ﺑﺎﺯﮔﺸﺖ ﺑﻪ ﺻﻔﺤﻪ ﻗﺒﻠﯽ
خرید پکیج
تعداد آیتم قابل مشاهده باقیمانده : 3 مورد
نسخه الکترونیک
medimedia.ir

Flecainide: Pediatric drug information

Flecainide: Pediatric drug information
(For additional information see "Flecainide: Drug information" and see "Flecainide: Patient drug information")

For abbreviations, symbols, and age group definitions used in Lexicomp (show table)
ALERT: US Boxed Warning
Mortality:

Flecainide was included in the National Heart Lung and Blood Institute's Cardiac Arrhythmia Suppression Trial (CAST), a long-term, multicenter, randomized, double-blind study in patients with asymptomatic non-life-threatening ventricular arrhythmias who had an MI more than 6 days but less than 2 years previously. An excessive mortality or nonfatal cardiac arrest rate was seen in patients treated with flecainide compared with that seen in patients assigned to a carefully matched placebo-treated group. This rate was 5.1% for flecainide and 2.3% for the matched placebo. The average duration of treatment with flecainide in this study was 10 months.

The applicability of the CAST results to other populations (eg, those without recent MI) is uncertain, but at present, it is prudent to consider the risks of Class ΙC agents (including flecainide), coupled with the lack of any evidence of improved survival, generally unacceptable in patients without life-threatening ventricular arrhythmias, even if the patients are experiencing unpleasant, but not life-threatening, symptoms or signs.

Ventricular proarrhythmic effects in patients with atrial fibrillation/flutter:

A review of the world literature revealed reports of 568 patients treated with oral flecainide for paroxysmal atrial fibrillation/flutter (PAF). Ventricular tachycardia was experienced in 0.4% of these patients. Of 19 patients in the literature with chronic atrial fibrillation (CAF), 10.5% experienced ventricular tachycardia (VT) or ventricular fibrillation (VF). Flecainide is not recommended for use in patients with CAF. Case reports of ventricular proarrhythmic effects in patients treated with flecainide for atrial fibrillation/flutter have included increased premature ventricular contractions (PVCs), VT, VF, and death.

As with other Class Ι agents, patients treated with flecainide for atrial flutter have been reported with 1:1 atrioventricular conduction due to slowing the atrial rate. A paradoxical increase in the ventricular rate also may occur in patients with atrial fibrillation who receive flecainide. Concomitant negative chronotropic therapy such as digoxin or beta-blockers may lower the risk of this complication.

Brand Names: Canada
  • AG-Flecainide;
  • APO-Flecainide;
  • Auro-Flecainide;
  • JAMP Flecainide;
  • MAR-Flecainide;
  • NRA-Flecainide;
  • Tambocor
Therapeutic Category
  • Antiarrhythmic Agent, Class I-C
Dosing: Neonatal
Supraventricular tachycardia, suppression

Supraventricular tachycardia (SVT), suppression: Very limited data available; optimal dose not established: Flecainide has been used alone and in combination with digoxin, propranolol, or sotalol.

BSA-directed dosing:

Initial: Oral: 70 to 100 mg/m2/day divided every 12 hours. Dosing should be titrated based on response and serum concentrations (Ref). Dosing based on a retrospective review of 10 patients, including 6 neonates (age range: 1 to 17 days), with refractory SVT who were treated with flecainide and sotalol. The median starting dose of flecainide was 70 mg/m2/day in 2 divided doses; the median dose required to reach therapeutic trough goal of 200 to 800 ng/mL was 100 mg/m2/day (dose range: 70 to 150 mg/m2/day). Suppression of SVT was achieved in all patients; no proarrhythmic activity was reported (Ref).

Weight-directed dosing: Note: In clinical trials, this dose was initiated after acute SVT controlled with IV flecainide (not available in US) (Ref).

Initial: Oral: 2 mg/kg/day divided every 12 hours; titrate to clinical response, monitor serum concentration; usual dose range in infants and children is 3 to 6 mg/kg/day (Ref); doses >8 mg/kg/day have been associated with a higher incidence of proarrhythmic effects in children (Ref).

Dosing based on a prospective and retrospective study; in both studies, acute SVT was initially controlled with IV flecainide (not available in US) and then converted to preventative oral therapy (Ref). The prospective study enrolled 20 neonates (mean PNA: 11.5 ± 11.07 days; mean GA: 36.8 ± 3 weeks; mean birthweight: 2.8 ± 0.8 kg) with paroxysmal SVT without any structural heart disease; following acute restoration of sinus rhythm, oral flecainide was administered to suppress further SVT episodes; a mean dose of 3.35 ± 1.35 mg/kg/day completely controlled SVT in 17 neonates; 3 patients required the addition of propranolol; this study did not report resultant serum concentrations (Ref). In a retrospective analysis of 39 neonates and infants treated with digoxin and/or flecainide to prevent the recurrence of SVT (median PNA at treatment: 12 days; range: 1 to 330 days; neonates: n=32), 25 of the patients received flecainide at an initial dose of 6 to 8 mg/kg/day divided every 12 hours and titrated based on response and serum concentrations; final doses ranged from 3.2 to 13.5 mg/kg/day and successfully suppressed SVT in 96% of patients. The authors noted high variability in serum concentrations with initial dosing (0.23 to 1.14 mcg/mL) (Ref).

Dosing: Pediatric
Arrhythmias

Arrhythmias:

BSA-directed dosing: Use caution with dose titration, as small change in dose may result in disproportionate increase in plasma concentrations.

Infants ≤6 months: Oral: Initial: 50 mg/m2/day divided every 8 to 12 hours; may titrate dose at 4-day intervals; maximum daily dose: 200 mg/m2/day; higher doses have been associated with an increased risk of proarrhythmic effects.

Infants >6 months, Children, and Adolescents: Oral: Initial: 100 mg/m2/day divided every 8 to 12 hours; may titrate dose at 4-day intervals; maximum daily dose: 200 mg/m2/day; higher doses have been associated with an increased risk of proarrhythmic effects.

Weight-based dosing: Limited data available; dosing regimens variable: Infants, Children, and Adolescents: Oral: Initial: 1 to 3 mg/kg/day divided every 8 hours; may titrate dose at 4-day intervals; usual maintenance range: 3 to 6 mg/kg/day (Ref); an average effective dose of 4 mg/kg/day was reported in an expert analysis of literature and clinical experience (Ref); maximum daily dose: 8 mg/kg/day (Ref); higher doses have been associated with an increased risk of proarrhythmic effects.

Dosage adjustment for concomitant therapy: Significant drug interactions exist, requiring dose/frequency adjustment or avoidance. Consult drug interactions database for more information.

Dosing: Kidney Impairment: Pediatric

There are no pediatric specific recommendations; based on experience in adult patients, dosage adjustment suggested.

Dosing: Hepatic Impairment: Pediatric

There are no dosage adjustments provided in the manufacturer's labeling; however, elimination from the plasma may be slower in patients with hepatic impairment. Use with caution; obtain plasma concentrations to guide dosage adjustments. Dose increases should be made very cautiously at intervals >4 days and serum concentrations monitored frequently. Frequent plasma level monitoring is required in patients with severe hepatic impairment; if unavailable, use is not recommended.

Dosing: Adult

(For additional information see "Flecainide: Drug information")

Fetal tachycardia, sustained

Fetal tachycardia, sustained (maternal/transplacental administration) (off-label use): Oral: 100 to 300 mg/day in divided doses administered every 8 to 12 hours (Ref). Adjust dose to fetal response. Some studies targeted maternal blood levels between 0.2 and 1 mcg/mL. Maximum dose: 450 mg/day (Ref).

Paroxysmal atrial fibrillation/flutter and paroxysmal supraventricular tachycardias

Paroxysmal atrial fibrillation/flutter and paroxysmal supraventricular tachycardias (prevention): Oral: Initial: 50 mg every 12 hours; increase by 50 mg twice daily at 4-day intervals; maximum dose: 300 mg/day. The AHA/ACC/HRS atrial fibrillation guidelines recommend a maximum dose of 400 mg/day (Ref).

Ventricular arrhythmias

Ventricular arrhythmias (prevention): Oral: Initial: 50 to 100 mg every 12 hours; increase by 50 mg twice daily at 4-day intervals; maximum: 400 mg/day (Ref). Some patients inadequately controlled with or intolerant to dosing every 12 hours may require dosing every 8 hours. Note: Initiate therapy in a hospital setting in patients with sustained ventricular tachycardia. Use of higher initial doses and more rapid dosage adjustments have resulted in an increased incidence of proarrhythmic events and congestive heart failure, particularly during the first few days. Do not use a loading dose.

