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Abstract Heart failure. Digoxin therapy has no effect on mortality in heart failure. How does digoxin work? Digoxin in heart failure Randomised controlled trials The role of digoxin in the management of heart failure was clarified by a number of well-designed randomised placebo-controlled clinical trials in the s Box 2.
What is the optimal dose of digoxin? Digoxin in diastolic heart failure Diastolic heart failure has been increasingly recognised as a clinical entity, particularly in the elderly and in women.
Recommendations Digoxin is indicated for the management of heart failure. Digoxin for arrhythmia While there is little doubt that appropriate doses of digoxin see above will slow the resting ventricular rate in most patients with chronic atrial fibrillation E1 , it has been known for many years that digoxin is far less successful in controlling exercise-induced or stress-induced tachycardia in atrial fibrillation in many patients, even when plasma drug concentrations are near the upper end of the accepted therapeutic range.
Atrial flutter Most studies of digoxin in atrial fibrillation or flutter have either enrolled patients with atrial fibrillation only, or have combined patients with atrial fibrillation and atrial flutter. View this article on Wiley Online Library. Competing interests:. Withering W. An account of the foxglove and some of its medical uses, with practical remarks on dropsy and other diseases. Classics of cardiology: a collection of classic works on the heart and circulation with comprehensive biographic accounts of the authors.
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Circulation ; Effect of digitalis treatment on survival after acute myocardial infarction. Am J Cardiol ; Effect of oral milrinone on mortality in severe chronic heart failure. N Engl J Med ; Meijler FL. An "account" of digitalis and atrial fibrillation.
Packer M. The development of positive inotropic agents for chronic heart failure: how have we gone astray? Double-blind placebo-controlled study of ibopamine and digoxin in patients with mild to moderate heart failure: results of the Dutch Ibopamine Multicenter Trial DIMT.
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Drugs are metabolized in the liver along with the kidney and lungs; however, liver metabolism is decreased with age. In addition, kidney function maybe be reduced with age, hence decrease the elimination rate.
Digoxin has a narrow therapeutic index which means that it will put patients at risk for severe toxicity [20]. Digoxin has both therapeutic and toxic effects, which can directly or indirectly affect the cardiovascular system, central nervous system, and gut [2]. Curie et al. Cognitive dysfunction is a comorbidity seen in heart failure patients, therefore, digoxin therapy relieves the symptoms of cognitive dysfunction in elderly patients.
This sodium pump is necessary to maintain the normal resting potential; however, the drug digoxin inhibits this process. Inhibition of Na-K-ATPase results in an increase in intracellular sodium concentration, also, the reduction in calcium contributes to the increase intracellular sodium, as a results increases cardiac contractility [2].
The increased intracellular calcium leads to increase potassium conductance which results in decrease action potential. Autonomic action of digoxin involves both sympathetic and parasympathetic which predominates, such as the atropine-blockade effects of digoxin. This innervation affects the atrial and atrioventricular nodes, more than the purkinji or ventricular function [2].
Cardiologist, Pincus, stated that digoxin dosage has been reduced over the past decade; the new recommended range to treat heart failure is 0.
Although, the recommended range is lowered, there has been a decline in digoxin use, hence digoxin toxicity [21]. In a study by the Australian Institute of Health, stated that chronic toxicity is more common. Patients are usually given antidote or treatment for any drug overdose or toxicity; however, there is no recommended guideline to treat mild to moderate digoxin toxicity [21]. Digoxin-specific fab antibody fragment is used to treat severe toxicity for which patients may present with life threatening arrhythmia, cardiac arrest, hyperkalemia [21].
Digoxin-specific fab antibodies have high affinity for digoxin and will reverse its toxicity. However, in the case of severe toxicity with cardiac involvement digoxin-specific fab fragment should be administered immediately [22]. Activated charcoal is another effective agent used to treat digoxin toxicity. It is useful for patients with recent overdose, or in event where digoxin-specific antibody is not available, also no cardiac involvement [22].
Activated charcoal may increase clearance of digoxin by binding to digoxin in the intestinal lumen and gastrointestinal dialysis. Other drugs such as colestipol and cholestyramine will bind to digoxin in order to be eliminated from the system.
Important to note, activated charcoal is unpalatably and can cause severe nausea, vomiting and a risk of aspiration, therefore, assessing the quantity and reason for the overdose is necessary [22].
Dosing rate exceeding 3. In a case report, Gowda et al. It is stated that the treatment is also effective in treating toad venom exposure. Digoxin toxicity can also occur with drug-drug interaction such as diabetic patients treated with sulfonureas who may be treated simultaneously with clarithromycin.
