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

We conducted a prospective, double-blind, placebo-controlled multicenter trial in order to evaluate the long-term effects of captopril (50 mg/day), digoxin (0.25 mg/day) and placebo on quality of life, cardiovascular events, clinical symptoms and exercise tolerance in patients with documented myocardial infarction, resulting in regional wall motion abnormalities, and with mild heart failure (NYHA class II to III without treatment) and exercise not limited by angina. 222 patients were studied, 63 were randomized to captopril, 66 to digoxin, 67 to placebo. Follow-up was conducted for two years. Base line characteristics in the three treatment groups were similar. After one year of therapy, digoxin had significantly improved general well-being (p < 0.01 vs captopril), symptom score (p < 0.05 vs captopril and placebo), and vitality (p < 0.05 vs captopril). Digoxin improved NYHA class in 45% as compared to placebo (28%, p < 0.05). Worsening of angina was more frequent with captopril as compared to digoxin (p < 0.05). However, cardiovascular events during follow-up were lower in the captopril group as compared to placebo and digoxin (p < 0.01 captopril vs placebo). No differences between groups were observed in baseline and follow-up exercise tolerance between the three groups. Dizziness during upright tilt and cough were more frequent with captopril as compared to digoxin or placebo. After two years of follow-up (captopril n = 32, digoxin n = 29, placebo n = 27) general well-being was improved with both digoxin and captopril (p < 0.004 and p < 0.03 vs placebo).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Captopril versus digoxin in patients with coronary artery disease and mild heart failure. A prospective, double-blind, placebo-controlled multicenter study. The CADS Study Group. 812 24

The efficacy of captopril (capoten) and digoxin was comparatively studied in long-term randomized, double blind trials of 22 male patients with postinfarction cardiosclerosis, functional classes I-III and preserved sinus rhythm. The optimal doses of the drugs proved to be small (0.31 and 35 mg/day of digoxin and capoten, respectively). No adverse effects were noted. The mortality rate was 10 and 16.7% with digoxin and captopril, respectively. The drugs equally improved the functional class by 0.51 and 0.45 and VO2 max by 1.5 and 1.7 ml/min. Digoxin had a mild effect on heart rate (-8.4%) and ejection fraction (+5.7%) and deteriorated diastolic relaxation, by slowing down the early peak of transmitral Doppler spectrum by 16.2%. Captopril significantly improved diastolic function by increasing the early peak by 17.2%. No significant changes in left ventricular sizes were recorded. The clinical efficacy of captopril was explained by a significant decrease in angiotension II (70%) and norepinephrine (40%) levels and by associated normalization of baroreflex regulation. Digoxin insignificantly affected the levels of angiotensin II and norepinephrine, but improved the baroreceptor regulation of sympathetic control impaired in chronic heart failure. It is concluded that extracardiac mechanisms play a major role in the action of not only captopril, but digoxin in the treatment of patients with postinfarct cardiosclerosis and chronic heart failure with sinus rhythm.
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PMID:[Comparative study on use of angiotensin-converting enzyme inhibitors and cardiac glycosides in the treatment of cardiac insufficiency]. 819 54

The influence of chronic perindopril treatment on digoxin pharmacokinetics was investigated in 10 patients with mild chronic heart failure under stable diuretic and digitalis treatment and normal renal function. Digoxin was administered at a dose of 0.125 mg/day (n = 2) or 0.250 mg/day (n = 8). The 24-hour steady-state digoxin profile was assessed before and after concomitant administration of perindopril for 1 month at doses of 2 mg once a day for the first 8 days and 4 mg once a day for the remaining 21 days. Chronic treatment with perindopril produced no significant effect on mean (+/- standard deviation) digoxin serum area under the curve for 24 hours (17.9 +/- 7.4 versus 16.3 +/- 4.4 ng/mL.h), peak digoxin concentration (1.3 +/- 0.54 versus 1.2 +/- 0.36 ng/mL), time to peak concentration (3 versus 4 hours), and apparent oral clearance of digoxin (237.7 +/- 109.6 versus 237.4 +/- 79.5 mL/min). Clinical and biologic tolerance of perindopril was good throughout the study. Chronic administration of perindopril did not alter steady-state digoxin kinetics in patients with mild chronic heart failure and normal renal function, indicating that no adaptation of the digoxin dose is required during co-prescription with perindopril in such patients.
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PMID:Digoxin pharmacokinetics and perindopril in heart failure patients. 844 Jul 63