Ventricular premature beats

Ventricular premature beats (off-label use) : Oral: 50 to 200 mg every 12 hours (Ref). According to the prescribing information, may increase by 50 mg twice daily at 4-day intervals; maximum: 400 mg/day.

Atrial fibrillation/flutter

Atrial fibrillation/flutter (pharmacological cardioversion) (off-label dose): Oral: Note: May be used on an outpatient basis (“Pill-in-the-pocket”). An initial inpatient cardioversion trial should have been successful before sending patient home on this approach. Patient must be taking an AV nodal-blocking agent (eg, beta-blocker, nondihydropyridine calcium channel blocker) prior to initiation of antiarrhythmic (Ref).

<70 kg: 200 mg; may not repeat in ≤24 hours

≥70 kg: 300 mg; may not repeat in ≤24 hours

Conversion from another antiarrhythmic agent: Allow for 2 to 4 half-lives of the other agent after discontinuation to pass before initiating flecainide therapy.

Dosage adjustment for concomitant therapy: Significant drug interactions exist, requiring dose/frequency adjustment or avoidance. Consult drug interactions database for more information.

Dosing: Kidney Impairment: Adult

The renal dosing recommendations are based upon the best available evidence and clinical expertise. Senior Editorial Team: Bruce Mueller, PharmD, FCCP, FASN, FNKF; Jason A. Roberts, PhD, BPharm (Hons), B App Sc, FSHP, FISAC; Michael Heung, MD, MS.

Note: Flecainide has a narrow therapeutic index, and the half-life is prolonged in patients with kidney impairment. In patients with kidney impairment, monitor serum trough concentrations (especially in patients with CrCl ≤35 mL/minute/1.73 m2) and ECG parameters frequently following initiation of therapy or dose adjustments and periodically during therapy (Ref).

No dosage adjustment is likely to be necessary for pharmacological cardioversion of atrial fibrillation or flutter “pill-in-the-pocket” dosing, as use of this approach should be infrequent enough to avoid accumulation (Ref).

Altered kidney function:

CrCl ≥60 mL/minute/1.73 m2: No dosage adjustment necessary (Ref).

CrCl >35 to <60 mL/minute/1.73 m2: Initial: No dosage adjustment necessary; consider obtaining serum trough concentrations to guide dosage adjustments in addition to the anticipated clinical response; dose increases should be made cautiously and at intervals of ~7 days (Ref).

CrCl ≤35 mL/minute/1.73 m2: Initial: Administer 50% of the usual indication-specific initial dose in 1 to 2 divided doses (Ref); subsequent dose adjustments should preferentially be determined based on serum trough concentrations in addition to the anticipated clinical response; the manufacturer's labeling recommends not to use flecainide if monitoring of trough concentrations is not available in patients with severe impairment (Ref); dose increases should be made no more frequently than every 7 days (Ref).

Hemodialysis, intermittent (thrice weekly): Not dialyzable (Ref): Note: Use with extreme caution. In a retrospective evaluation of 5 dialysis patients receiving chronic flecainide therapy, significant variability (>7-fold) of dose-corrected steady-state plasma concentrations was observed (Ref).

Initial: Administer 50% of the usual indication-specific initial dose in 1 to 2 divided doses (Ref); subsequent dose adjustments should preferentially be determined based on serum trough concentrations in addition to the anticipated clinical response; the manufacturer's labeling recommends not to use flecainide if monitoring of trough concentrations is not available in patients with severe kidney impairment (Ref); dose increases should be made no more frequently than every 7 days (Ref).

Peritoneal dialysis: Not dialyzable (Ref): Note: Use with extreme caution. In a retrospective evaluation of 5 dialysis patients receiving chronic flecainide therapy, extreme variability (>7-fold) of dose-corrected steady-state plasma concentrations was observed (Ref).

Initial: Administer 50% of the usual indication-specific initial dose in 1 to 2 divided doses (Ref); subsequent dose adjustments should preferentially be determined based on serum trough concentrations in addition to the anticipated clinical response; the manufacturer's labeling recommends not to use flecainide if monitoring of trough concentrations is not available in patients with severe kidney impairment (Ref); dose increases should be made no more frequently than every 7 days (Ref).

CRRT: Not significantly removed (Ref):

Initial: Administer 50% of the usual indication-specific initial dose in 1 to 2 divided doses (Ref); subsequent dose adjustments should preferentially be determined based on serum trough concentrations in addition to the anticipated clinical response; the manufacturer's labeling recommends not to use flecainide if monitoring of trough concentrations is not available in patients with severe kidney impairment (Ref); dose increases should be made no more frequently than every 7 days (Ref).

PIRRT (eg, sustained, low-efficiency diafiltration): Not likely to be significantly removed (Ref):

Initial: Administer 50% of the usual indication-specific initial dose in 1 to 2 divided doses (Ref); subsequent dose adjustments should preferentially be determined based on serum trough concentrations in addition to the anticipated clinical response; the manufacturer's labeling recommends not to use flecainide if monitoring of trough concentrations is not available in patients with severe kidney impairment (Ref); dose increases should be made no more frequently than every 7 days (Ref).

Dosing: Hepatic Impairment: Adult

There are no dosage adjustments provided in the manufacturer’s labeling; however elimination from the plasma may be slower in patients with hepatic impairment. Use with caution; obtain plasma concentrations to guide dosage adjustments. Dose increases should be made very cautiously at intervals >4 days and serum concentrations monitored frequently. Frequent plasma level monitoring is required in patients with severe hepatic impairment; if unavailable, use is not recommended.

Adverse Reactions (Significant): Considerations
Proarrhythmic effects/conduction disturbances

Potentially fatal proarrhythmic effects (including ventricular premature contractions, ventricular tachycardia, and ventricular fibrillation) have been reported in patients with atrial fibrillation without structural heart disease who received flecainide (Ref). Additionally, prolongation of P-R interval on ECG, widened QRS complex on ECG, and prolonged QT interval on ECG, atrioventricular block, or right bundle branch block are possible, leading to sinus bradycardia, sinus pause, sinoatrial arrest, or torsades de pointes (Ref). The incidence of proarrhythmic effects with flecainide use is lower in patients without structural heart disease (Ref); one study noted a <3% incidence of sustained ventricular arrhythmia (Ref).

Mechanism: Dose-related; related to the pharmacologic action; flecainide may unmask the ECG pattern of Brugada syndrome, thereby inducing ventricular tachycardia (Ref). Additionally, flecainide may promote reentry in ventricular tissue via inhibition of rapid sodium channels (slowing phase 0) and inhibition of the slow calcium channel (Ref). Sodium channel blockade also slows conduction through all cardiac conduction pathways, leading to widened QRS, bundle branch block, and prolonged PR interval (Ref).

Onset: Varied; most patients experience proarrhythmic effects or conduction disturbances within the first 1 to 3 weeks of therapy (Ref). Another study reported events within the 12-week period of treatment (Ref).

Risk factors:

• Large dose escalations (Ref)

• Sick sinus syndrome (or other sinus node dysfunction) (Ref)

• Sustained ventricular tachycardia (Ref)

• Atrioventricular conduction abnormalities (Ref)

1:1 Atrioventricular conduction

When treating atrial fibrillation or atrial flutter, 1:1 atrioventricular (AV) conduction may occur, resulting in a rapid ventricular rate and hemodynamic compromise (Ref). The conduction is reversible with cardioversion (Ref).

Mechanism: Related to the pharmacologic action; the effects of flecainide on rhythm allow for the organization of atrial fibrillation into atrial flutter. Additionally, flecainide slows conduction through sodium channel blockade, resulting in a slower atrial flutter rate, facilitating 1:1 conduction through the AV node (Ref).

Onset: Rapid; symptoms associated with 1:1 conduction occur within 30 minutes to a few hours after a dose (Ref).

Risk factors:

• Physical activity after a dose (Ref)

• Dual AV conduction pathways (Ref)

• Absence of AV nodal blocking agent (eg, beta blocker, non-dihydropyridine calcium channel blocker, digoxin) used concurrently (Ref)

Fatal complications associated with structural heart disease (SDH)

Flecainide use in patients with structural heart disease (SHD) (heart failure, myocardial infarction/ischemia) may exacerbate proarrhythmic events (eg, ventricular arrhythmias) and increase the risk of death (Ref). Acute decompensated worsening of heart failure is possible in patients with chronic heart failure (Ref).

Mechanism: Related to the pharmacologic action. In ischemic tissue, flecainide causes significant rate-dependent slowing of conduction via sodium channel inhibition, leading to heterogeneous conduction and reentry pathways (Ref). Flecainide also exhibits significant negative inotropic properties, which can significantly impact patients with poor cardiac function at baseline (Ref).

