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In patients with anterior MI, despite contemporary treatment, ventricular remodeling is still a common event. In addition, diastolic function can have an important role as a predictor of remodeling in this scenario.
The stability of amrinone and digoxin, procainamide hydrochloride, propranolol hydrochloride, sodium bicarbonate, potassium chloride, or verapamil hydrochloride in intravenous admixtures was studied. Admixtures of amrinone and digoxin were studied at one concentration. Amrinone admixtures with propranolol hydrochloride, sodium bicarbonate, potassium chloride, and verapamil hydrochloride were studied at two concentrations. In general, 0.45% sodium chloride injection was used as the diluent; 5% dextrose injection was also used for the procainamide hydrochloride experiments. Duplicate solutions of each test admixture and single-drug control admixture were prepared and stored for four hours at 22-23 degrees C under fluorescent light. Samples were analyzed by visual inspection, tested for pH, and assayed by high-performance liquid chromatography. Admixtures containing amrinone 1.25 or 2.5 mg/mL (as the lactate salt) and sodium bicarbonate 37.5 mg/mL precipitated immediately or within 10 minutes. No changes in pH or visual appearance were noted for amrinone admixtures with procainamide hydrochloride, digoxin, propranolol hydrochloride, potassium chloride, and verapamil hydrochloride. Appreciable degradation of both amrinone and procainamide was observed after four hours when the two were mixed in 5% dextrose. No degradation of amrinone or procainamide was seen when the 5% dextrose was replaced by 0.45% sodium chloride. Amrinone and sodium bicarbonate were incompatible in intravenous admixtures. Amrinone was compatible with digoxin, propranolol hydrochloride, potassium chloride, and verapamil hydrochloride. Amrinone and procainamide were compatible in 0.45% sodium chloride injection but not in 5% dextrose injection.
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Many relapses of atrial fibrillation (AF) occur, especially during the first week(s) after electrical cardioversion (ECV). The aim of the present study was to compare in a randomized design the efficacy of verapamil (intracellular calcium lowering) versus digoxin (calcium increasing) for maintenance of sinus rhythm after ECV.
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A total of 154,058 patients were identified as the study cohort; from these, 595 cases and 27,020 matched controls were selected for study. The prescription of clarithromycin at 7, 14, and 30 days prior to the index date was associated with a 4.36- (95% CI 1.28–14.79), 5.07- (95% CI 2.36–10.89), and 2.98-fold (95% CI 1.59–5.63) increase in hospitalization for digoxin intoxication, respectively. The results of the dose–response relationship also indicated that clarithromycin prescribed with a prescribed daily dose (PDD)/defined daily dose (DDD) ratio >2 led to a 55.41-fold (95% CI 9.31–329.9) increase of the risk, which is significantly greater than that prescribed with a 1–2 PDD/DDD ratio (adjusted OR 4.81; 95% CI 1.88–12.30) or with a <1 PDD/DDD ratio (adjusted OR 0.78; 95% CI 0.19–3.20).
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The bile acid-binding resin cholestyramine was administered in a dose of 4 g every six hours to a patient with digoxin intoxication. The serum digoxin concentration declined rapidly, and the digoxin half-life decreased from 75.5 hours to 19.9 hours while cholestyramine was administered. All signs and symptoms of toxic reaction subsided during the period of cholestyramine therapy, which correlated with the decline in digoxin concentrations. Cholestyramine and a related agent, colestipol, presumably interrupt the enterohepatic recycling of digoxin to enhance elimination. These agents represent potentially useful adjunctive measures in the management of non-life-threatening digitalis intoxication.
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Heart failure is common in the elderly and is associated with a significant morbidity and mortality. It accounts for about 5% of adult medical admissions and the expenditure of 1% of the total National Health Service budget. Clinical presentation in old age may be with the classical symptoms of heart failure but often, due to multiple pathology and low functional ability, presentation is atypical. Both nonspecific symptoms and signs of heart failure, are often a delayed presentation in this population, make diagnosis difficult. Treatment of the failing heart in an older person is similar to the young however, diligence is required when prescribing due to age-related pharmacokinetic changes and co-existent morbidity. This may result in polypharmacy and an increase in drug interactions which themselves may have deleterious consequences. However, knowledge of the aetiology of heart failure in old age and the possible atypical presentation as well as available treatments, will result in better management and improved quality of life and reduced mortality in the elderly heart failure population.
Digoxin toxicity diagnosis without DIF treatment accounted for 19,543 cases; 5,004 patients received DIF of whom 3086 had a diagnosis of toxicity. Most patients were >65 years old (88%). The predictors of DIF use were urgent/emergent admission, hyperkalemia, arrhythmia associated with digoxin toxicity, acute renal failure, or suicidal intent (odds ratios 1.7, 2.4, 3.6, 2.1, and 3.7, respectively; p < 0.0001 for all). The majority (78%) of DIF was administered on days 1 and 2 of the hospitalization; 10% received treatment after day 7. Digoxin was used after DIF administration in 14% of cases. Among patients who received DIF within 2 days of admission, there was no difference for in-hospital mortality or length of stay compared with patients not receiving DIF.