Controversy surrounds the safety of digoxin use in patients recovering from acute myocardial infarction. Previous observations yielded contradictory conclusions. To determine whether digoxin therapy is associated with increased mortality in patients recovering from acute myocardial infarction, we analyzed data from 1731 survivors of acute myocardial infarction enrolled in the Secondary Prevention Reinfarction Israeli Nifedipine Trial (SPRINT), from which patients with severe heart failure were excluded. At the time of hospital discharge, 175 patients (10%) were taking digoxin. Mortality over 1 year after infarction was significantly higher in patients treated with digoxin than in patients who were not receiving digoxin [27 of 175 (15%) vs. 60 of 1556 (4%); p < 0.0001]. Digoxin administration was associated with increased mortality in several subsets of patients. Since patients treated with digoxin had baseline characteristics predictive of mortality more frequently than their counterparts, we adjusted for these differences. Multivariate analysis performed by the Cox proportional hazards model identified treatment with digoxin as an independent determinant associated with increased death during the first year after myocardial infarction [relative risk (RR) 2.8; 90% confidence interval (CI) 1.8-4.2]. Subgroup multivariate analysis indicated digoxin as an independent predictor of first year death in 464 patients who developed heart failure during their hospital stay (RR 2.3; 90% CI 1.3-4.0), as well as among 1267 patients who did not (RR 3.4; 90% CI 1.7-6.9). The present study suggests a significant excess mortality associated with digoxin therapy after myocardial infarction. The increased mortality risk may be related to unidentified variables associated with the severity of disease in patients treated with digoxin. However, our findings raise concern that the administration of digoxin may contribute to increased mortality in survivors of acute myocardial infarction.
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PMID:Digoxin and mortality in survivors of acute myocardial infarction: observations in patients at low and intermediate risk. The SPRINT Study Group. Secondary Prevention Reinfarction Israeli Nifedipine Trial. 854 12

Digoxin therapy has been suggested to increase mortality risk in survivors of acute myocardial infarction. Since digoxin is a drug with a narrow therapeutic/toxic ratio, we raised the hypothesis that the association between digoxin and post myocardial infarction mortality may have a dose-dependent relationship. The purpose of this study was to evaluate this hypothesis. We retrospectively analyzed data from 1731 survivors of acute myocardial infarction. At the time of hospital discharge, 175 patients (10%) were taking digoxin. The exact dosage of digoxin was ascertained in 153 (87%) patients. Patients were divided into two groups based on the weekly dosage of digoxin at hospital discharge: The first group included 41 patients who were treated with a low dose (< or = 1.5 mg per week, usually 0.125 mg daily). The second group included 112 patients treated with a full dose (> 1.5 mg per week, usually 0.25 mg daily). Both groups were comparable with regard to mean age, gender, history of prior myocardial infarction, diabetes mellitus, hypertension, and prior angina. There were no significant differences in the incidence of in-hospital complications, such as heart failure, atrial fibrillation, ventricular tachycardia, ventricular fibrillation, and postinfarction angina. One year mortality was significantly higher among patients treated with a full dose [19 of 112 (17%)] than patients treated with a low dose of digoxin [1 of 41 (2%); p < 0.02] Multivariate analysis performed by the Cox proportional hazards model identified treatment with a full dose of digoxin as an independent determinant associated with increased death during the first year after myocardial infarction (hazard ratio 10.7; 95% confidence interval 1.4-80.5). Thus, mortality among myocardial infarction survivors treated with digoxin was related to a full-dose therapy. Patients treated with a low dose experienced a low mortality rate. Our findings raise concern that digoxin may exert a dose-dependent deleterious effect upon the survival of patients recovering from acute myocardial infarction.
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PMID:Digoxin and increased mortality among patients recovering from acute myocardial infarction: importance of digoxin dose. The SPRINT Study Group. 857 56

Because of its prevalence in the population and its associated underlying diseases and morbidity, atrial fibrillation (AF) is an important and costly health problem. Advancing age, diabetes, heart failure, valvular disease, hypertension, and myocardial infarction predict the occurrence of AF within a population. The management of AF is complex and involves prevention of thromboembolic complications and treatment of arrhythmia-related symptoms. Stroke occurs in 4.5% of untreated patients with AF per year. Independent risk factors for stroke in nonrheumatic patients with AF are advanced age; a history of prior embolism, hypertension, or diabetes; and echocardiographic findings of left atrial enlargement and left ventricular dysfunction. Warfarin decreases stroke by two-thirds and death by one-third; aspirin is only about half as effective overall and is insufficient therapy for those with risk factors for stroke. Options for thromboembolic prophylaxis are use of warfarin for all in whom it is safe or, alternatively, warfarin for those with risk factors and aspirin for those without risk factors. One-half of the patients with AF are 75 years of age or older. The uniform applicability and relative safety of warfarin therapy in this age-group are controversial. Specific therapy for the arrhythmia should be dictated by the need to control symptoms. Symptomatic treatments include rate-control medications and strategies designed to terminate and prevent arrhythmia recurrence. Digoxin, beta-adrenergic blockers, verapamil, and diltiazem slow excessive ventricular rates in patients with AF and may favorably manage comorbid conditions. The efficacy of anti-arrhythmic medications is only 40 to 70% per year in preventing recurrences of AF, and these agents, except amiodarone, may increase the risk of sudden death in patients with certain types of organic heart disease and AF. The use of nonpharmacologic symptomatic therapies such as atrioventricular node modification or ablation with a rate-response pacemaker or surgical intervention is increasing.
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PMID:Management of atrial fibrillation in adults: prevention of thromboembolism and symptomatic treatment. 857 89