Onset: Varied. For patients with heart failure with reduced ejection fraction, flecainide significantly increased the risk of decompensation over a 1-year follow-up (Ref). In the CAPS study, an onset of ~3 months was suggested based on the Kaplan Meier curve for percent free from new or worsening heart failure (Ref). In the CAST trial, patients were followed up to 10 months; cardiac events and death began nearly immediately after initiation of flecainide and continued to occur over the 10-month period (Ref).

Risk factors:

• Myocardial infarction (Ref)

• Chronic heart failure (Ref)

Adverse Reactions

The following adverse drug reactions and incidences are derived from product labeling unless otherwise specified.

>10%:

Cardiovascular: Ventricular arrhythmia (new or exacerbated: 7% to 13%)

Nervous system: Dizziness (19%)

Ophthalmic: Visual disturbances (16%; including accommodation disturbance, blurred vision, seeing spots)

1% to 10%:

Cardiovascular: Bradycardia (1%), cardiac arrhythmia (new or worsened: 1% to 7%), cardiac failure (≤9%), chest pain (5%), edema (4%), flushing (1% to 3%), palpitations (6%), sinoatrial arrest (1% to 3%), sinus bradycardia (≤1%), sinus pause (1% to 3%), syncope (1% to 3%), tachycardia (1% to 3%), worsening of heart failure (≤9%)

Dermatologic: Diaphoresis (1% to 3%), skin rash (1% to 3%)

Gastrointestinal: Abdominal pain (3%), anorexia (1% to 3%), constipation (4%), diarrhea (1% to 3%), dyspepsia (1% to 3%), nausea (9%), vomiting (1% to 3%)

Nervous system: Anxiety (1% to 3%), ataxia (1% to 3%), depression (1% to 3%), drowsiness (1% to 3%), fatigue (8%), headache (10%), hypoesthesia (1% to 3%), insomnia (1% to 3%), malaise (1% to 3%), paresis (1% to 3%), paresthesia (1% to 3%), vertigo (1% to 3%)

Neuromuscular & skeletal: Asthenia (5%), tremor (5%)

Ophthalmic: Diplopia (1% to 3%)

Otic: Tinnitus (1% to 3%)

Respiratory: Dyspnea (10%)

Miscellaneous: Fever (1% to 3%)

<1%:

Cardiovascular: Angina pectoris, complete atrioventricular block, hypertension, hypotension, second degree atrioventricular block

Dermatologic: Alopecia, exfoliative dermatitis, pruritus, urticaria

Endocrine & metabolic: Decreased libido

Gastrointestinal: Dysgeusia, flatulence, swelling of lips, swelling of mouth, swollen tongue, xerostomia

Genitourinary: Impotence, urinary retention

Hematologic & oncologic: Granulocytopenia, leukopenia, thrombocytopenia

Nervous system: Abnormal dreams, amnesia, apathy, confusion, depersonalization, euphoria, neuropathy, seizure, speech disturbance, stupor, twitching

Neuromuscular & skeletal: Arthralgia, myalgia

Ophthalmic: Eye irritation, eye pain, nystagmus disorder, photophobia

Renal: Polyuria

Respiratory: Bronchospasm, pneumonitis, pulmonary infiltrates

Frequency not defined: Cardiovascular: Bundle branch block, prolongation of J-T interval on ECG, prolongation P-R interval on ECG (Echt 2020), torsades de pointes (Echt 2020), widened QRS complex on ECG (Echt 2020)

Postmarketing:

Cardiovascular: Exacerbation of cardiac arrhythmias (Echt 2020), prolonged QT interval on ECG (Echt 2020), supraventricular cardiac arrhythmias (Echt 2020), ventricular fibrillation (Echt 2020), ventricular premature contractions (Echt 2020), ventricular tachyarrhythmia (Echt 2020), ventricular tachycardia (Echt 2020), wide complex tachycardia (Echt 2020)

Hepatic: Increased serum alkaline phosphatase, increased serum transaminases

Contraindications

Hypersensitivity to flecainide or any component of the formulation; pre-existing second- or third-degree AV block or with right bundle branch block when associated with a left hemiblock (bifascicular block) (except in patients with a functioning artificial pacemaker); cardiogenic shock; concurrent use of ritonavir.

Significant drug interactions exist, requiring dose/frequency adjustment or avoidance. Consult drug interactions database for more information.

According to the American College of Cardiology/American Heart Association/European Society of Cardiology, the use of flecainide is considered contraindicated in patients with structural heart disease (ACC/AHA/HRS [Page 2015]; AHA/ACC/HRS [Al-Khatib 2017])

Warnings/Precautions

Disease-related concerns:

• AV block: If second- or third-degree AV block, or right bundle branch block associated with a left hemiblock occur, flecainide therapy should be discontinued unless a temporary or implanted ventricular pacemaker is in place to ensure an adequate ventricular rate.

• Electrolyte imbalance: Correct electrolyte disturbances, especially hypokalemia or hypomagnesemia, prior to use and throughout therapy.

• Hepatic impairment: Use with caution in patients with significant hepatic impairment; benefit should outweigh risk. Consider careful monitoring during initiation of therapy. Dose titration should occur only after steady state has been achieved (≥4 days after initiation). Frequent plasma level monitoring is required in patients with severe hepatic impairment; if unavailable, use is not recommended.

• Renal impairment: Use with caution in patients with significant renal impairment. Frequent plasma level monitoring is required in patients with severe renal impairment; if unavailable, use is not recommended.

• Structural or ischemic heart disease: According to the manufacturer, use with extreme caution in patients with structural heart disease as the risk of death and cardiac events may be increased. Avoid use in patients with structural or ischemic heart disease (ACC/AHA/HRS [Page 2015]).

Special populations:

• Pediatric: Small changes in dose may lead to disproportionate increases in plasma concentrations in pediatric patients. Following initiation of therapy or changes in dose, obtain plasma trough concentrations and ECG once steady state has been achieved (>5 doses after initiation or change); regular monitoring of trough concentrations and ECG is recommended by the manufacturer during the first year of therapy and during major changes in dietary milk intake as milk may interfere with the absorption of flecainide in pediatric patients (Russell 1989; Thompson 2012; manufacturer's labeling); consider dose reductions when milk is removed from the diet (eg, during weaning or bouts of gastroenteritis).

Other warnings/precautions:

• Pacemakers: Use with caution in patients with permanent pacemakers or temporary pacing wires; can increase endocardial pacing thresholds and suppress ventricular escape rhythms. Do not use in patients with existing poor thresholds or nonprogrammable pacemakers unless suitable pacing rescue is available. The pacing threshold in patients with pacemakers should be determined at baseline, 1 week after initiation and at regular intervals thereafter.

Dosage Forms: US

Excipient information presented when available (limited, particularly for generics); consult specific product labeling.

Tablet, Oral, as acetate:

Generic: 50 mg, 100 mg, 150 mg

Generic Equivalent Available: US

Yes

Pricing: US

Tablets (Flecainide Acetate Oral)

50 mg (per each): $1.74 - $2.56

100 mg (per each): $2.73 - $4.01

150 mg (per each): $3.76 - $5.52

Disclaimer: A representative AWP (Average Wholesale Price) price or price range is provided as reference price only. A range is provided when more than one manufacturer's AWP price is available and uses the low and high price reported by the manufacturers to determine the range. The pricing data should be used for benchmarking purposes only, and as such should not be used alone to set or adjudicate any prices for reimbursement or purchasing functions or considered to be an exact price for a single product and/or manufacturer. Medi-Span expressly disclaims all warranties of any kind or nature, whether express or implied, and assumes no liability with respect to accuracy of price or price range data published in its solutions. In no event shall Medi-Span be liable for special, indirect, incidental, or consequential damages arising from use of price or price range data. Pricing data is updated monthly.

Dosage Forms: Canada

Excipient information presented when available (limited, particularly for generics); consult specific product labeling.

Tablet, Oral, as acetate:

Tambocor: 50 mg, 100 mg

Generic: 50 mg, 100 mg

Extemporaneous Preparations

20 mg/mL Oral Suspension (ASHP Standard Concentration) (ASHP 2017)

A 20 mg/mL oral liquid suspension may be made from tablets and one of three different vehicles (cherry syrup, a 1:1 mixture of Ora-Sweet and Ora-Plus, or a 1:1 mixture of Ora-Sweet SF and Ora-Plus). Crush twenty-four 100 mg tablets in a mortar and reduce to a fine powder. Add 20 mL of the chosen vehicle and mix to a uniform paste; mix while adding the vehicle in incremental proportions to almost 120 mL; transfer to a calibrated bottle, rinse mortar with vehicle, and add quantity of vehicle sufficient to make 120 mL. Label “shake well” and “protect from light.” Stable for 60 days when stored in amber plastic prescription bottles in the dark at room temperature or refrigerated.

