Digoxin Therapy in Heart Failure and Atrial Fibrillation
Summary
Digoxin, a cardiac glycoside derived from the foxglove plant, has been a mainstay of treatment in systolic heart failure and in rate control for atrial fibrillation. By inhibiting the cardiac Na+/K+-ATPase pump, digoxin increases intracellular calcium, enhancing myocardial contractility and exerting a positive inotropic effect. In heart failure with reduced ejection fraction, it improves symptoms, functional capacity and quality of life, although its impact on long-term mortality remains modest. In atrial fibrillation, digoxin slows atrioventricular nodal conduction to control ventricular rate, particularly at rest. Its narrow therapeutic window demands careful dosing and monitoring of serum levels, renal function and electrolyte balance to prevent toxicity. Global patterns of use vary widely: in resource-limited settings, affordability has maintained digoxin as a cornerstone therapy, whereas in regions with broader access to beta-blockers and non-dihydropyridine calcium-channel blockers its use has declined. Contemporary practice emphasises individualised dosing algorithms, rigorous monitoring and integration with other standard therapies such as renin–angiotensin system inhibitors and mineralocorticoid receptor antagonists. Despite its age, digoxin remains relevant through ongoing debates about patient selection, toxicity prevention and optimal adjunctive regimens.
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Digoxin Therapy in Heart Failure and Atrial Fibrillation publication trend
The graph below shows the total number of articles in digoxin therapy in heart failure and atrial fibrillation across all publications each year (not limited to Nature Index journals).
Technical terms
Ejection fraction: The percentage of blood ejected from the left ventricle with each heartbeat, used to classify heart failure severity.
Na+/K+-ATPase: A membrane enzyme that exchanges intracellular sodium for extracellular potassium; its inhibition by digoxin increases cardiac contractility.
Positive inotropy: Enhancement of myocardial contractile force, as achieved by digoxin to improve cardiac output.
Atrioventricular (AV) node: A key relay station in cardiac conduction; slowing its conduction rate controls ventricular response in atrial fibrillation.
Narrow therapeutic window: A small margin between effective and toxic drug concentrations, necessitating close monitoring of serum levels and renal function.
References
- Digitalis Medication in Treatment of Heart Failure. Chinese Medicine (2024).
- Safety profile of intravenous digoxin in Chinese patients with acute heart failure with reduced ejection fraction: a small-scale prospective cohort study. Frontiers in Pharmacology (2023).
- Expert Consensus on the Diagnosis and Management of Digoxin Toxicity. The American Journal of Medicine (2024).
- Digoxin Use and Adverse Outcomes in Patients With Atrial Fibrillation. Medicine (2016).
- Digoxin Use and Subsequent Clinical Outcomes in Patients With Atrial Fibrillation With or Without Heart Failure in the ENGAGE AF‐TIMI 48 Trial. Journal of the American Heart Association (2017).
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