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

To evaluate the effects of compensated heart failure (HF) on digoxin pharmacokinetic properties in cats, 6 cats with dilated cardiomyopathy were compared with 6 clinically normal (control) cats. Digoxin tablets were administered at a dosage of 0.01 mg/kg of body weight, q 48 h for approximately 10 days, until presumed steady state was reached. Both groups were treated concomitantly with aspirin, furosemide, and a commercial low-salt diet. Retrospectively, control and HF cats were calculated to be at 95% and 97% steady state, respectively. At the time blood samples were collected, HF cats were clinically compensated. Serum digoxin concentration [( DXN]) was determined by radioimmunoassay on samples drawn immediately before and 1, 2, 4, 8, 12, 24, 34, and 48 hours after digoxin administration. Measured and calculated values (peak, 8-hour, and mean [DXN]; elimination half-life [t1/2]; oral clearance; and hours during which [DXN] was in the toxic range) were not significantly different between control and HF cats. To predict individual propensity for digoxin intoxication, serum creatinine and urea concentrations and sulfobromophthalein dye retention were measured in control and HF cats prior to the onset of treatment with digoxin. There was no statistically significant correlation between serum creatinine and urea concentrations when compared with sulfobromophthalein dye retention nor between any of these values and digoxin peak, 8-hour, and mean concentrations or t1/2, oral clearance, or hours during which [DXN] was in the toxic range. Mean serum creatinine and urea nitrogen concentrations were significantly greater (P less than 0.01) and sulfobromophthalein dye retention approached significant prolongation (P less than 0.06) in HF cats, compared with that in control cats.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of compensated heart failure on digoxin pharmacokinetics in cats. 279 76

A pregnancy complicated by twin transfusion syndrome is presented. When signs of cardiac failure (edema, ascites and hydramnios) persisted in the recipient twin, maternal digoxin therapy was instituted at 27 weeks' gestation. The signs of failure resolved, and the twins were delivered electively by cesarean section at 34 weeks. At birth, the syndrome was confirmed by examination of the infants and placenta. Both infants survived. Digoxin therapy is recommended for fetal heart failure from circulatory overload in twin transfusion.
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PMID:Twin transfusion syndrome: successful in utero treatment with digoxin. 286 81

433 patients aged 29-80 with mild to moderate heart failure entered a multicentre double-blind randomised between-patient comparison of xamoterol 200 mg twice daily, digoxin 0.125 mg twice daily, and placebo. Patients were assessed at baseline and after three months. Of 349 who completed the double-blind phase, 300 had valid exercise tests. Compared with placebo, xamoterol significantly increased exercise duration and work done on a bicycle ergometer and improved breathlessness and tiredness during daily life as assessed by visual analogue scale and by Likert scale. Digoxin showed no statistically significant advantage over placebo on any of the measures except the Likert scale. Exercise performance and work done were significantly higher with xamoterol than with digoxin.
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PMID:Double-blind placebo-controlled comparison of digoxin and xamoterol in chronic heart failure. The German and Austrian Xamoterol Study Group. 289 16

The interaction between digoxin and the beta-sympathomimetic drug doxaminol was investigated in cats with acute heart failure induced by pentobarbital sodium. Doxaminol, 50 micrograms/kg X min, infused for 60 min caused a dose-dependent rise in dp/dtmax with little increase in heart rate. The maximum increase of 4.3 mHg/s was obtained after about 37 min. Digoxin, 10 micrograms/kg X min, and the combination of both drugs were infused until cardiac arrest. The maximum increase of dp/dtmax was observed after 29 min in both experiments; it was 5.7 mHg/s with digoxin alone and 7.3 mHg/s with the combination (p = 0.025). The combined infusion of epinephrine (0.3 micrograms/kg X min) plus digoxin (10 micrograms/kg X min) caused a maximal increase of dp/dtmax by 7.9 mHg/s. The cardiotoxic dose of digoxin was markedly reduced by epinephrine, not by doxaminol. The relevance of this difference to man cannot be assessed definitely because the ECG changes produced by digoxin in cats are different from those seen in man.
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PMID:Increase in the cardiotonic action and in the therapeutic margin of digoxin by the adrenergic beta-stimulant doxaminol in cats. 300 17

In this article literature concerning the major drugs used in the treatment of heart failure is reviewed. Because of major discrepancies in results from short term and uncontrolled studies versus long term randomised control trials, only the latter group of studies are addressed in detail. Of 3 randomised control trials of digoxin, 1 has been positive, and 2 negative. Digoxin is probably of benefit to a minority of heart failure patients. Four randomised control trials of oral nitrates have shown a reduction in left ventricular filling pressure, and trends favouring active treatment for the indices of exercise capacity and functional status. Of 2 randomised control trials of hydralazine one is totally negative, the other difficult to interpret because of major loss of patients to followup. Of 5 trials of quinazolone derivatives (prazosin and trimazosin), 2 have been positive, 2 showed non-statistically significant trends favouring active treatment, and 1 was completely negative. These results are consistent with a modest benefit of prazosin and trimazosin in some heart failure patients. Five trials of angiotensin-converting enzyme inhibitors (captopril and enalapril) have shown dramatic and consistent benefit in exercise capacity and functional status. These results support a clinical policy of initial treatment with diuretics and addition of either captopril or enalapril for patients who remain symptomatic on optimal diuretic therapy. A trial of digoxin is warranted in patients whose functional capacity remains reduced on this regimen.
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PMID:The treatment of heart failure. A methodological review of the literature. 302 49