Allen LV, Erickson III MA. Stability of baclofen, captopril, diltiazem, hydrochloride, dipyridamole, and flecainide acetate in extemporaneously compounded oral liquids. Am J Health Syst Pharm. 1996;53:2179-2184.8879325
Administration: Pediatric

Oral: Administer around-the-clock to promote less variation in peak and trough serum levels. May be administered in children without regard to food; however, administration with milk or milk-based formulas may decrease absorption; monitor serum concentrations closely with any changes in milk or milk-based formula consumption; dose adjustments may be necessary (Ref).

Administration: Adult

Oral: When used for the management of fetal tachycardia (maternal/transplacental administration; off-label use), oral doses are administered to the mother.

Storage/Stability

Store at 20°C to 25°C (68°F to 77°F) in a tight, light-resistant container

Use

Prevention and suppression of documented life-threatening ventricular arrhythmias (ie, sustained ventricular tachycardia); prevention of symptomatic, disabling supraventricular tachycardias in patients without structural heart disease (FDA approved in pediatric patients [age not specified] and adults).

Medication Safety Issues
Sound-alike/look-alike issues:

Flecainide may be confused with fluconazole

Tambocor [DSC] may be confused with Pamelor, Temodar, tamoxifen, Tamiflu

Metabolism/Transport Effects

Substrate of CYP1A2 (minor), CYP2D6 (major); Note: Assignment of Major/Minor substrate status based on clinically relevant drug interaction potential

Drug Interactions

Note: Interacting drugs may not be individually listed below if they are part of a group interaction (eg, individual drugs within “CYP3A4 Inducers [Strong]” are NOT listed). For a complete list of drug interactions by individual drug name and detailed management recommendations, use the Lexicomp drug interactions program by clicking on the “Launch drug interactions program” link above.

Alkalinizing Agents: May decrease the excretion of Flecainide. Risk C: Monitor therapy

Amiodarone: May enhance the QTc-prolonging effect of Flecainide. Amiodarone may increase the serum concentration of Flecainide. Management: Decrease flecainide dose by 50%. Monitor for QTc interval prolongation and ventricular arrhythmias, and consider monitoring for elevated flecainide concentrations. Patients with additional risk factors for QTc prolongation may be at even higher risk. Risk D: Consider therapy modification

Amisulpride (Oral): May enhance the QTc-prolonging effect of QT-prolonging Agents (Moderate Risk). Risk C: Monitor therapy

Antihepaciviral Combination Products: May increase the serum concentration of Flecainide. Management: Canadian labeling recommends avoiding this combination. Risk C: Monitor therapy

Artemether and Lumefantrine: May increase the serum concentration of CYP2D6 Substrates (High risk with Inhibitors). Risk C: Monitor therapy

Asunaprevir: May increase the serum concentration of Flecainide. Risk X: Avoid combination

Bradycardia-Causing Agents: May enhance the bradycardic effect of other Bradycardia-Causing Agents. Risk C: Monitor therapy

Carbonic Anhydrase Inhibitors: May decrease the excretion of Flecainide. Risk C: Monitor therapy

Ceritinib: Bradycardia-Causing Agents may enhance the bradycardic effect of Ceritinib. Management: If this combination cannot be avoided, monitor patients for evidence of symptomatic bradycardia, and closely monitor blood pressure and heart rate during therapy. Risk D: Consider therapy modification

CYP2D6 Inhibitors (Moderate): May increase the serum concentration of Flecainide. Risk C: Monitor therapy

CYP2D6 Inhibitors (Strong): May increase the serum concentration of Flecainide. Risk C: Monitor therapy

Dabrafenib: May enhance the QTc-prolonging effect of QT-prolonging Class IC Antiarrhythmics (Moderate Risk). Management: Monitor for QTc interval prolongation and ventricular arrhythmias when these agents are combined. Patients with additional risk factors for QTc prolongation may be at even higher risk. Risk C: Monitor therapy

Digoxin: Flecainide may increase the serum concentration of Digoxin. Risk C: Monitor therapy

Domperidone: QT-prolonging Agents (Moderate Risk) may enhance the QTc-prolonging effect of Domperidone. Management: Consider alternatives to this drug combination. If combined, monitor for QTc interval prolongation and ventricular arrhythmias. Patients with additional risk factors for QTc prolongation may be at even higher risk. Risk D: Consider therapy modification

Encorafenib: May enhance the QTc-prolonging effect of QT-prolonging Class IC Antiarrhythmics (Moderate Risk). Management: Monitor for QTc interval prolongation and ventricular arrhythmias when these agents are combined. Patients with additional risk factors for QTc prolongation may be at even higher risk. Risk C: Monitor therapy

Etrasimod: May enhance the bradycardic effect of Bradycardia-Causing Agents. Risk C: Monitor therapy

Etravirine: May decrease the serum concentration of Flecainide. Risk C: Monitor therapy

Fexinidazole: May increase the serum concentration of MATE1/2-K Substrates (Clinically Relevant with Inhibitors). Management: Avoid use of fexinidazole with MATE1/2-K substrates when possible. If combined, monitor for increased MATE1/2-K substrate toxicities. Risk D: Consider therapy modification

Fingolimod: Bradycardia-Causing Agents may enhance the bradycardic effect of Fingolimod. Management: Consult with the prescriber of any bradycardia-causing agent to see if the agent could be switched to an agent that does not cause bradycardia prior to initiating fingolimod. If combined, perform continuous ECG monitoring after the first fingolimod dose. Risk D: Consider therapy modification

Fluorouracil Products: QT-prolonging Class IC Antiarrhythmics (Moderate Risk) may enhance the QTc-prolonging effect of Fluorouracil Products. Management: Monitor for QTc interval prolongation and ventricular arrhythmias, including torsades de pointes when these agents are combined. Patients with additional risk factors for QTc prolongation may be at even higher risk. Risk C: Monitor therapy

Foslevodopa: May increase the serum concentration of MATE1/2-K Substrates (Clinically Relevant with Inhibitors). Risk C: Monitor therapy

Haloperidol: QT-prolonging Class IC Antiarrhythmics (Moderate Risk) may enhance the QTc-prolonging effect of Haloperidol. Management: Monitor for QTc interval prolongation and ventricular arrhythmias when these agents are combined. Patients with additional risk factors for QTc prolongation may be at even higher risk. Risk C: Monitor therapy

Ivabradine: Bradycardia-Causing Agents may enhance the bradycardic effect of Ivabradine. Risk C: Monitor therapy

Lacosamide: Bradycardia-Causing Agents may enhance the AV-blocking effect of Lacosamide. Risk C: Monitor therapy

Lacosamide: QT-prolonging Class IC Antiarrhythmics (Moderate Risk) may enhance the adverse/toxic effect of Lacosamide. Specifically the risk for bradycardia, ventricular tachyarrhythmias, or a prolonged PR interval may be increased. Risk C: Monitor therapy

Levoketoconazole: QT-prolonging Agents (Moderate Risk) may enhance the QTc-prolonging effect of Levoketoconazole. Risk X: Avoid combination

Midodrine: May enhance the bradycardic effect of Bradycardia-Causing Agents. Risk C: Monitor therapy

Nirmatrelvir and Ritonavir: May increase the serum concentration of Flecainide. Risk X: Avoid combination

Ondansetron: QT-prolonging Class IC Antiarrhythmics (Moderate Risk) may enhance the QTc-prolonging effect of Ondansetron. Management: Monitor for QTc interval prolongation and ventricular arrhythmias when these agents are combined. Patients with additional risk factors for QTc prolongation may be at even higher risk. Risk C: Monitor therapy

Ozanimod: May enhance the bradycardic effect of Bradycardia-Causing Agents. Risk C: Monitor therapy

PAZOPanib: QT-prolonging Class IC Antiarrhythmics (Moderate Risk) may enhance the QTc-prolonging effect of PAZOPanib. Management: Monitor for QTc interval prolongation and ventricular arrhythmias when these agents are combined. Patients with additional risk factors for QTc prolongation may be at even higher risk. Risk C: Monitor therapy

Peginterferon Alfa-2b: May decrease the serum concentration of CYP2D6 Substrates (High risk with Inhibitors). Peginterferon Alfa-2b may increase the serum concentration of CYP2D6 Substrates (High risk with Inhibitors). Risk C: Monitor therapy

Pentamidine (Systemic): QT-prolonging Class IC Antiarrhythmics (Moderate Risk) may enhance the QTc-prolonging effect of Pentamidine (Systemic). Management: Monitor for QTc interval prolongation and ventricular arrhythmias when these agents are combined. Patients with additional risk factors for QTc prolongation may be at even higher risk. Risk C: Monitor therapy

