30 min (25 +/- 1.8 to 42 +/- 1.6 mmHg at 80 min). Both right and left diastolic pressures increased after HgCl2 treatment, suggesting the development of diastolic ventricular dysfunction. Since HgCl2 could be increasing pulmonary vascular resistance, isolated lungs (N = 10) were perfused for 80 min with Krebs solution (continuous flow of 10 ml/min) containing or not 5 microM HgCl2. A continuous increase in pulmonary vascular resistance was observed, suggesting the direct effect of Hg2+ on the pulmonary vessels (12 +/- 0.4 to 29 +/- 3.2 mmHg at 30 min). To examine the interactions of Hg2+ and changes in cholinergic activity we analyzed the effects of acetylcholine (Ach) on mean arterial blood pressure (ABP) in anesthetized rats (N = 9) before and after Hg2+ treatment (5 mg/kg). Using the same amount and route used to study the hemodynamic effects we also examined the effects of Hg2+ administration on heart and plasma cholinesterase activity (N = 10). The in vivo hypotensive response to Ach (0.035 to 10.5 microg) was reduced after Hg2+ treatment. Cholinesterase activity (microM h-1 mg protein-1) increased in heart and plasma (32 and 65%, respectively) after Hg2+ treatment. In conclusion, the reduction in ABP produced by Hg2+ is not dependent on a putative increase in cholinergic activity. HgCl2 mainly affects cardiac function. The increased pulmonary vascular resistance and cardiac failure due to diastolic dysfunction of both ventricles are factors that might contribute to the reduction of cardiac output and the fall in arterial pressure.
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PMID:Effects of mercury on the arterial blood pressure of anesthetized rats. 1045 61

Alzheimer's disease (AD), the leading cause of disability in people older than 75 years of age, has direct and indirect medical costs estimated at $100 billion per year. Yet underdiagnosis, coding, and reimbursement barriers result in most patients with AD receiving inadequate care. The vast majority of managed care organizations (MCOs) still lack formal disease management programs for AD. In several documented studies, the total costs for managing patients with AD increased significantly over age- and comorbidity-matched controls without AD. Importantly, these extra costs include not only nursing home care but also medical claims for inpatient stays, emergency department visits, and outpatient care. The extra costs are especially high in those patients with comorbidities such as diabetes or heart failure. Emerging pharmacoeconomic data indicate potential savings in medical care costs associated with early treatment of AD and the potential cost effectiveness of cholinesterase inhibitors such as donepezil. These studies document that Medicare MCOs are in need of directed efforts to improve medical management for members with AD.
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PMID:The pharmacoeconomics of Alzheimer's disease. 1114 78

A 45-year-old woman was referred to our hospital because of hyperthyroidism complicated by atrial fibrillation and heart failure. Laboratory data revealed pancytopenia, with a white blood cell count of 2,600/microliter, red blood cell count of 330 x 10(4)/microliter, and platelet count of 6.2 x 10(4)/microliter. The patient had normal transaminase levels, but tests for hepaplastin and cholinesterase showed values of 34% and 1.4 U/ml, respectively, indicating liver dysfunction. There was also decreased excretion of indocyanine green. After initiation of treatment with 30 mg thiamazole and 20 mg propranolol daily, the patient's thyroid function normalized and the other abnormal laboratory findings such as pancytopenia and liver dysfunction also disappeared. Pancytopenia is a rare complication of hyperthyroidism. In this case, various laboratory abnormalities were normalized by antithyroid therapy alone, indicating that the hyperthyroidism itself was closely related to the pathogenesis of pancytopenia and liver dysfunction.
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PMID:[Recovery from pancytopenia and liver dysfunction after administration of thiamazole for hyperthyroidism]. 1119 44

Cardiac parasympathetic activity reduces susceptibility to potentially lethal ventricular arrhythmias in heart failure and ischemic heart disease. This influence is mediated in large part by antagonism of the adverse cardiac effects of sympathetic overactivity ("indirect" parasympathetic activity) in addition to the "direct" effects of muscarinic stimulation. Nitric oxide modulates parasympathetic cardiac signaling in some animal models, but human data are lacking. We have investigated the influence of endogenous nitric oxide on cardiac responses to parasympathetic stimulation in healthy humans. In 18 volunteers, we studied chronotropic and inotropic responses to muscarinic stimulation, both before and after prestimulation with isoproterenol. Cardiac muscarinic stimulation was achieved using an intravenous bolus of the short-acting cholinesterase inhibitor, edrophonium. Responses were assessed during a background infusion of a nitric oxide synthase inhibitor (N(G)-monomethyl-L-arginine [L-NMMA]), placebo (saline), or phenylephrine (vasoconstrictor control) in a single-blind, random order, crossover protocol. L-NMMA did not affect chronotropic responses to edrophonium alone (direct parasympathetic activity). The decrease in heart rate attributable to "indirect" parasympathetic activity (derived by comparison with the effect of edrophonium during concurrent adrenergic stimulation) was substantially attenuated by L-NMMA in comparison to both control infusions. No modification of muscarinic inotropic responses by L-NMMA was apparent in comparison to the vasoconstrictor control. Nitric oxide exerts a powerful facilitating influence on indirect (antiadrenergic) but not direct human cardiac parasympathetic control. Stimulation of the endogenous nitric oxide pathway might enhance parasympathetic protection against the adverse influences of cardiac sympathetic overactivity.
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PMID:Nitric oxide and cardiac muscarinic control in humans. 1503 54

