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)

Twenty-five neonates (16 boys and 9 girls) who had atrial flutter were identified. Diagnosis was made on or before the first day of life in 18 (72%). Heart failure were present in 9 patients, and hydrops fetalis was present in another 5. Atrial and ventricular rates did not differ between symptomatic and asymptomatic patients. Atrioventricular conduction was variable in 16 patients, and documented 1:1 conduction occurred in 5. Digoxin was the initial drug therapy given to 21 patients, with 7 reverting to sinus rhythm. Electrical cardioversion (pacing or synchronized shock) was attempted in 13 of the 14 cases in which digoxin was not successful and was attempted as the first treatment in 3 cases. Sustained sinus rhythm was achieved in 9. Two infants died of complications from prematurity but without having been successfully converted to sinus rhythm. No patient had atrial flutter during long-term follow-up (median 23 months). Neonatal atrial flutter has significant morbidity but an excellent long-term prognosis.
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PMID:Neonatal atrial flutter: significant early morbidity and excellent long-term prognosis. 906 Jul 98

The effect on heart rate variability of adding digoxin to a diuretic and ACE inhibitor was studied in patients with chronic stable cardiac failure. Digoxin was found to increase heart rate variability, especially those measures of heart rate variability thought to represent parasympathetic activity. The withdrawal of digoxin led to a decrease in heart rate variability to pre-treatment levels. Whilst digoxin in standard doses does not alter prognosis in chronic cardiac failure, it does have potentially beneficial neurohumoral effects. If the increase in heart rate variability, which represents beneficial neurohumoral modulation, can be divorced from the potentially detrimental effects, perhaps by using smaller doses, then there may be a role for digoxin in the treatment of chronic cardiac failure.
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PMID:Effects of digoxin on time domain measures of heart rate variability in patients with stable chronic cardiac failure: withdrawal and comparison group studies. 908 23

Improvement of symptoms, increase in exercise capacity and prevention of disease progression are the aims of drug therapy in patients with congestive heart failure. At present only the ACE inhibitors are able to achieve all therapeutic targets and should therefore be regarded as drugs of first choice in systolic dysfunction. Diuretics are also necessary in most patients since they rapidly reduce pulmonary congestion and peripheral oedema, but have no documented beneficial long term effects on the course of CHF. Digoxin remains a useful drug to treat symptomatic patients who do not respond adequately to the combination of ACE inhibitors and diuretics, as well as in patients with atrial fibrillation. However, a reduction of mortality by digitalis glycosides cannot be expected. A new trend in the treatment of CHF is the utilisation of beta blockers. These drugs showed positive effects in chronic CHF in several studies, particularly in patients with dilated cardiomyopathy. Newer drugs such as carvedilol, seem to improve the symptoms and reduce complications even in CHF due to coronary artery disease. The role of beta blockers in the routine management of patients with heart failure requires further evaluation.
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PMID:[Drug treatment of cardiac insufficiency with systolic dysfunction]. 913 44

This study investigated the effect of chronic digitalis glycoside use on beta-adrenergic sympathetic activities in heart failure. Twenty-two Japanese white rabbits were anesthetized by intravenous injection of chloral hydrate. Aortic regurgitation (AR) was produced by perforating aortic valves in 14 rabbits. Digoxin was given for 1 week to 7 rabbits with AR (AR + Dig) and saline to 7 rabbits with AR (AR + C). Sham operation was performed in the remaining 8 rabbits (S). The left ventricular end-diastolic pressure was higher in AR + C than S (p < 0.05). It was lower in AR + Dig than AR + C (p < 0.05). Cardiac output was lower in AR + C than S (p < 0.05). There was no difference between AR + Dig and S. Both the left ventricular end-diastolic and end-systolic diameters were larger in AR + C (p < 0.05) than S, but they were similar between AR + Dig and S. Plasma norepinephrine level was lower in AR + Dig than AR + C. Myocardial beta-adrenergic receptors number determined by radioligand binding assay using 30-800 pM 125I-iodocyanopindolol was lower in AR + C than S (28.8 +/- 7.9 vs. 69.9 +/- 12.3 fmol/mg protein, p < 0.05). It was higher in AR + Dig (39.9 +/- 9.8) than AR + C (p < 0.05). Myocardial norepinephrine content was lower in both AR + C (p < 0.05) and AR + Dig than S (p < 0.05). Thus, digitalis glycosides exert favorable effects on beta-adrenergic sympathetic activities in addition to the effects on hemodynamic variables in this animal model of heart failure.
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PMID:Effect of chronic digoxin on beta-adrenergic receptors in rabbits with heart failure. 920 Nov 13

