Flecainide was approved for medical use in the United States in 1985.[1] It is available as ageneric medication.[2] In 2023, it was the 223rd most commonly prescribed medication in the United States, with more than 1million prescriptions.[4][5]
It also has limited use in the treatment of certain forms ofventricular tachycardia (VT). In particular, flecainide has been useful in the treatment of ventricular tachycardias that are not in the setting of an acute ischemic event. It has use in the treatment of right ventricular outflow tract (RVOT) tachycardia[6] and in the suppression of arrhythmias inarrhythmogenic right ventricular dysplasia (ARVD).[7] Studies (notably theCardiac Arrhythmia Suppression Trial) have shown an increased mortality when flecainide is used to suppress ventricularextrasystoles in the setting of acute myocardial infarction.[8][9]
In individuals suspected of having theBrugada syndrome, the administration of flecainide may help reveal theelectrocardiography (ECG) findings that are characteristic of the disease process. This may help make the diagnosis of the disease in equivocal cases.[11]
Results of a medical study known as theCardiac Arrhythmia Suppression Trial (CAST) demonstrated that patients with structural heart disease (such as a history of MI (heart attack), or left ventricular dysfunction) and also patients with ventricular arrhythmias, should not take this drug. The results were so significant that the trial was stopped early and preliminary results were published.[12]
The dose may need to be adjusted in certain clinical scenarios. As with all otherantiarrhythmic agents, there is a risk ofproarrhythmia associated with the use of flecainide. This risk is probably increased when flecainide is co-administered with other class Ic antiarrhythmics, such asencainide. The risk of proarrhythmia may also be increased byhypokalemia.[13] The risk of proarrhythmia is not necessarily associated with the length of time an individual is taking flecainide, and cases of late proarrhythmia have been reported.[14]
Because of the negative inotropic effects of flecainide, it should be used with caution in individuals with depressedejection fraction, and may worsencongestive heart failure in these individuals. It should be avoided in people with ischaemic heart disease and the elderly.[15]
Treatment of flecainide cardiac toxicity involves increasing the excretion of flecainide, blocking its effects in the heart, and (rarely) institution of cardiovascular support to avoid impending lethal arrhythmias. Modalities that have had success include administration of a beta-sympathomimetic agent,[18] and administration of a sodium load[18](often in the form ofhypertonicsodium bicarbonate). Placing the individual oncardiopulmonary bypass support may be necessary in order to temporarily remove the need for a beating heart and to increase blood flow to the liver.[19][20]
Flecainide has highbioavailability after an oral dose,[27] meaning that most of the drug that is ingested will enter the systemic blood stream. Peak serum concentrations can be seen 1 to 6 hours after ingestion of an oral dose. While the plasmahalf-life is about 20 hours, it is quite variable, and can range from 12 to 27 hours.[28] During oral loading with flecainide, a steady state equilibrium is typically achieved in 3 to 5 days.
The majority of flecainide is eliminated by thekidneys, with the remainder metabolized by thecytochrome P450 2D6 isoenzyme in the liver.[29] Therefore, alterations in renal function or urine pH will greatly affect the elimination of flecainide, as more is eliminated by the kidney than by the hepatic route.
Because of the dual elimination routes of flecainide and its tendency to decreasemyocardial contractility,[15] flecainide interacts with numerous pharmaceuticals and can potentiate the effects of other myocardial depressants and AV node blocking agents.
Flecainide intoxication is rare but serious due to the cardiogenic shock that it provokes. Its diagnosis can be difficult in the lack of contributing anamnestic elements. Clinical and paraclinical signs are not specific. Treatment is primarily symptomatic, which gives good results thanks to the hypertonic solution of sodium salts. Organ donation is possible in the case of braindead patients who had a flecainide intoxication.[30]
The effect of flecainide on thesodium channels of the heart increases as the heart rate increases; This is known as use-dependence and is why that flecainide is useful to break atachyarrhythmia.[32]
Flecainide also inhibitsryanodine receptor 2 (RyR2),[33] a major regulator ofsarcoplasmic release of stored calcium ions. It can reducecalcium sparks and thus arrhythmogenic calcium waves in the heart.[34] While Flecainide therapy has been shown to suppress ventricular arrhythmias in patients withcatecholaminergic polymorphic ventricular tachycardia (CPVT) and mouse models of this disease, the relative contribution from the inhibition of sodium channels and of RyR2 in this effect on CPVT is unclear.[35]
Flecainide is sold under the brand name Tambocor (manufactured by3M pharmaceuticals). Flecainide went off-patent in February 2004. In addition to being marketed as Tambocor, it is available in generic version and under the brand names Almarytm, Apocard, Ecrinal, and Flécaine.