A novel electrochemical enzyme immunoassay system with a 10 ng L(-1) level detection limit was developed for the determination of B-type natriuretic peptide (BNP), an important marker for the diagnosis of heart failure. Sample BNP was added to a solution containing a certain concentration of acetylcholinesterase(AChE)-labeled anti-BNP antibody to undergo an immunological reaction. After the immunological reaction, we proposed two assay schemes. One involves measuring the amount of antibody-enzyme conjugate that reacted with two BNP molecules (reacted conjugate). The other involves measuring the amount of antibody-enzyme conjugate with at least one free binding site (unreacted conjugate). Then the amount of reacted or unreacted conjugate was determined by measuring the AChE activity after the recovery of each conjugate from the immunological reaction mixture. To determine the trace level of the recovered antibody-enzyme conjugate, the AChE activity was determined with high sensitivity on the basis of the chemisorption/electrochemical desorption process of thiocholine, which was produced through the enzymatic reaction, on a silver surface. The thiocholine chemisorption (i.e., accumulation) on the silver electrode surface resulted in a sensitivity for the electrochemical determination of the AChE activity that was 2 orders of magnitude greater than that obtained when using direct measurement without accumulation. The procedure for determining the AChE activity of unreacted conjugate after its recovery on a BNP-modified disk was applied to the determination of BNP in serum samples. This procedure involves the removal of the immunological reaction mixture before the enzymatic reaction process, which allows the AChE activity to be measured without any interference from endogenous pseudocholinesterase, which exists with high activity in serum. With both procedures, the BNP could be measured within an hour. The detection limits were 20 and 40 ng L(-1) using the reacted and unreacted conjugate measuring procedures, respectively.
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PMID:Electrochemical enzyme immunoassay of a peptide hormone at picomolar levels. 1598 32

Heart failure is correlated with attenuation of parasympathetic nervous function and enhanced sympathetic activity. Carvedilol, a third-generation beta-blocker, may improve the prognosis of heart failure better than selective beta(1)-blockers. Not all of its effects, however, can be explained by direct actions on the sympathetic nervous system. This study was therefore performed to investigate the possible alterations of muscarinic cholinergic (M)(2) receptors and cholinesterase-positive nerves in different regions of the adriamycin-induced failing rat heart, and the potential effects of carvedilol on these M(2) receptors and cholinesterase-positive nerves. Karnovsky-Roots histochemical staining combined with point counting methods, and immunochemical streptavidin-biotin complex staining and image analysis were used to test the distribution of cholinesterase-positive nerves and the expression of M(2) receptors, respectively. Our results show that the cholinesterase-positive nerve system was downregulated in the adriamycin-induced failing heart group, while the density of M(2) receptors was increased in the carvedilol 3- and 10-mg/kg body weight groups, especially in the endocardial tissues of the left-ventricular free wall. It is concluded that upregulation of M(2) receptors may be one of the potential mechanisms by which carvedilol exert its action on heart failure.
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PMID:Effects of carvedilol on M2 receptors and cholinesterase-positive nerves in adriamycin-induced rat failing heart. 1679 4

The objective of this review was to assess the benefits and risks of medication withdrawal in older people as documented in published trials of medication withdrawal. This was done by systematic review of the evidence from clinical trials of withdrawal of specific classes of medications in patient populations with a mean age of >or=65 years. We identified all relevant articles published between 1966 and 2007 initially through electronic searches on PubMed and manual searches of review articles. Numerous search terms related to the withdrawal of medication in older people were utilized. Clinical trials identified were reviewed according to predetermined inclusion/exclusion criteria. Only trials that focused on the withdrawal of specific classes of medication were included. Thirty-one published studies (n = 8972 subjects) met the inclusion criteria, including four randomized and placebo-controlled studies (n = 448 subjects) of diuretic withdrawal, nine open-label and prospective observational studies (n = 7188 subjects) of withdrawal of antihypertensives (including diuretics), 16 studies (n = 1184 patients) of withdrawal of sedative, antidepressant, cholinesterase inhibitor and antipsychotic medications, and 1 study each of withdrawal of nitrates and digoxin. These studies were of heterogeneous study design, patient selection criteria and follow-up. Withdrawal of diuretics was maintained in 51-100% of subjects and was unsuccessful primarily when heart failure was present. Adverse effects from medication withdrawal were infrequently encountered. After withdrawal of antihypertensive therapy, many subjects (20-85%) remained normotensive or did not require reinstatement of therapy for between 6 months and 5 years, and there was no increase in mortality. Withdrawal of psychotropic medications was associated with a reduction in falls and improved cognition. In conclusion, there is some clinical trial evidence for the short-term effectiveness and/or lack of significant harm when medication withdrawal is undertaken for antihypertensive, benzodiazepine and psychotropic agents in older people.
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PMID:Medication withdrawal trials in people aged 65 years and older: a systematic review. 1902 1


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