Pimozide: May enhance the QTc-prolonging effect of QT-prolonging Agents (Moderate Risk). Risk X: Avoid combination

Pindolol: Flecainide may enhance the bradycardic effect of Pindolol. The negative inotropic effects of Pindolol may also be enhanced. Risk C: Monitor therapy

Ponesimod: Bradycardia-Causing Agents may enhance the bradycardic effect of Ponesimod. Management: Avoid coadministration of ponesimod with drugs that may cause bradycardia when possible. If combined, monitor heart rate closely and consider obtaining a cardiology consult. Do not initiate ponesimod in patients on beta-blockers if HR is less than 55 bpm. Risk D: Consider therapy modification

QT-prolonging Agents (Highest Risk): May enhance the QTc-prolonging effect of Flecainide. Management: Consider alternatives to this combination. Patients with other risk factors (eg, older age, female sex, bradycardia, hypokalemia, hypomagnesemia, heart disease, and higher drug concentrations) are likely at greater risk for these toxicities. Risk D: Consider therapy modification

QT-prolonging Antidepressants (Moderate Risk): QT-prolonging Class IC Antiarrhythmics (Moderate Risk) may enhance the QTc-prolonging effect of QT-prolonging Antidepressants (Moderate Risk). Management: Monitor for QTc interval prolongation and ventricular arrhythmias when these agents are combined. Patients with additional risk factors for QTc prolongation may be at even higher risk. Risk C: Monitor therapy

QT-prolonging Antipsychotics (Moderate Risk): QT-prolonging Class IC Antiarrhythmics (Moderate Risk) may enhance the QTc-prolonging effect of QT-prolonging Antipsychotics (Moderate Risk). Management: Monitor for QTc interval prolongation and ventricular arrhythmias when these agents are combined. Patients with additional risk factors for QTc prolongation may be at even higher risk. Risk C: Monitor therapy

QT-prolonging Class IC Antiarrhythmics (Moderate Risk): May enhance the QTc-prolonging effect of other QT-prolonging Class IC Antiarrhythmics (Moderate Risk). Management: Monitor for QTc interval prolongation and ventricular arrhythmias when these agents are combined. Patients with additional risk factors for QTc prolongation may be at even higher risk. Risk C: Monitor therapy

QT-Prolonging Inhalational Anesthetics (Moderate Risk): May enhance the QTc-prolonging effect of QT-prolonging Class IC Antiarrhythmics (Moderate Risk). Management: Monitor for QTc interval prolongation and ventricular arrhythmias when these agents are combined. Patients with additional risk factors for QTc prolongation may be at even higher risk. Risk C: Monitor therapy

QT-prolonging Kinase Inhibitors (Moderate Risk): QT-prolonging Class IC Antiarrhythmics (Moderate Risk) may enhance the QTc-prolonging effect of QT-prolonging Kinase Inhibitors (Moderate Risk). Management: Monitor for QTc interval prolongation and ventricular arrhythmias when these agents are combined. Patients with additional risk factors for QTc prolongation may be at even higher risk. Risk C: Monitor therapy

QT-prolonging Miscellaneous Agents (Moderate Risk): May enhance the QTc-prolonging effect of QT-prolonging Class IC Antiarrhythmics (Moderate Risk). Management: Monitor for QTc interval prolongation and ventricular arrhythmias when these agents are combined. Patients with additional risk factors for QTc prolongation may be at even higher risk. Risk C: Monitor therapy

QT-prolonging Moderate CYP3A4 Inhibitors (Moderate Risk): QT-prolonging Class IC Antiarrhythmics (Moderate Risk) may enhance the QTc-prolonging effect of QT-prolonging Moderate CYP3A4 Inhibitors (Moderate Risk). Management: Monitor for QTc interval prolongation and ventricular arrhythmias when these agents are combined. Patients with additional risk factors for QTc prolongation may be at even higher risk. Risk C: Monitor therapy

QT-prolonging Quinolone Antibiotics (Moderate Risk): May enhance the QTc-prolonging effect of QT-prolonging Class IC Antiarrhythmics (Moderate Risk). Management: Monitor for QTc interval prolongation and ventricular arrhythmias when these agents are combined. Patients with additional risk factors for QTc prolongation may be at even higher risk. Risk C: Monitor therapy

QT-prolonging Strong CYP3A4 Inhibitors (Moderate Risk): QT-prolonging Class IC Antiarrhythmics (Moderate Risk) may enhance the QTc-prolonging effect of QT-prolonging Strong CYP3A4 Inhibitors (Moderate Risk). Management: Monitor for QTc interval prolongation and ventricular arrhythmias when these agents are combined. Patients with additional risk factors for QTc prolongation may be at even higher risk. Risk C: Monitor therapy

Quinidine (Non-Therapeutic): May enhance the QTc-prolonging effect of QT-prolonging CYP2D6 Substrates. Quinidine (Non-Therapeutic) may increase the serum concentration of QT-prolonging CYP2D6 Substrates. Risk X: Avoid combination

Risdiplam: May increase the serum concentration of MATE1/2-K Substrates (Clinically Relevant with Inhibitors). Management: Avoid use of risdiplam with MATE substrates if possible. If the combination cannot be avoided, monitor closely for adverse effects. Consider a reduced dose of the MATE substrate according to that substrate's labeling if appropriate. Risk D: Consider therapy modification

RisperiDONE: May enhance the QTc-prolonging effect of QT-prolonging Class IC Antiarrhythmics (Moderate Risk). Management: Monitor for QTc interval prolongation and ventricular arrhythmias when these agents are combined. Patients with additional risk factors for QTc prolongation may be at even higher risk. Risk C: Monitor therapy

Ritonavir: May increase the serum concentration of Flecainide. Risk X: Avoid combination

Sertindole: May enhance the QTc-prolonging effect of QT-prolonging Agents (Moderate Risk). Risk X: Avoid combination

Simeprevir: May increase the serum concentration of Flecainide. Risk C: Monitor therapy

Siponimod: Bradycardia-Causing Agents may enhance the bradycardic effect of Siponimod. Management: Avoid coadministration of siponimod with drugs that may cause bradycardia. If combined, consider obtaining a cardiology consult regarding patient monitoring. Risk D: Consider therapy modification

Sodium Bicarbonate (Systemic): May decrease the excretion of Flecainide. Risk C: Monitor therapy

Tafenoquine: May increase the serum concentration of MATE1/2-K Substrates (Clinically Relevant with Inhibitors). Management: Avoid use of MATE substrates with tafenoquine, and if the combination cannot be avoided, monitor closely for evidence of toxicity of the MATE substrate and consider a reduced dose of the MATE substrate according to that substrate's labeling. Risk D: Consider therapy modification

Tipranavir: May increase the serum concentration of Flecainide. Risk X: Avoid combination

Tobacco (Smoked): May decrease the serum concentration of Flecainide. Risk C: Monitor therapy

Tofacitinib: May enhance the bradycardic effect of Bradycardia-Causing Agents. Risk C: Monitor therapy

Verapamil: May enhance the adverse/toxic effect of Flecainide. In particular, this combination may significantly impair myocardial contractility and AV nodal conduction. Risk C: Monitor therapy

Food Interactions

Clearance may be decreased in patients following strict vegetarian diets due to urinary pH ≥8. Milk may interfere with the absorption of flecainide (Russell 1989; Thompson 2012). Management: Dose reduction should be considered when milk is removed from the diet (eg, during weaning or bouts of gastroenteritis). Plasma trough flecainide levels should be monitored during major changes in dietary milk intake.

Pregnancy Considerations

Flecainide crosses the placenta (Palmer 1990). Placental transfer is not decreased when fetal hydrops is present. Neonatal conduction abnormalities have been reported (AHA [Donofrio 2014]).

Untreated maternal arrhythmias may cause adverse events in the mother and fetus. Flecainide may be used for the ongoing management of pregnant women with highly symptomatic supraventricular tachycardia (SVT). The lowest effective dose is recommended; avoid use during the first trimester if possible (ACC/AHA/HRS [Page 2015]). Use is also recommended for the prevention of SVT in patients with Wolff-Parkinson-White (WPW) syndrome. Until more information is available, when prevention of SVT in patients without WPW syndrome, atrial tachycardia, or atrial fibrillation is needed in pregnancy, flecainide is generally reserved for use when other agents are not effective (ESC [Regitz-Zagrosek 2018]).