Endogenous Digitalis-Like Factor (DLF) is a putative hypothalamic Na+,K+-ATPase inhibitor that mediates natriuresis in response to intravascular volume expansion or sodium loading. The precise structure of this substance remains unknown; however, it cross-reacts with antibody to digoxin. Using a radioimmunoassay, we measured DLF concentrations in 26 normal subjects: mean value of this factor was 0.512 ng digoxin-equivalents/ml +/- 0.038 SEM; DLF correlated significantly with serum sodium levels (r = 0.59 - p less than 0.01) and daily urinary sodium excretion (r = 0.48 - p less than 0.05). Our results confirm that endogenous digitalis-like factor has a physiological role as regulator of natriuresis, in response to plasma sodium concentrations.
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The SOLVD prevention (4228 patients) and the SOLVD treatment (2569 patients) trials were randomized, double-blind trials that studied the effect of enalapril in patients with reduced left-ventricular function or congestive heart failure. We combined both SOLVD populations and compared the results of a univariate analysis to a multivariate approach in which 3 patient subgroups were defined according to baseline risks for the combined end point of death or hospitalization for heart failure.
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Most pharmacokinetic and biologic attributes of digitalis are age dependent. They are determined in great measure by the chemical structure of the specific cardiac glycoside being used. These effects differ in the intact normal circulation and in heart failure because of the altered autonomic nervous system and hormonal control that exist in the latter. Digitalis is effective only in the presence of myocardial dysfunction, but in a clinical setting, cardiac performance may be difficult to gauge; improved tools are needed for this purpose. The dosages of digoxin recommended for infants and children have been steadily reduced in the past decade, and there is no good evidence that more favorable risk-to-benefit ratios are achieved when higher doses are used or when higher plasma concentrations are sought. Massive digitalis toxicity is a serious, often fatal, complication in young infants, especially when the drug is given parenterally; it may be difficult to diagnose early. The only reliable deterrent for this complication is the adoption of careful safety standards whenever the drug is employed. Experience with digoxin antibodies is still scarce in children, especially in infancy, but their use generally has been associated with a favorable outcome. Endogenous substances that interfere with the digoxin radioimmunoassay (DLIS) occasionally yield clinically relevant, erroneously high, plasma digoxin concentration readings in neonates. An interesting hypothesis currently being investigated is the physiologic and pathologic role of these compounds in sodium hemostasis; they may be part of a putative endogenous NaK-ATP-ase inhibitor involved in the pathogenesis of hypertension and renal diseases.
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Guidelines for the management of patients with chronic heart failure have undergone change in recent years, with beta-blockers and spironolactone shown to reduce mortality when added to angiotensin converting enzyme (ACE) inhibitors, diuretics and digoxin. The aim of this study was to examine the therapeutic management of heart failure in patients admitted to Tasmania's three major public hospitals, with an assessment of the appropriateness of the therapy according to contemporary published guidelines.
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A quantitative, sensitive and specific assay for digoxin was developed using a high-performance liquid chromatographic (HPLC) system with post-column (PC) fluorogenic derivatization. Separation of digoxin from its metabolites was accomplished using a 15 cm X 4.6 mm I.D., 3-microns octadecylsilyl HPLC column and an optimum mobile phase of methanol-ethanol-isopropanol-dehydroascorbic acid (52:3:1:45, v/v). Concentrated hydrochloric acid, used as the PC derivatization reagent, was delivered by hexane displacement from a polyvinyl chloride pressure vessel. Construction of the pressure vessel is described. The mixture of HPLC effluent and PC reagent was passed into a 20-m knitted reactor (PTFE tubing) maintained at 79.0 +/- 0.2 degrees C. The resultant fluorophores were monitored by a fluorescence detector equipped with a 360-nm excitation filter and a 425-nm emission filter. Specificity of this HPLC-PC assay for digoxin in the presence of its metabolites was demonstrated. Also, numerous steroids evaluated did not produce fluorescence under these conditions. An extraction procedure for evaluating digoxin in serum without interference from endogenous compounds was also developed. Detector response to digoxin was linear from 0.5 to 3.3 ng extracted from serum.
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In this study, endogenous digoxin-like substance within the plasma was measured by radio-immunoassay in 122 children with the systolic blood pressure equal to or greater than the 75th percentile (age = 12.3 +/- 2.5 years) and 136 children with the systolic blood pressure at or less than the 50th percentiles (age = 11.9 +/- 2.8 years) after a follow-up of one year. The levels of digoxin-like substance in the plasma of children with the higher blood pressure were much higher than those in the controls (32.7 +/- 17.3 versus 22.7 +/- 12.7 pg/ml, P less than 0.001) and were positively correlated to the blood pressure (r = 0.21, P less than 0.05 for systolic blood pressure; and r = 0.41, P less than 0.01 for diastolic), and to the sodium content of the red cells (r = 0.36, P less than 0.001), plasma (r = 0.25, P less than 0.01) and 8-hour overnight urinary output (r = 0.32, P less than 0.05). The children in the group with higher blood pressure exhibited an exaggerated natriuresis after an oral saline-water load. We believe that a circulating inhibitor of sodium transport may play an important role in the early stage of the evolution of hypertension.
