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As the oldest cardiac glycoside with a narrow therapeutic index and complex pharmacokinetic profile, digoxin is still used to treat many conditions such as congestive heart failure (CHF), atrial fibrillation or flutter, and certain cardiac arrhythmias.1 Its distribution in the heart and muscles might increase due to hyperthyroidism or hypokalaemia and decrease due to hyperkalaemia or hyponatraemia.1 Digoxin is the minor substrate of cytochrome-P450 (CYP) 3A4 and the major substrate of P-glycoprotein/ABCB1.1
In general, the incidence of toxicity is reported to be about 1% in patients with CHF treated with digoxin.1 Increased intracellular calcium due to inhibition of Na–K transporter is the primary pathway of digoxin toxicity.2 Factors such as renal function, …
Contributors All authors contributed equally.
Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.
Competing interests None declared.
Provenance and peer review Not commissioned; internally peer reviewed.