Flecainide (administered maternally) may be considered for the in utero management of fetal SVT or atrial flutter with hydrops or ventricular dysfunction. Flecainide may also be considered for SVT without hydrops or ventricular dysfunction if heart rate is ≥200 bpm, or other rare tachycardias with an average heart rate of ≥200 bpm. In addition, flecainide may be considered for fetal ventricular tachycardia (VT) with normal QTc with or without hydrops but is contraindicated for the treatment of fetal VT when long QT syndrome is suspected or confirmed (AHA [Donofrio 2014]).

Monitoring Parameters

ECG, blood pressure, pulse, periodic serum concentrations after at least 5 doses when doses are started or changed or with dietary changes (eg, changes in milk or milk-based formula consumption due to maturation or concurrent illness [eg, gastroenteritis]), liver enzymes.

Reference Range

Therapeutic trough: 0.2 to 1 mcg/mL (SI: 0.4 to 2 micromoles/L). Note: Pediatric patients may respond at the lower end of the recommended therapeutic range (0.2 to 0.5 mcg/mL) but up to 0.8 mcg/mL may be required. Note: Hemolysis during blood sampling may cause a falsely elevated flecainide concentration (Vento 2007).

Mechanism of Action

Class Ic antiarrhythmic; slows conduction in cardiac tissue by altering transport of ions across cell membranes; causes slight prolongation of refractory periods; decreases the rate of rise of the action potential without affecting its duration; increases electrical stimulation threshold of ventricle, His-Purkinje system; possesses local anesthetic and moderate negative inotropic effects

Pharmacokinetics (Adult Data Unless Noted)

Absorption: Oral: Nearly complete; may be decreased when administered with milk in pediatric patients (Thompson 2012; manufacturer's labeling).

Protein binding: ~40%.

Half-life elimination:

Newborns: Up to ≤29 hours; 3 months: 11 to 12 hours; 12 months: 6 hours.

Children: ~8 hours.

Adolescents 12 to 15 years: ~11 to 12 hours.

Adults: ~20 hours (range: 12 to 27 hours); increased in patients with heart failure (NYHA Class III) or renal dysfunction.

Time to peak, serum: ~3 hours (range: 1 to 6 hours).

Excretion: Urine (30% [range: 10% to 50%] as unchanged drug); feces (5%).

Pharmacokinetics: Additional Considerations (Adult Data Unless Noted)

Altered kidney function: In patients with end-stage kidney disease, renal clearance is very low as compared to patients with moderate kidney impairment, and the plasma half-life may extend up to 58 hours (Conard 1984).

Brand Names: International
International Brand Names by Country
For country code abbreviations (show table)