In the Rh-sensitized pregnancy, direct treatment of the fetus has been practiced for over two decades. Although Rh immune prophylaxis has markedly decreased the incidence of Rh sensitization, there are still fetal deaths due to this disease. Current management of the severe form of Rh disease includes serial transabdominal intrauterine transfusions, preterm delivery and intensive neonatal care. Heart failure in the fetus may be treated by administering medications to the mother. Ascites or pericardial effusion are easy to detect with ultrasound imaging. Digoxin and diuretics have been used to reverse the ultrasound evidence of fetal congestive heart failure. Recently, direct fetal intravascular transfusion by fetoscopy has proven effective. In some instances, hydrops fetalis appears to be reversed by such transfusions. The use of promethazine and plasmapheresis have only limited success in ameliorating the disease in the fetus.
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PMID:Fetal transfusion. 314 69

Three-day ECG monitoring before and after digitalization of 55 patients with heart failure (HF) was performed. Digoxin did not make a considerable effect on the frequency of detection of high gradations of ventricular arrhythmias. Nevertheless it significantly reduced the mean number of ventricular extrasystoles (VES) per hour and the mean number of complex VES per hour in 8 (33.3%) patients out of 24 with frequent extrasystoles. A significant increase in the VES mean number per hour and in the complex VES mean number per hour was observed in 6 (25%) patients out of 24 with basal frequent extrasystoles. In patients with the antiarrhythmic effect of digoxin indices of the central hemodynamics (diastolic pressure in the pulmonary artery and ejection fraction) were significantly better and in patients with the arrhythmogenic effect of digoxin significantly worse in the absence of a significant difference between digoxin and K+ concentration in the plasma. Digoxin possessed a moderately pronounced antiarrhythmic effect mainly in the patients with HF early stages and in moderately pronounced disturbances of the central hemodynamics. In patients with severe manifestations of HF and with considerable deterioration of indices of the central hemodynamics digoxin in therapeutic concentrations can make an arrhythmogenic effect.
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PMID:[Anti-arrhythmia and arrhythmogenic actions of digoxin in ventricular rhythm disorders in patients with circulatory insufficiency]. 342 96

We have designed a simple nomogram for predicting digoxin dosage and have tested it prospectively in two consecutive studies. These were both conducted in hospital inpatients who were not already taking digoxin but who required drug therapy for atrial tachyarrhythmias and/or cardiac failure. Study I. Sixty-seven patients received digoxin according to the nomogram and 50 completed the ten day course of the study. Forty-one of these patients were eligible for the final analysis. On the tenth day of treatment, 28 patients were within the therapeutic range for plasma digoxin (0.8 to 2.0 ng.ml-1), 12 were subtherapeutic (less than 0.8 ng.ml) and one was potentially toxic (greater than 2.0 ng.ml-1). Study II. Thirty patients completed the second study. Digoxin was prescribed according to the nomogram with the addition of a dosage correction based on the plasma digoxin level on Day 3. On the tenth day of treatment, 24 patients were within the therapeutic range, one in the subtherapeutic and 5 in the potentially toxic. This simple digoxin nomogram, with or without the Day 3 dosage correction, should prove to be a useful aid to prescribing in patients who do not require rapid digitalisation. It is particularly relevant to elderly inpatients with atrial tachyarrhythmias and/or cardiac failure.
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PMID:A simple aid to digoxin prescribing. 342 37

The hemodynamic effects of digitalis were examined in ten patients with acute cardiac failure. Administration of 10 micrograms/kg of digoxin iv resulted in significant increases in cardiac index, stroke volume index, and left ventricular stroke work index within one hour in five patients with acute myocardial infarction (AMI) and five patients with atherosclerotic heart disease without AMI. These increases were maintained 2 h after digoxin therapy. Indirect assessment of global myocardial oxygen supply (coronary perfusion pressure) and demand (heart rate X systolic arterial pressure X wedge pressure product) did not reveal adverse changes. Digoxin therapy results in rapid improvement in cardiac function during acute cardiac failure in patients with and without AMI.
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PMID:Hemodynamic effects of digoxin during acute cardiac failure: a comparison in patients with and without acute myocardial infarction. 367 40

The relationship between the pharmacokinetics and dynamics of digoxin was investigated using a skin blistering technique that allows experimental access to tissue fluid concentrations. Eight healthy volunteers received digoxin, 1.0 mg, and placebo intravenously according to a double-blind crossover design. Drug concentrations were determined during a 72-hour period in serum, urine, and cantharides blister fluid (CBF). Digoxin levels in the hypothetic peripheral compartments were calculated from serum concentrations. Digoxin effects (total electromechanical systole [QS2c], left ventricular ejection time [LVETc], preejection period [PEPc], QTc time, heart rate, and T wave amplitude) were measured simultaneously. Peak levels in the shallow and deep compartments occurred at 12 1/2 to 20 minutes and 3 hours and the maximum concentration in CBF (2.75 +/- 0.48 ng/ml) occurred at 1 hour. Digoxin effects on QS2c, PEPc, and the ratio PEP/LVET were not related to serum concentrations but were closely related to CBF concentrations (r = 0.90). CBF concentrations were then within the range of serum digoxin concentrations usually associated with the treatment of heart failure. Thus, CBF allows experimental access to active drug concentrations after a single intravenous dose.
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PMID:Digoxin concentrations in serum and cantharides blister fluid: correlations with cardiac response. 369 Sep 39


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