Digoxin Use in Modern Medicine

Shan Chen, PharmD Candidate; Troy Khusial, PharmD Candidate; Dipen Patel, PharmD Candidate; Satinder Singh, PharmD Candidate; Tatyana Yakubova, PharmD Candidate; Amy Wang, PharmD, BCPS, MBA; Timothy Nguyen, PharmD, BCPS, CCP, FASCP


US Pharmacist. 2015;40(2):44-48. 

In This Article

Abstract and Introduction


Digoxin, a cardiac glycoside, has inotropic effects in addition to effects on cardiac output. It is used to treat heart failure and atrial fibrillation and has other off-label uses. Digoxin has been shown to reduce hospitalization rates without affecting mortality rates in patients with heart failure. Digoxin is effective for rate control in patients with atrial fibrillation, but its influence on mortality rates is a source of controversy. The use of digoxin is limited because the drug has a narrow therapeutic index and requires close monitoring. Digoxin can cause many adverse events, is involved in multiple drug interactions, and can result in toxicity. Despite its limitations, however, digoxin has a place in therapy.


Digoxin is a cardiac glycoside derived from the purple foxglove flower. In 1785, the English chemist, botanist, and physician Sir William Withering published his findings that Digitalis purpurea could be used to treat cardiac dropsy (congestive heart failure; CHF).[1] Digoxin has been in use for many years, but was not approved by the FDA for treatment of heart failure (HF) until the late 1990s.[2,3] Another FDA indication for digoxin is atrial fibrillation (AF).[3] Digoxin also has numerous off-label uses, such as in fetal tachycardia, supra-ventricular tachycardia, cor pulmonale, and pulmonary hypertension.[3]

Digoxin acts by inhibiting the sodium-potassium adenosine triphosphatase pump, promoting sodiumcalcium exchange; this results in an upsurge of intracellular calcium, thereby increasing myocardial contractility. Digoxin also has parasympathomimetic properties. By increasing vagal tone in the sinoatrial and atrioventricular (AV) nodes, it slows the heart rate and AV nodal conduction.[4] Table 1 provides a brief overview of digoxin.

Digoxin has been around for centuries, but its use has been limited by several factors. Because of its narrow therapeutic window, digoxin requires close monitoring. Also, two major drawbacks of digoxin are its adverse effects (AEs) and multiple drug interactions. Despite these limitations, digoxin still plays a role in therapy for HF, AF, and several off-label uses. It is considered adjunctive therapy, rather than first-line therapy, for these indications.[5,6]

According to current guidelines, digoxin may be used as additive therapy with beta-blockers and/or ACE inhibitors/angiotensin receptor blockers (ACEIs/ARBs) in the management of CHF.[5] Digoxin possesses negative chronotropic properties and has been shown to decrease morbidity in patients with AF. It is used mainly as add-on therapy in AF patients whose heart rates are not adequately controlled on beta-blockers alone.[6] Because of its positive inotropic effects, digoxin may have benefits in pulmonary arterial hypertension (PAH), but more studies are needed to assess long-term effects in this patient population.[7]