  • (AE) United Arab Emirates: Apo-flecainide | Tambocor;
  • (AR) Argentina: Diondel | Flenomid xr | Tambocor;
  • (AT) Austria: Aristocor;
  • (AU) Australia: Flecainide sandoz | Flecatab | Tambocor;
  • (BE) Belgium: Apocard | Apocard retard | Docflecai | Flecainide eg | Flecainide merck-generics | Flecainide retard eg | Flecainide sandoz | Flecateva | Flecateva retard | Tambocor;
  • (BG) Bulgaria: Amarhyton | Felkarid;
  • (CH) Switzerland: Tambocor;
  • (CL) Chile: Tambocor;
  • (CZ) Czech Republic: Tambocor;
  • (DE) Germany: Flecadura | Flecagamma | Flecainid 1A Pharma | Flecainid aaa | Flecainid AWD | Flecainid Hexal | Flecainid isis | Flecainid micro labs | Flecainid puren | Flecainid ratiopharm | Flecainid sandoz | Flecainid tillomed | Flecainidacetat actavis | Flecainidacetat AL | Flecainidacetat aurobindo | Tambocor;
  • (DK) Denmark: Flecainid alpharma;
  • (EE) Estonia: Flecainid ratiopharm | Flecainidacetat puren | Tambocor;
  • (ES) Spain: Apocard | Flecainida apotex | Flecainida aurovitas | Flecainida normon | Flecainida qualigen | Flecard;
  • (FI) Finland: Flecainid alpharma | Flecainide orion | Tambocor;
  • (FR) France: Flecaine | Flecainide Arrow | Flecainide Biogaran | Flecainide Dci | Flecainide eg | Flecainide Qualimed | Flecainide rpg | Flecainide sandoz | Flecainide teva | Flecainide zentiva;
  • (GB) United Kingdom: Flecainide | Flecainide cox | Flecainide kent | Tambocor;
  • (GR) Greece: Flecardia | Flecarythm | Tambocor;
  • (HK) Hong Kong: Apo-flecainide | Tambocor | Vick Flecainide;
  • (HU) Hungary: Tambocor;
  • (IE) Ireland: Flecainide | Tambocor;
  • (IL) Israel: Tambocor;
  • (IT) Italy: Almarytm | Flecainide | Flecainide aurobindo | Flecainide Doc generici | Flecainide eg | Flecainide Ratiopharm | Flecainide sandoz | Fleiderina | Frequil;
  • (JO) Jordan: Tambocor;
  • (JP) Japan: Flecainide acetate ko | Flecainide acetate pfizer | Tambocor;
  • (KR) Korea, Republic of: Fulcard | Tambocor;
  • (KW) Kuwait: Tambocor;
  • (LB) Lebanon: Flecain | Flecainide | Flecainide biogaran l.p. | Tambocor;
  • (LT) Lithuania: Flecadura | Flecainid aaa | Flecainid isis | Flecainid puren | Flecainideacetaat aurobindo | Tambocor;
  • (LU) Luxembourg: Apocard | Flecainide eg | Flecainide sandoz | Tambocor;
  • (LV) Latvia: Apocard | Flecagamma | Flecainid isis | Flecainid rth | Flecainid sandoz | Tambocor;
  • (MA) Morocco: Flecainide | Tambocor;
  • (MX) Mexico: Tambocor;
  • (MY) Malaysia: Tambocor;
  • (NL) Netherlands: Flecainide | Flecainide-acetaat | Flecainide-Acetaat Actavis | Flecainide-Acetaat Sandoz | Tambocor;
  • (NO) Norway: Flecainid sandoz | Tambocor | Tambocor retard;
  • (NZ) New Zealand: Flecainide bnm | Flecainide Controlled Release | Tambocor;
  • (PH) Philippines: Flecainide | Tambocor;
  • (PL) Poland: Apocard | Aristocor | Flecadura | Flecaine lp | Flecainid Hexal | Flecainide acetate holsten | Flecainide Biogaran | Flecainide mylan | Tambocor;
  • (PR) Puerto Rico: Tambocor;
  • (PT) Portugal: Apocard | Tambocor;
  • (PY) Paraguay: Apocard;
  • (RO) Romania: Amarhyton | Tambocor;
  • (SA) Saudi Arabia: Apo-flecainide;
  • (SE) Sweden: Flecainide alternova | Flekainid sandoz | Flekainid stada | Tambocor;
  • (SG) Singapore: Tambocor;
  • (SI) Slovenia: Felkarid | Tambocor;
  • (SK) Slovakia: Flekainid sandoz | Tambocor;
  • (TH) Thailand: Tambocor;
  • (TN) Tunisia: Flecaine | Flecav;
  • (TW) Taiwan: Tambocor;
  • (UA) Ukraine: Flekainid sandoz | Lixarit;
  • (UY) Uruguay: Diondel | Tambocor;
  • (ZA) South Africa: Tambocor
  1. Al-Khatib SM, Stevenson WG, Ackerman MJ, et al. 2017 AHA/ACC/HRS guideline for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society. Circulation. Published online October 30, 2017. doi:10.1161/CIR.0000000000000549 [PubMed 29084731]
  2. Alboni P, Botto GL, Baldi N, et al. Outpatient Treatment of Recent-Onset Atrial Fibrillation With the "Pill-in-the-Pocket" Approach. N Engl J Med. 2004;351(23):2384-2391. [PubMed 15575054]
  3. Alsaied T, Baskar S, Fares M, et al. First-line antiarrhythmic transplacental treatment for fetal tachyarrhythmia: a systematic review and meta-analysis. J Am Heart Assoc. 2017;6(12):e007164. doi:10.1161/JAHA.117.007164 [PubMed 29246961]
  4. Anderson JL, Gilbert EM, Alpert BL, et al; Flecainide Supraventricular Tachycardia Study Group. Prevention of symptomatic recurrences of paroxysmal atrial fibrillation in patients initially tolerating antiarrhythmic therapy. A multicenter, double-blind, crossover study of flecainide and placebo with transtelephonic monitoring. Circulation. 1989;80(6):1557-1570. doi:10.1161/01.cir.80.6.1557 [PubMed 2513143]
  5. Anderson PO, Sauberan JB. Modeling drug passage into human milk. Clin Pharmacol Ther. 2016;100(1):42-52. doi:10.1002/cpt.377 [PubMed 27060684]
  6. Andrikopoulos GK, Pastromas S, Tzeis S. Flecainide: Current status and perspectives in arrhythmia management. World J Cardiol. 2015;7(2):76-85. doi:10.4330/wjc.v7.i2.76 [PubMed 25717355]
  7. Aronoff GR, Bennett WM, Berns JS, et al. Drug Prescribing in Renal Failure: Dosing Guidelines for Adults and Children. 5th ed. American College of Physicians; 2007.
  8. ASHP. Standardize 4 Safety Initiative Compounded Oral Liquid Version 1.01. July 2017. https://www.ashp.org/-/media/assets/pharmacy-practice/s4s/docs/s4s-ashp-oral-compound-liquids.ashx?la=en&hash=4C2E4F370B665C028981B61F6210335AD5D0D1D6.
  9. Bailie GR, Waldek S. Pharmacokinetics of flecainide in a patient undergoing continuous ambulatory peritoneal dialysis. J Clin Pharm Ther. 1988;13(2):121-124. doi:10.1111/j.1365-2710.1988.tb00167.x [PubMed 3134365]
  10. Barman M. Proarrhythmic effects of antiarrhythmic drugs: case study of flecainide induced ventricular arrhythmias during treatment of atrial fibrillation. J Atr Fibrillation. 2015;8(4):1091. doi:10.4022/jafib.1091 [PubMed 27957216]
  11. Benhorin J, Taub R, Goldmit M, et al. Effects of flecainide in patients with new SCN5A mutation: mutation-specific therapy for long-QT syndrome? Circulation. 2000;11;101(14):1698-1706. [PubMed 10758053]
  12. Blomstrom-Lundqvist C, Scheinman MM, Aliot EM; American Heart Association Task Force on Practice Guidelines; European Society of Cardiology Committee for Practice Guidelines. Writing Committee to Develop Guidelines for the Management of Patients With Supraventricular Arrhythmias. ACC/AHA/ESC guidelines for the management of patients with supraventricular arrhythmias--executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Develop Guidelines for the Management of Patients With Supraventricular Arrhythmias). Circulation. 2003;108(15):1871-1909. [PubMed 14557344]
  13. Borgeat A, Biollaz J, Freymond B, Bayer-Berger M, Chiolero R. Hemofiltration clearance of flecainide in a patient with acute renal failure. Intensive Care Med. 1988;14(3):236-237. doi:10.1007/BF00717997 [PubMed 3132493]
  14. Chorin E, Taub R, Medina A, et al. Long-term flecainide therapy in type 3 long QT syndrome. Europace. 2018;20(2):370-376. doi:10.1093/europace/euw439 [PubMed 28339995]
  15. Colangelo T, Johnson D, Ho R. Flecainide-induced atrial flutter with 1:1 conduction complicated by ventricular fibrillation after electrical cardioversion. Tex Heart Inst J. 2021;48(2):e197099. doi:10.14503/THIJ-19-7099 [PubMed 34086956]
  16. Comelli I, Pigna F, Cervellin G. 1:1 atrial flutter induced by flecainide, whilst the patient was at rest. Am J Emerg Med. 2018;36(11):2131.e3-2131.e5. doi:10.1016/j.ajem.2018.07.040 [PubMed 30033133]
  17. Conard GJ, Ober RE. Metabolism of flecainide. Am J Cardiol. 1984;53(5):41B-51B. [PubMed 6364769]
  18. de Paola AA, Horowitz LN, Morganroth J, et al. Influence of left ventricular dysfunction on flecainide therapy. J Am Coll Cardiol. 1987;9(1):163-168. doi:10.1016/s0735-1097(87)80096-7 [PubMed 3098817]
  19. Donofrio MT, Moon-Grady AJ, Hornberger LK, et al; American Heart Association Adults with Congenital Heart Disease Joint Committee of the Council on Cardiovascular Disease in the Young and Council on Clinical Cardiology, Council on Cardiovascular Surgery and Anesthesia, and Council on Cardiovascular and Stroke Nursing. Diagnosis and treatment of fetal cardiac disease: a scientific statement from the American Heart Association. Circulation. 2014;129(21):2183-2242. doi:10.1161/01.cir.0000437597.44550.5d [PubMed 24763516]
  20. Echt DS, Liebson PR, Mitchell LB, et al. Mortality and morbidity in patients receiving encainide, flecainide, or placebo. The Cardiac Arrhythmia Suppression Trial. N Engl J Med. 1991;324(12):781-788. doi:10.1056/NEJM199103213241201 [PubMed 1900101]
  21. Echt DS, Ruskin JN. Use of flecainide for the treatment of atrial fibrillation. Am J Cardiol. 2020;125(7):1123-1133. doi:10.1016/j.amjcard.2019.12.041 [PubMed 32044037]
  22. Ekiz A, Kaya B, Bornaun H, et al. Flecainide as first-line treatment for fetal supraventricular tachycardia. J Matern Fetal Neonatal Med. 2018;31(4):407-412. doi:10.1080/14767058.2017.1286317 [PubMed 28114840]
  23. European Society of Gynecology (ESG); Association for European Paediatric Cardiology (AEPC); German Society for Gender Medicine (DGesGM), Regitz-Zagrosek V, Blomstrom Lundqvist C, Borghi C, et al; ESC Committee for Practice Guidelines. ESC Guidelines on the management of cardiovascular diseases during pregnancy: the Task Force on the Management of Cardiovascular Diseases during Pregnancy of the European Society of Cardiology (ESC). Eur Heart J. 2011;32(24):3147-3197. doi:10.1093/eurheartj/ehr218 [PubMed 21873418]