Hyperkalemia is a presentation seen in digoxin toxicity, which is also seen among patients treated with ACE-Inhibitor and potassium sparing diuretics, this combination can lead to life threatening hyperkalemia [23].
Drug-drug interaction is of major concern with elderly patients with several co-morbidities, treated by multiple physicians, and accidental combination of multiple drugs.
Drug interaction can also be alarming with numerous hospital admissions in that patients are not informed of their list of medications and can lead to drug intoxication [23]. It is stated that with computerized prescribing system, the incidence of digoxin toxicity will be decreased since there are prompt alert to potential clinical error [24].
Drug intoxication in elderly can also be related to impairment of renal function, digoxin is excreted from the body by the kidney and if impaired the patient may have an increase amount of digoxin in the plasma. The debate concerning digoxin use continues Rathore et al.
CHF statistics is alarming and the need for effective treatment is inevitable, the Framinigham study shed light on the incidence, prevalence, and prognosis of CHF and the therapies administered was not effective. The question of administering digoxin as a treatment for heart failure continued, although, specific guidelines regarding the use of digoxin in treating heart failure was established [27].
The recommended treatment for heart failure includes digoxin, beta blockers, angiotensin-converting enzyme inhibitor, calcium channel blockers, and diuretics for which digoxin has been proven effective along with other treatment for various comorbidities associated with heart failure.
Many researchers have supported the effectiveness of digoxin and reassures that its low doses are safe and important for the improvement of symptoms of heart failure. It is also suggested that there is a need to optimize current therapies and improve strategies for selecting therapy [11]. Digoxin is effective in patients with CHF because of its positive inotropic properties. Although studies have shown that digoxin reduces hospitalizations and improves symptoms of HF, it has not been proven to decrease mortality.
One double-blind, controlled trial of digoxin for CHF treatment randomized subjects with cardiac dysfunction to digoxin or placebo for 7 weeks. Cardiac function, as measured by ejection fraction EF , was significantly improved in digoxin patients. Digoxin may also be considered in patients with stage C HF structural heart disease with prior or current symptoms of HF or stage D HF HF symptoms at rest and recurrent hospitalizations despite therapy.
Although digoxin is prescribed for patients with HF and AF, concomitant beta-blocker therapy is usually more effective at controlling ventricular response, particularly during exercise. The initial dosage of digoxin is 0. The target serum level of digoxin in HF is 0. Digoxin has been shown effective for decreasing HF symptoms, and its effect on morbidity and mortality has been assessed as well.
The primary outcome was mortality; secondary outcomes were a composite of mortality from cardiovascular causes, death from worsening HF, and hospitalization for other causes digoxin toxicity.
In the intent-to-treat analysis, there were 1, deaths in the digoxin group and 1, deaths in the placebo group Fewer digoxin patients than placebo patients were hospitalized and 1,, respectively; risk ratio 0. Also, the risk associated with the combined outcome of death due to worsening HF or hospitalization was lower in the digoxin group 1, vs. The conclusion was that although digoxin had no effect on overall mortality, it significantly decreased the overall number of hospitalizations attributed to worsening HF.
AF is a common arrhythmia in which irregular electrical impulses are conducted through the heart. These irregular electrical impulses lead to uncoordinated and inefficient heart contractions. As a result, blood pools in the heart, increasing the likelihood of a blood clot, which may lead to serious consequences such as myocardial infarction or stroke. AF can be managed by utilizing either rate or rhythm control agents. Digoxin exhibits its benefit in AF by controlling the heart rate.
One multicenter, randomized, double-blind, crossover trial evaluated the benefit of digoxin versus placebo in 43 patients with paroxysmal AF. The study endpoint was time to occurrence of one or two AF episodes as documented by patient-activated monitors. The median time to two episodes was The median time to one episode was 3. It was concluded that digoxin reduced the frequency of symptomatic AF episodes and that the effect, although small, may be due to a reduction in ventricular rate rather than an antiarrhythmic action.
Digoxin is one of the medications used to manage heart rate, which is considered controlled when the ventricular response is 60 to 80 bpm at rest and 90 to bpm during moderate exercise. First-line therapies for rate control include diltiazem, verapamil, esmolol, and other beta-blockers. Digoxin is not considered first-line therapy, owing to its narrow therapeutic index which requires monitoring and numerous drug interactions.
Patients at higher risk for digoxin toxicity i. PAH is a progressive disease in which restricted blood flow through the pulmonary arteries leads to increased pulmonary vascular resistance and, ultimately, right HF. Pulmonary hypertension is often associated with neurohormonal sympathetic activation, so digoxin may be used because of its sympatholytic properties.
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