Digitalis has been widely used in the treatment of cardiac disease for more than 200 years. The present article reviews the current role of digitalis in the management of heart failure and atrial fibrillation (AF) in light of recent study findings. Generally, first-line therapy for the management of heart failure due to systolic dysfunction should include an ACE inhibitor and a diuretic. In patients who remain symptomatic despite the use of these drugs, the addition of digoxin should be considered. Because digoxin has been shown to reduce the number of hospital admissions attributable to worsening heart failure, more liberal use of digoxin in the management of heart failure may be justified. Digoxin may be adequate as monotherapy for ventricular rate control in patients with chronic AF, particularly in sedentary and elderly patients. A beta-blocker or calcium antagonist (either alone or in combination with digoxin) is indicated when digoxin is ineffective for ventricular rate control. Digoxin is ineffective in restoring sinus rhythm, preventing paroxysms or controlling rate in paroxysmal AF. The elderly are at an increased risk of digoxin toxicity. Low dosages of digoxin appear to be effective in the treatment of heart failure due to systolic dysfunction and may reduce the incidence of digitalis toxicity in these patients. In elderly patients with AF and inadequate rate control who are receiving digitalis monotherapy, adding another atrioventricular nodal blocking drug may be more appropriate than increasing the digoxin dose, in order to avoid toxic digoxin levels.
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PMID:When, and when not, to use digoxin in the elderly. 920 47

Digitalis has been used for more than 250 years, but its role in the treatment of chronic heart failure has been intensively investigated only during the past two decades. Digoxin increases cardiac output both at rest and during exercise, alone or in combination with ACE inhibitors, and these hemodynamic effects are sustained during chronic therapy. A daily dose of digoxin that achieves a serum concentration of approximately 1.2 ng/ml is associated with a significant improvement in central hemodynamics, particularly in patients with impaired cardiac function despite pretreatment with diuretics and ACE inhibitors. Acute administration of digoxin in patients with chronic heart failure has an immediate sympathoinhibitory effect, and chronic therapy is associated with a sustained decrease in serum norepinephrine concentration. Discontinuation of digoxin in patients with chronic heart failure resulted in hemodynamic deterioration, which was reversed when the drug was readministered. Randomized withdrawal of digoxin in patients receiving only diuretics (PROVED study), or its withdrawal in patients receiving diuretics and ACE inhibitors (RADIANCE study), was associated with worsening of the clinical evidence of heart failure and a decrease in left ventricular systolic function in both studies. In the only large-scale, placebo-controlled mortality study reported thus for (DIG Trial), 7788 patients received standard drug treatment for chronic heart failure in addition to either digoxin or placebo. Digoxin had no impact on survival over the 37 months of follow-up, but the incidence of hospitalizations due to worsening heart failure was significantly reduced in patients receiving the drug compared with those receiving placebo.
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PMID:Digoxin therapy in chronic heart failure. 921 Oct 21

Despite advances in medical treatment, the annual mortality associated with severe heart failure remains over 40%, and even in mild heart failure the associated mortality is 40% over 4 years. Once it has been demonstrated that the morbidity and mortality to heart failure can be adequately addressed by combinations of drug therapy, then it is logical to attempt to strip out redundant components of these therapeutic regimes. In the meantime, however, combination therapy is required to counter many of the pathophysiological facets of the heart failure syndrome, including fluid retention, neuroendocrine activation, progressive ventricular dysfunction, and sudden cardiac death. Diuretics and ACE inhibitors are well-established drug treatments. Digoxin appears to lessen the rate of progression of heart failure without altering survival. New evidence suggests that beta-blockers may be useful additions to the heart failure therapeutic armamentarium, although whether all beta-blockers are equally effective remains to be established.
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PMID:Combination drug therapy in chronic heart failure: is treatment part of the problem in heart failure? 921 Oct 24