Congestive heart failure is a frequent disorder with an estimated prevalence of 0.4-2% in the general population. Despite recent advances in our understanding of the pathophysiology of this disorder and new developments in its treatment, the prognosis of heart failure remains poor. All patients with heart failure should undergo diagnostic evaluation to determine the type of cardiac dysfunction, establish its etiology and orient treatment. Angiotensin converting enzyme (ACE) inhibitors, diuretics and digoxin are the standard therapy for chronic congestive heart failure caused by systolic dysfunction. ACE inhibitors are indicated in all stages of heart failure, even in asymptomatic patients. Diuretics should be added in the presence of fluid retention. Digoxin remains an important component in the management of refractory symptoms and atrial fibrillation. Symptomatic improvement and reduced morbidity have been shown with all these drugs. However, improved survival has been documented for ACE inhibitors only. Currently, numerous drugs with different mechanisms of action are being evaluated in ongoing clinical trials. Promising results have been published, mainly with beta-receptor blockers and newer positive inotropic substances. Rapidly growing evidence from basic research will advance our understanding of heart failure and hopefully pave the way for new preventive and therapeutic strategies in the near future.
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PMID:[Drug therapy of cardiac insufficiency: status 1995]. 869 14

Digoxin has been a controversial drug since its introduction >200 years ago. Although its efficacy in patients with heart failure and atrial fibrillation is clear, its value in patients with heart failure and sinus rhythm has often been questioned. In the 1980s, reports of some large-scale trials indicated that digoxin, with or without vasodilators or angiotensin-converting enzyme inhibitors, reduced signs and symptoms of congestive heart failure and improved exercise tolerance. This beneficial influence was mainly found in patients with more advanced heart failure and dilated ventricles, whereas the effect in those with mild disease appeared to be less pronounced. In the last few years, new data have shown that digoxin may also have clinical value in mild heart failure, either when used in combination with other drugs or when administered alone. As neurohumoral activation has increasingly been recognized to be a contributing factor in the disease progression of chronic heart failure, the modulating effects of digoxin on neurohumoral and autonomic status have received more attention. Also, there is evidence that relatively low doses of digoxin may be at least as effective as higher doses and have a lower incidence of side effects. Further, the recognition that the use of digoxin too early after myocardial infarction may be harmful and the development of other drugs, in particular angiotensin-converting enzyme inhibitors, have obviously changed the place of digoxin in the treatment of chronic heart failure. The large-scale survival trial by the Digitalis Investigators Group (DIG), whose preliminary results have recently been presented, has shown that although digoxin has a neutral effect on total mortality during long-term treatment, it reduces the number of hospital admissions and deaths due to worsening heart failure. The potentially new features of the old drug digoxin are discussed in this review.
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PMID:Value of digoxin in heart failure and sinus rhythm: new features of an old drug? 883 53

In his study the author deals with etiopathogenesis, diagnosis and therapy of heart failure in acute infarction of myocardium (AMI) with special attention paid to haemodynamic monitoring. The therapy of AMI is based especially on thrombolysis, or urgent revascularisation. In therapy of left ventricular failure we prefer nitrates, diuretics, and ACE-inhibitors. A severe heart failure requires haemodynamic monitoring and administration of positive inotropic substances (dopamine, dobutamine, amrinone) and sodium nitroprusside. Digoxin is indicated only in atrial fibrillation and flutter with fast response of ventricles. In cardiogenic shock it is necessary to introduce an intraaortic balloon contrapulsation and urgent revascularisation (coronary angioplasty, or aortocoronary bypass). Special attention has to be paid to the diagnosis and therapy of AMI of the right ventricle. We avoid the administration of diuretics, nitrates, or morphine which cause hypotension. The therapy is based on thrombolysis, hypotension requires volume expansion, sustained hypotension needs administration of dobutamine, and haemodynamic monitoring. In case of complete AV block, sequence atrioventricular cardiostimulation is recommended. (Ref. 11.).
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PMID:[Heart failure in acute myocardial infarct and the importance of hemodynamic monitoring]. 896 99

The goals of therapy for congestive heart failure (CHF) are to improve quality of life and to prolong it. Improvement in patients with CHF can only be realized, however, if a multidisciplinary healthcare team can provide effective management in both the inpatient and outpatient settings. Inhibition of compensatory mechanisms that perpetuate CHF is the first step in achieving treatment goals. Combination therapy with diuretics, digoxin (Lanoxicaps, Lanoxin), and vasodilators is used for patients with symptomatic heart failure and volume overload. Because angiotensin-converting enzyme inhibitors improve survival rates more than other vasodilators, they are preferred in patients with systolic dysfunction.
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PMID:Drug therapy for congestive heart failure. Appropriate choices can prolong life. 900 90


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