^Sakurada H, Hiyoshi Y, Tejima T, Yanase O, Tokuyasu Y, Watanabe K, et al. (May 1990). "[Effects of oral flecainide treatment of refractory tachyarrhythmias]".Kokyu to Junkan. Respiration & Circulation.38 (5):471–476.PMID2115193.
^Gasparini M, Priori SG, Mantica M, Napolitano C, Galimberti P, Ceriotti C, et al. (January 2003). "Flecainide test in Brugada syndrome: a reproducible but risky tool".Pacing and Clinical Electrophysiology.26 (1P2):338–341.doi:10.1046/j.1460-9592.2003.00045.x.PMID12687841.S2CID555793.
^Cardiac Arrhythmia Suppression Trial (CAST) Investigators (August 1989). "Preliminary report: effect of encainide and flecainide on mortality in a randomized trial of arrhythmia suppression after myocardial infarction".The New England Journal of Medicine.321 (6):406–412.doi:10.1056/NEJM198908103210629.PMID2473403.
^Ohki R, Takahashi M, Mizuno O, Fujikawa H, Mitsuhashi T, Katsuki T, et al. (January 2001). "Torsades de pointes ventricular tachycardia induced by mosapride and flecainide in the presence of hypokalemia".Pacing and Clinical Electrophysiology.24 (1):119–121.doi:10.1046/j.1460-9592.2001.00119.x.PMID11227957.S2CID41090195.
^Morganroth J (February 1992). "Early and late proarrhythmia from antiarrhythmic drug therapy".Cardiovascular Drugs and Therapy.6 (1):11–14.doi:10.1007/BF00050910.PMID1533532.S2CID22653784.
^abSantinelli V, Arnese M, Oppo I, Matarazzi C, Maione S, Palma M, et al. (April 1993). "Effects of flecainide and propafenone on systolic performance in subjects with normal cardiac function".Chest.103 (4):1068–1073.doi:10.1378/chest.103.4.1068.PMID8131440.
^Fornieles-Pérez H, Montoya-García M, Levine PA, Sanz O (May 2002). "Documentation of acute rise in ventricular capture thresholds associated with flecainide acetate".Pacing and Clinical Electrophysiology.25 (5):871–872.doi:10.1046/j.1460-9592.2002.00871.x.PMID12049386.S2CID7180036.
^Ozkan M, Dweik RA, Ahmad M (September 2001). "Drug-induced lung disease".Cleveland Clinic Journal of Medicine.68 (9):782–785,789–795.doi:10.3949/ccjm.68.9.782 (inactive 1 July 2025).PMID11563482.S2CID45036873.{{cite journal}}: CS1 maint: DOI inactive as of July 2025 (link)
^Camus P, Fanton A, Bonniaud P, Camus C, Foucher P (2004). "Interstitial lung disease induced by drugs and radiation".Respiration; International Review of Thoracic Diseases.71 (4):301–326.doi:10.1159/000079633.PMID15316202.S2CID16315007.
^Pesenti S, Lauque D, Daste G, Boulay V, Pujazon MC, Carles P (2002). "Diffuse infiltrative lung disease associated with flecainide. Report of two cases".Respiration; International Review of Thoracic Diseases.69 (2):182–185.doi:10.1159/000056325.PMID11961436.S2CID72367121.
^Haas M, Pérault MC, Bonnefoy P, Rodeau F, Caron F (2001). "[Interstitial pneumopathy due to flecainide]".Presse Médicale.30 (21): 1062.PMID11471279.
^Robain A, Perchet H, Fuhrman C (February 2000). "Flecainide-associated pneumonitis with acute respiratory failure in a patient with the LEOPARD syndrome".Acta Cardiologica.55 (1):45–47.doi:10.2143/ac.55.1.2005718.PMID10707759.S2CID20721407.
^Padrini R, Piovan D, Busa M, al-Bunni M, Maiolino P, Ferrari M (January 1993). "Pharmacodynamic variability of flecainide assessed by QRS changes".Clinical Pharmacology and Therapeutics.53 (1):59–64.doi:10.1038/clpt.1993.9.PMID8422742.S2CID23471140.
^Wang Z, Fermini B, Nattel S (November 1993). "Mechanism of flecainide's rate-dependent actions on action potential duration in canine atrial tissue".The Journal of Pharmacology and Experimental Therapeutics.267 (2):575–581.doi:10.1016/S0022-3565(25)39407-3.PMID8246130.
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