Flecainide is an antiarrhythmic medicine used to prevent paroxysmal supraventricular tachycardias, paroxysmal atrial fibrillation/flutter and certain serious ventricular arrhythmias. It is effective but can provoke new arrhythmias (proarrhythmic effect), so its use is reserved for patients in whom the benefit outweighs the risk and, in many cases, initiated in hospital.
Also known as: Tambocor, flecainide acetate
Amiodarone raises flecainide and both prolong the QT.
Flecainide is metabolised by CYP2D6; amiodarone inhibits this enzyme and also CYP2C9 and P-glycoprotein, potentially increasing flecainide concentrations by 50–100%. As both drugs depress conduction (widen QRS) and amiodarone prolongs QT, the proarrhythmia risk (ventricular tachycardia, blocks) increases. When the combination is needed (e.g. AF), reduce the flecainide dose by half, monitor the ECG (QRS, QT) and flecainide plasma levels if available.
Flecainide + amiodarone: amiodarone inhibits CYP2D6 and may double flecainide levels (proarrhythmia risk). Reduce the flecainide dose by 50% and monitor the ECG.
Amiodarone inhibits flecainide metabolism (CYP2D6/CYP3A4) and adds class III QT effect.
ECG (QT, QRS), proarrhythmia signs.
Torsades de pointes, syncope, worsening heart failure.
Reduce flecainide and monitor the ECG; avoid if baseline QT is long.
DailyMed (FDA) — approved Flecainide label: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=74c1eb2a-a37f-4f33-86bf-51e0d1d0c2bc ; approved Amiodarone label: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=51a88e8e-da02-4b97-9e7e-442fbffd908d — additional reference: Prontuário Terapêutico do INFARMED (11th ed., 2012)
Flecainide may raise digoxin by up to about 20%.
Flecainide and digoxin have additive effects on atrioventricular conduction, with a risk of AV block, and flecainide can slightly raise digoxin concentrations (possible inhibition of efflux transport). The combination is used in cardiology (e.g. control of atrial arrhythmias), but requires vigilance: monitor the ECG (PR interval, QRS duration), digoxin levels and signs of toxicity of both (flecainide can be proarrhythmic and digoxin causes arrhythmias at high levels).
Flecainide + digoxin: flecainide can slightly raise digoxin levels and both depress AV conduction. Monitor ECG and digoxin levels.
Flecainide slightly reduces renal clearance of digoxin, chiefly in the elderly and renal impairment.
Digoxin levels, heart rate, gastrointestinal symptoms.
Nausea, bradycardia or arrhythmia.
Monitor digoxin levels and signs of toxicity.
DailyMed (FDA) — approved Flecainide label: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=74c1eb2a-a37f-4f33-86bf-51e0d1d0c2bc ; approved Digoxin label: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=e61d2108-d871-44c0-b12a-2e61fbb56967 — additional reference: Prontuário Terapêutico do INFARMED (11th ed., 2012)
Grapefruit juice inhibits intestinal P-glycoprotein and CYP3A4, which may reduce flecainide clearance and increase its exposure.
Avoid regular grapefruit juice intake during flecainide treatment.
EMC-UK (MHRA) — approved Flecainide SmPC: https://www.medicines.org.uk/emc/product/3086/smpc
Flecainide is contraindicated in structural heart disease or ventricular dysfunction because of the risk of proarrhythmia and sudden death.
Do not use in structural heart disease, prior myocardial infarction or left ventricular dysfunction.
EMC-UK (MHRA) — approved Flecainide SmPC: https://www.medicines.org.uk/emc/product/3086/smpc
Flecainide crosses the placenta; data in pregnancy are limited but have not shown consistent teratogenicity.
Use only if the benefit outweighs the risk, particularly for clinically significant maternal arrhythmias.
Flecainide is excreted into breast milk in small amounts; available data suggest low risk to the infant.
No specific additional contraception is required, but the decision to treat in pregnancy should be documented.
EMC-UK (MHRA) — approved Flecainide SmPC: https://www.medicines.org.uk/emc/product/3086/smpc
Clinical and educational support tool. The information does not replace a medical prescription or the opinion of a qualified healthcare professional.
Class IC antiarrhythmic (membrane stabiliser), used for the prevention and treatment of ventricular and supraventricular arrhythmias (including atrial fibrillation in selected patients without structural heart disease). Negative inotropic effect and proarrhythmic risk — reserved for patients under specialist supervision. Almost complete oral absorption with no first-pass effect; half-life ~20 h (12-27 h).
Local anaesthetic activity; belongs to the membrane-stabilising (Class IC) group of antiarrhythmics. Produces a dose-related decrease in intracardiac conduction in all parts of the heart, with the greatest effect on the His-Purkinje system (H-V conduction); effects on refractory periods are observed only in the ventricle. Suppresses premature ventricular complexes and recurrent ventricular tachycardia (plasma levels 0.2-1 mcg/mL).
Almost complete oral absorption, with peak plasma levels at ~3 hours (range 1-6 h); no relevant first-pass metabolism. Food and antacids do not affect absorption (milk may inhibit it in infants). Plasma protein binding ~40%. Steady state is reached within 3-5 days of multiple dosing.
Metabolised in the liver, involving CYP2D6 (cytochrome P450IID6); the two major urinary metabolites are meta-O-dealkylflecainide (active, about one-fifth as potent) and the meta-O-dealkylated lactam (inactive). About 30% of an oral dose (10-50%) is excreted unchanged in urine and only 5% in faeces. Elimination depends on renal function; very alkaline urine (pH ≥8) slows elimination.
Mean apparent plasma half-life of ~20 hours after multiple oral doses (range 12-27 h); ~14 h in healthy volunteers, ~19 h in NYHA class III heart failure, prolonged in renal impairment. In children aged 1-12 years ~8 h; in adolescents 11-12 h. Plasma levels above 0.7-1 mcg/mL are associated with more cardiac adverse effects.
Medicines from the same therapeutic group (ATC classification) or the same pharmacological class.