The evidence supporting the efficacy of digoxin in patients with heart failure who are in sinus rhythm is substantial. Digoxin improves hemodynamics, exercise capacity, symptoms, and quality of life and reduces hospitalizations. All of this is accomplished with a drug that is very inexpensive and can be given once daily. Its safety has been established through the DIG trial. Although digoxin does not decrease mortality beyond that of diuretics and ACE inhibitors, it does not increase mortality, unlike many positive inotropes. Furthermore, digoxin, in addition to ACE inhibitors and a diuretic, decreases the hospitalization rate due to worsening of heart failure. From a managed care perspective, as well as that of the patient, this is of enormous benefit. A pharmacoeconomic analysis estimated that continuation of digoxin in patients with stable congestive heart failure could save the healthcare system an estimated $ 400 million, based on costs from one hospital. The issue is not whether to use digoxin in these patients, but rather, how early to initiate therapy. From some of the recent data in patients with systolic dysfunction and mild heart failure, as well as knowledge of the neurohormonal activation that occurs early in these patients, it could be suggested that early use of neurohormonal modulators, including digoxin, would decrease the progression of heart failure. Thus, rather than waiting for symptoms despite optimal doses of an ACE inhibitor and diuretic, as suggested by the AHCPR practice guideline for heart failure, initiation of digoxin therapy in patients as early as NYHA class II at a dosage that will achieve a serum concentration of 1.0 ng/mL or less should occur. With the understanding of digoxin's effect on the neurohormonal systems, its role in patients with preserved systolic function needs to be reexplored. The debate can now focus on asymptomatic patients or those with preserved systolic function. Could these patients benefit from therapy with digoxin as well?
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PMID:Is there an expanded role for digoxin in patients with heart failure and sinus rhythm? A protagonist viewpoint. 922 52

Although the role of digoxin therapy has been the subject of debate, the drug is generally accepted as effective in the treatment of heart failure due to systolic dysfunction and as therapy for atrial fibrillation and supraventricular tachyarrhythmias. Serum digoxin concentrations are commonly used to gauge patient response to digoxin. Digoxin pharmacokinetics are complex, and many factors can confound the interpretation of digoxin concentrations. The exact therapeutic range of serum digoxin varies in the literature but should be considered to be from 0.8 to 2.0 ng per mL, on the basis of population data regarding therapeutic response and toxicity. Renal function plays a major role in digoxin pharmacokinetics and is an important factor in determining digoxin doses. Many medications, including quinidine, amiodarone and verapamil, alter digoxin pharmacokinetics and can result in two- to three-fold increases in the serum digoxin concentration. Effective interpretation of the digoxin concentration requires consideration of the patient's renal function and clinical status, possible drug interactions, time of the assay and other variables.
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PMID:The serum digoxin concentration: ten questions to ask. 953 8

Digoxin is widely used in the transplacental therapy of fetal tachyarrhythmia. Unfortunately, in cases with severe cardiac insufficiency and hydrops fetalis, transplacental passage of digoxin is often hampered and therapy therefore ineffective. The present study was designed to establish the isolated placental lobule to quantify transplacental digoxin passage under different experimental conditions. Ten human placentas were obtained immediately after delivery, and a lobule was dually perfused after cannulating a small artery and vein of the chorionic plate and piercing four catheters through the corresponding basal plate. Flow rates were 12 ml/min in the maternal circuit and 6 (I) respectively 3 ml/min (II) in the fetal circuit. The maternal circuit was spiked with digoxin to 6.18 +/- 0.40 ng/ml, and transplacental passage was calculated from repeated fetal and maternal perfusate samples (Fluorescence-Polarization-Immunoassay; TDx, Abbott Laboratories). Within three hours of recirculating perfusion with a fetal flow rate of 6 ml/min (I), digoxin concentrations in the maternal circuit (400 ml) declined to 3.56 +/- 0.09 ng/ml, whereas digoxin levels in the fetal compartment (200 ml) increased to 2.58 +/- 0.37 ng/ml. With a fetal perfusion rate of 3 ml/min (II), the efflux of digoxin out of the maternal circuit was lower (p < 0.05) and the influx in the total compartment was reduced (fetal digoxin concentrations reached only 26.9 +/- 10.6% vs. 39.1 +/- 5.5% of the initial maternal digoxin concentrations). These data suggest that severe fetal cardiac insufficiency with reduced placental perfusion may be in part responsible for the decrease of transplacental digoxin passage in fetuses with hydrops.
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PMID:[Modification of transplacental digoxin transfer in the isolated placental lobule]. 941 May 33


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