Audience: heart-failure clinicians, general physicians and trainees. Evidence reviewed: September 2026.
Key message
Digoxin remains useful for selected patients, but it is not a foundational mortality-reducing therapy for heart failure. Its narrow therapeutic index makes indication, renal function, dose, drug interactions and clinical monitoring inseparable from prescribing.
Two distinct indications
| Setting | Potential role | What it does not establish |
|---|---|---|
| HFrEF in sinus rhythm | May reduce heart-failure hospitalisation in persistently symptomatic patients despite guideline-directed therapy | No proven survival benefit in the pivotal DIG trial |
| HFrEF with atrial fibrillation | May support resting rate control, often with another agent | Less reliable rate control during exertion |
Evidence in HFrEF
In the Digitalis Investigation Group trial, digoxin did not reduce all-cause mortality but reduced hospital admission for worsening heart failure. The trial pre-dated angiotensin-receptor neprilysin inhibitors, SGLT2 inhibitors and widespread modern device therapy, so absolute benefits in present practice are uncertain. Contemporary guidelines therefore position digoxin as an option for selected symptomatic HFrEF rather than routine foundational treatment.
Choosing and monitoring treatment
- Confirm the goal: symptom/hospitalisation reduction or ventricular-rate control.
- Use a low maintenance dose tailored to age, lean body mass and renal function; loading is rarely needed in stable chronic care.
- Check renal function and potassium before treatment and after clinically important changes.
- Review interacting medicines, including amiodarone, verapamil, macrolides and other P-glycoprotein inhibitors.
- If a serum concentration is required, sample at steady state and at least 6–8 hours after the last dose; interpret the result with symptoms, ECG and renal function.
For heart failure, many experts aim for a low serum concentration, commonly 0.5–0.9 ng/mL, when measurement is clinically indicated. A number within a laboratory “therapeutic range” does not exclude toxicity, particularly in older adults, renal impairment, hypokalaemia, hypomagnesaemia or hypothyroidism.
Recognising toxicity
Toxicity may cause anorexia, nausea, confusion, visual disturbance, bradyarrhythmia, atrioventricular block or almost any tachyarrhythmia. Stop digoxin, obtain an ECG, electrolytes, renal function and an appropriately timed level, and assess severity urgently. Life-threatening arrhythmia or significant hyperkalaemia may require digoxin-specific antibody fragments under emergency/toxicology guidance.
When to reconsider
Reassess digoxin when renal function changes, interacting therapy is added, bradycardia develops, the original indication disappears or adherence/monitoring is unreliable. Withdrawal may worsen symptoms or rate control in some patients, so deprescribing should be planned rather than automatic.
Selected references
- The Digitalis Investigation Group. The effect of digoxin on mortality and morbidity in patients with heart failure. N Engl J Med. 1997.
- 2026 ESC guideline for acute and chronic heart failure.
- 2022 AHA/ACC/HFSA heart-failure guideline.
Educational material only. Dose and monitoring must follow the current product information, renal function, local formulary and individual clinical context.
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