  24. Evers J, Eichelbaum M, Kroemer HK. Unpredictability of flecainide plasma concentrations in patients with renal failure: relationship to side effects and sudden death? Ther Drug Monit. 1994;16(4):349-351. doi:10.1097/00007691-199408000-00003 [PubMed 7974623]
  25. Expert opinion. Senior Renal Editorial Team: Bruce Mueller, PharmD, FCCP, FASN, FNKF; Jason A. Roberts, PhD, BPharm (Hons), B App Sc, FSHP, FISAC; Michael Heung, MD, MS.
  26. Fenrich AL Jr, Perry JC, Friedman RA. Flecainide and Amiodarone: Combined Therapy for Refractory Tachyarrhythmias in Infants. J Am Coll Cardiol. 1995;25(5):1195-1198. [PubMed 7897134]
  27. Ferlini M, Colli AM, Bonanomi C, et al. Flecainide as First-Line Treatment for Supraventricular Tachycardia in Newborns. J Cardiovasc Med (Hagerstown). 2009;10(5):372-375. [PubMed 19300276]
  28. Flaker GC, Blackshear JL, McBride R, Kronmal RA, Halperin JL, Hart RG. Antiarrhythmic drug therapy and cardiac mortality in atrial fibrillation. The Stroke Prevention in Atrial Fibrillation Investigators. J Am Coll Cardiol. 1992;20(3):527-532. doi:10.1016/0735-1097(92)90003-6 [PubMed 1512329]
  29. Flecainide acetate [prescribing information]. Laurelton, NY: Epic Pharma LLC; August 2022.
  30. Forland SC, Cutler RE, McQuinn RL, et al. Flecainide pharmacokinetics after multiple dosing in patients with impaired renal function. J Clin Pharmacol. 1988;28(8):727-735. doi:10.1002/j.1552-4604.1988.tb03207.x [PubMed 3145942]
  31. Greene HL, Richardson DW, Hallstrom AP, et al. Congestive heart failure after acute myocardial infarction in patients receiving antiarrhythmic agents for ventricular premature complexes (Cardiac Arrhythmia Pilot Study). Am J Cardiol. 1989;63(7):393-398. doi:10.1016/0002-9149(89)90306-8 [PubMed 2464919]
  32. Hill GD, Kovach JR, Saudek DE, Singh AK, Wehrheim K, Frommelt MA. Transplacental treatment of fetal tachycardia: A systematic review and meta-analysis. Prenat Diagn. 2017;37(11):1076-1083. doi:10.1002/pd.5144 [PubMed 28833310]
  33. Ito S. Drug therapy for breast-feeding women. NEJM. 2000;343(2):118-126. [PubMed 10891521]
  34. Jaeggi ET, Carvalho JS, De Groot E, et al. Comparison of transplacental treatment of fetal supraventricular tachyarrhythmias with digoxin, flecainide, and sotalol: results of a nonrandomized multicenter study. Circulation. 2011;124(16):1747-1754. [PubMed 21931080]
  35. January CT, Wann LS, Alpert JS, et al. 2014 AHA/ACC/HRS Guideline for the Management of Patients With Atrial Fibrillation: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the Heart Rhythm Society. Circulation. Published online March 28, 2014. [PubMed 24682347]
  36. January CT, Wann LS, Calkins H,t al. 2019 AHA/ACC/HRS Focused Update of the 2014 AHA/ACC/HRS Guideline for the Management of Patients With Atrial Fibrillation: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society. Heart Rhythm. 2019. pii: S1547-5271(19)30037-2. doi:10.1016/j.hrthm.2019.01.024 [PubMed 30703530]
  37. Manolis AS. Ventricular premature beats. Post TW, ed. UpToDate. Waltham, MA: UpToDate Inc. http://www.uptodate.com. Accessed March 26, 2018.
  38. McNamara RL, Tamariz LJ, Segal JB, Bass EB. Management of atrial fibrillation: review of the evidence for the role of pharmacologic therapy, electrical cardioversion, and echocardiography. Ann Intern Med. 2003;139(12):1018-1033. doi:10.7326/0003-4819-139-12-200312160-00012 [PubMed 14678922]
  39. McQuinn RL, Pisani A, Wafa S, et al. Flecainide excretion in human breast milk. Clin Pharmacol Ther. 1990;48(3):262-267. [PubMed 2119270]
  40. Morganroth J. Risk factors for the development of proarrhythmic events. Am J Cardiol. 1987;59(11):32E-37E. doi:10.1016/0002-9149(87)90199-8 [PubMed 3107364]
  41. Musto B, Cavallaro C, Musto A, et al. Flecainide Single Oral Dose for Management of Paroxysmal Supraventricular Tachycardia in Children and Young Adults. Am Heart J. 1992;124(1):110-115. [PubMed 1615792]
  42. Nathan AW, Hellestrand KJ, Bexton RS, Spurrell RA, Camm AJ. The proarrhythmic effects of flecainide. Drugs. 1985;29(suppl 4):45-53. doi:10.2165/00003495-198500294-00010 [PubMed 4006779]
  43. Norvir (ritonavir) [prescribing information]. Chicago, IL: AbbVie Inc; March 2015.
  44. O'Sullivan JJ, Gardiner HM, Wren C. Digoxin or Flecainide for Prophylaxis of Supraventricular Tachycardia in Infants? J Am Coll Cardiol. 1995;26(4):991-994. [PubMed 7560629]
  45. Page RL, Joglar JA, Caldwell MA, et al. 2015 ACC/AHA/HRS Guideline for the Management of Adult Patients With Supraventricular Tachycardia: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society. J Am Coll Cardiol. 2016;67(13):e27-e115. doi:10.1016/j.jacc.2015.08.856 [PubMed 26409259]
  46. Palmer CM, Norris MC. Placental transfer of flecainide. Am J Dis Child. 1990;144(2):144. [PubMed 2105628]
  47. Park MK, ed. Park's Pediatric Cardiology for Practitioners. 6th ed. Elsevier/Mosby; 2014.
  48. Perry JC and Garson A Jr. Flecainide acetate for treatment of tachyarrhythmias in children: review of world literature on efficacy, safety, and dosing. Am Heart J. 1992;124(6):1614-1621. [PubMed 1462922]
  49. Perry JC, McQuinn RL, Smith RT Jr, et al. Flecainide Acetate for Resistant Arrhythmias in the Young: Efficacy and Pharmacokinetics. J Am Coll Cardiol. 1989;14(1):185-191. [PubMed 2500470]
  50. Price JF, Kertesz NJ, Snyder CS, Friedman RA, Fenrich AL. Flecainide and sotalol: a new combination therapy for refractory supraventricular tachycardia in children <1 year of age. J Am Coll Cardiol. 2002;39(3):517-520. [PubMed 11823091]
  51. Priestley KA, Ladusans EJ, Rosenthal E, et al. Experience With Flecainide for the Treatment of Cardiac Arrhythmias in Children. Eur Heart J. 1988;9(12):1284-1290. [PubMed 3147891]
  52. Preliminary Report: Effect of Encainide and Flecainide on Mortality in a Randomized Trial of Arrhythmia Suppression After Myocardial Infarction. The Cardiac Arrhythmia Suppression Trial (CAST) Investigators. N Engl J Med. 1989;321(6):406-412. [PubMed 2473403]
  53. Refer to manufacturer's labeling.
  54. Regitz-Zagrosek V, Roos-Hesselink JW, Bauersachs J, et al; ESC Scientific Document Group. 2018 ESC Guidelines for the management of cardiovascular diseases during pregnancy. Eur Heart J. 2018;39(34):3165-3241. doi:10.1093/eurheartj/ehy340 [PubMed 30165544]
  55. Russell GA, Martin RP. Flecainide toxicity. Arch Dis Child. 1989;64(6):860-862. [PubMed 2505692]
  56. Shiga T, Yoshioka K, Watanabe E, et al. Paroxysmal atrial fibrillation recurrences and quality of life in symptomatic patients: a crossover study of flecainide and pilsicainide. J Arrhythm. 2017;33(4):310-317. doi:10.1016/j.joa.2017.03.005 [PubMed 28765762]
  57. Skanes AC, Healey JS, Cairns JA, et al. Focused 2012 Update of the Canadian Cardiovascular Society Atrial Fibrillation Guidelines: Recommendations for Stroke Prevention and Rate/Rhythm Control. Can J Cardiol. 2012;28(2):125-136. [PubMed 22433576]
  58. Sridharan S, Sullivan I, Tomek V, et al. Flecainide versus digoxin for fetal supraventricular tachycardia: Comparison of two drug treatment protocols. Heart Rhythm. 2016;13(9):1913-1919. doi:10.1016/j.hrthm.2016.03.023 [PubMed 27554948]
  59. Strizek B, Berg C, Gottschalk I, Herberg U, Geipel A, Gembruch U. High-dose flecainide is the most effective treatment of fetal supraventricular tachycardia. Heart Rhythm. 2016;13(6):1283-1288. doi:10.1016/j.hrthm.2016.01.029 [PubMed 26829115]
  60. Tamargo J, Le Heuzey JY, Mabo P. Narrow therapeutic index drugs: a clinical pharmacological consideration to flecainide. Eur J Clin Pharmacol. 2015;71(5):549-567. doi:10.1007/s00228-015-1832-0 [PubMed 25870032]
  61. Taylor R, Gandhi MM, Lloyd G. Tachycardia due to atrial flutter with rapid 1:1 conduction following treatment of atrial fibrillation with flecainide. BMJ. 2010;340:b4684. doi:10.1136/bmj.b4684 [PubMed 20219811]
  62. Thompson B, Mangat J, Barton C, Hawcutt DB. Decreased milk drinking causing flecainide toxicity in an older child. BMJ Case Rep. 2012:bcr0220125810. [PubMed 22729333]
  63. Van der Werf C, Kannankeril PJ, Sacher F, et al. Flecainide therapy reduces exercise-induced ventricular arrhythmias in patients with catecholaminergic polymorphic ventricular tachycardia. J Am Coll Cardiol. 2011;57(22):2244-2254. doi:10.1016/j.jacc.2011.01.026 [PubMed 21616285]
  64. Vento M, Tudela BF, Escrig R, Sáenz P, Sánchez A, Cano A. Haemolysis alters plasma flecainide levels in newborn infants. Acta Paediatr. 2007;96(3):466-468. [PubMed 17407483]
  65. Vigneswaran TV, Callaghan N, Andrews RE, et al. Correlation of maternal flecainide concentrations and therapeutic effect in fetal supraventricular tachycardia. Heart Rhythm. 2014;11(11):2047-2053. doi:10.1016/j.hrthm.2014.07.031 [PubMed 25068572]
  66. Wagner X, Jouglard J, Moulin M, Miller AM, Petitjean J, Pisapia A. Coadministration of flecainide acetate and sotalol during pregnancy: lack of teratogenic effects, passage across the placenta, and excretion in human breast milk. Am Heart J. 1990;119(3 Pt 1):700-702. [PubMed 1689933]
  67. Watanabe H, van der Werf C, Roses-Noguer F, et al. Effects of flecainide on exercise-induced ventricular arrhythmias and recurrences in genotype-negative patients with catecholaminergic polymorphic ventricular tachycardia. Heart Rhythm. 2013;10(4):542-547. [PubMed 23286974]
  68. Zeigler V, Gillette PC, Ross BA, et al. Flecainide for Supraventricular and Ventricular Arrhythmias in Children and Young Adults. Am J Cardiol. 1988;62(10, pt 1):818-820. [PubMed 3138905]
Topic 13302 Version 288.0

آیا می خواهید مدیلیب را به صفحه اصلی خود اضافه کنید؟