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Oral amiodarone has been suggested by some authors for rate control in patients with persistent atrial fibrillation. In this study we evaluated the efficacy and safety of oral amiodarone versus placebo for rate control during exercise and daily activities in patients with chronic atrial fibrillation who had undergone digitalisation.
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Tumor necrosis factor-alpha (TNF-alpha) is a proinflammatory cytokine that produces left ventricular dysfunction and a negative inotropic effect in cardiac tissue when overexpressed in human subjects. Previous studies have shown that levels of circulating TNF-alpha are elevated in patients with advanced congestive heart failure (CHF) and especially in those with cardiac cachexia. To clarify the potential role of TNF-alpha in the unstable state of decompensated advanced CHF, we investigated the TNF-alpha serum activity in 25 cachectic and 22 non-cachectic CHF patients (New York Heart Association, NYHA functional classes III or IV), who were treated with intravenous diuretics and positive inotropic agents for acute decompensation of the disease, during a 5-day hospitalization period, as well as in 15 age-matched healthy control subjects. Cachectic CHF patients needed higher dosages of inotropic agents than non-cachectic patients and the determination of TNF-alpha serum concentrations in this patient group showed high levels of TNF-alpha at hospital admission (18.3 +/- 3.2 pg/ml) and a transient increase in circulating TNF-alpha during the treatment period with the highest levels on the 2nd day of hospitalization (32.5 +/- 7.1 pg/ml). The TNF-alpha serum levels were low in non-cachectic CHF patients and healthy controls on the 1st day (4.0 +/- 0.9 and 3.7 +/- 0.6 pg/ml, respectively) and did not change substantially during the course of the study. The present results show that TNF-alpha serum activity is transiently increased during the treatment of decompensated cachectic CHF patients only and may be related to the clinical instability and the consequent therapeutic interventions in this category of CHF patients.
Atrial fibrillation was present in 25% of patients with previous cardiovascular disease (6,194 patients), the prevalence being 4.8% (1,540/32,051) of the study population. Atrial fibrillation was more frequent in females 29%, (810/2,837) than in males, 22% (730/3,367), p < 0.005). Atrial fibrillation was present in 33% (469/1,420) of patients with heart failure and in 12% (387/3,226) of those with coronary heart disease. Arterial hypertension was diagnosed in 25% of the patients with atrial fibrillation. Only 33% of them were treated with oral anticoagulants (41% of the patients seen by cardiologists and 26% by primary-care physicians, p < 0.005). The antiarrhythmic drug most often used was digoxin (36%).
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The prevalence of T. cruzi infection was 37.6%. There was a graded and independent association between infection and the MMSE score (adjusted odds ratios estimated by ordinal logistic regression = 1.99; 95% CI 1.43-2.76). No significant associations between the MMSE score and ECG abnormalities or digoxin medication use were found.
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A significant relationship was observed between C3435T SNP and digoxin AUCs ( p<0,05). Homozygous TT subjects had 20% higher digoxin plasma concentrations than CT and CC subjects and a trend for higher 48 h digoxin urinary recoveries (TT>CT>CC). Similar results, although not statistically significant, were observed from the MDR1 G2677T/A SNP.
This article describes nonradioactive probing of a Northern blot. The method employs digoxigenin-labeled probes. Antidigoxigenin antibody/alkaline phosphate conjugate, and a chemiluminescent substrate are subsequently used in the detection system.
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Only 9 (47%) patients had effective pacing. The other 10 (53%) patients had 16.4 +/- 4.6% fusion and 23.5 +/- 8.7% pseudo-fusion beats. Long-term responders (> or =1 New York Heart Association functional class improvement) to CRT had a significantly higher percentage of fully paced beats (86.4 +/- 17.1% vs. 66.8 +/- 19.1%; p = 0.03) than nonresponders.
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During a six-month period, fourteen patients with beta-thalassemia major and heart failure without diabetes mellitus referred to pediatric cardiology clinic enrolled in this double blind, randomly assigned study. All patients were on anti failure therapy with Digoxin, Captopril and Furosemide. Carvedilol was started at a dosage of 3.12 mg bid and for patients who had a systolic blood pressure >100 mmHg, heart rate >60/min and no signs of low cardiac output the dosage was increased every two weeks to a maximum of 25 mg bid. Clinical signs and symptoms, systolic and diastolic echocardiographic indexes and Tissue Doppler Imaging (TDI) data were collected from each patient.
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Routine therapeutic drug-monitoring data from 106 patients who received oral digoxin at Seoul National University Bundang Hospital were retrospectively collected. The pharmacokinetics of digoxin were analyzed with a 1-compartment, open-label pharmacokinetic model by using a nonlinear mixed-effects modeling tool (NONMEM) and a multiple trough screening approach.