Flecainide Acetate (Page 2 of 6)

INDICATIONS AND USAGE

In patients without structural heart disease, Flecainide Acetate Tablets, USP are indicated for the prevention of:

  • paroxysmal supraventricular tachycardias (PSVT), including atrioventricular nodal reentrant tachycardia, atrioventricular reentrant tachycardia and other supraventricular tachycardias of unspecified mechanism associated with disabling symptoms
  • paroxysmal atrial fibrillation/flutter (PAF) associated with disabling symptoms

Flecainide Acetate Tablets, USP are also indicated for the prevention of:

  • documented ventricular arrhythmias, such as sustainedventricular tachycardia ( sustained VT), that in the judgment of the physician are life-threatening.

Use of Flecainide Acetate Tablets, USP for the treatment of sustainedVT, like other antiarrhythmics, should be initiated in the hospital. The use of Flecainide Acetate Tablets, USP is not recommended in patients with less severe ventricular arrhythmias even if the patients are symptomatic.

Because of the proarrhythmic effects of Flecainide Acetate Tablets, USP, its use should be reserved for patients in whom, in the opinion of the physician, the benefits of treatment outweigh the risks.

Flecainide Acetate Tablets, USP should not be used in patients with recent myocardial infarction. (See Boxed WARNINGS.)

Use of Flecainide Acetate Tablets, USP in chronic atrial fibrillation has not been adequately studied and is not recommended. (See Boxed WARNINGS.)

As is the case for other antiarrhythmic agents, there is no evidence from controlled trials that the use of Flecainide Acetate Tablets, USP favorably affects survival or the incidence of sudden death.

CONTRAINDICATIONS

Flecainide Acetate Tablets are contraindicated in patients with pre-existing second- or third-degree AV block, or with right bundle branch block when associated with a left hemiblock (bifascicular block), unless a pacemaker is present to sustain the cardiac rhythm should complete heart block occur. Flecainide Acetate Tablets are also contraindicated in the presence of cardiogenic shock or known hypersensitivity to the drug.

WARNINGS

Mortality

Flecainide acetate 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 a myocardial infarction more than six days but less than two years previously. An excessive mortality or non-fatal cardiac arrest rate was seen in patients treated with flecainide acetate compared with that seen in patients assigned to a carefully matched placebo-treated group. This rate was 16/315 (5.1%) for flecainide acetate and 7/309 (2.3%) for the matched placebo. The average duration of treatment with flecainide acetate in this study was ten months.

The applicability of the CAST results to other populations (e.g., those without recent myocardial infarction) is uncertain, but at present, it is prudent to consider the risks of Class IC agents (including flecainide acetate), 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 Pro-arrhythmic Effects in Patients with Atrial Fibrillation/Flutter

A review of the world literature revealed reports of 568 patients treated with oral flecainide acetate for paroxysmal atrial fibrillation/flutter (PAF). Ventricular tachycardia was experienced in 0.4% (2/568) of these patients. Of 19 patients in the literature with chronic atrial fibrillation (CAF), 10.5% (2) experienced VT or VF. FLECAINIDE IS NOT RECOMMENDED FOR USE IN PATIENTS WITH CHRONIC ATRIAL FIBRILLATION. Case reports of ventricular proarrhythmic effects in patients treated with flecainide acetate for atrial fibrillation/flutter have included increased PVCs, VT, ventricular fibrillation (VF), and death.

As with other Class I agents, patients treated with flecainide acetate 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 acetate. Concomitant negative chronotropic therapy such as digoxin or beta-blockers may lower the risk of this complication.

PROARRHYTHMIC EFFECTS

Flecainide acetate, like other antiarrhythmic agents, can cause new or worsened supraventricular or ventricular arrhythmias. Ventricular proarrhythmic effects range from an increase in frequency of PVCs to the development of more severe ventricular tachycardia, e.g., tachycardia that is more sustained or more resistant to conversion to sinus rhythm, with potentially fatal consequences. In studies of ventricular arrhythmia patients treated with flecainide acetate, three-fourths of proarrhythmic events were new or worsened ventricular tachyarrhythmias, the remainder being increased frequency of PVCs or new supraventricular arrhythmias. In patients treated with flecainide acetate for sustainedventricular tachycardia, 80% (51/64) of proarrhythmic events occurred within 14 days of the onset of therapy. In studies of 225 patients with supraventricular arrhythmia (108 with paroxysmal supraventricular tachycardia and 117 with paroxysmal atrial fibrillation), there were 9 (4%) proarrhythmic events, 8 of them in patients with paroxysmal atrial fibrillation. Of the 9, 7 (including the one in a PSVT patient) were exacerbations of supraventricular arrhythmias (longer duration, more rapid rate, harder to reverse) while 2 were ventricular arrhythmias, including one fatal case of VT/VF and one wide complex VT (the patient showed inducible VT, however, after withdrawal of flecainide acetate), both in patients with paroxysmal atrial fibrillation and known coronary artery disease.

It is uncertain if flecainide acetate’s risk of proarrhythmia is exaggerated in patients with chronic atrial fibrillation (CAF), high ventricular rate, and/or exercise. Wide complex tachycardia and ventricular fibrillation have been reported in two of 12 CAF patients undergoing maximal exercise tolerance testing.

In patients with complex ventricular arrhythmias, it is often difficult to distinguish a spontaneous variation in the patient’s underlying rhythm disorder from drug-induced worsening, so that the following occurrence rates must be considered approximations. Their frequency appears to be related to dose and to the underlying cardiac disease.

Among patients treated for sustainedVT (who frequently also had CHF, a low ejection fraction, a history of myocardial infarction and/or an episode of cardiac arrest), the incidence of proarrhythmic events was 13% when dosage was initiated at 200 mg/day with slow upward titration, and did not exceed 300 mg/day in most patients. In early studies in patients with sustainedVT utilizing a higher initial dose (400 mg/day) the incidence of proarrhythmic events was 26%; moreover, in about 10% of the patients treated proarrhythmic events resulted in death, despite prompt medical attention. With lower initial doses, the incidence of proarrhythmic events resulting in death decreased to 0.5% of these patients. Accordingly, it is extremely important to follow the recommended dosage schedule. (See DOSAGE AND ADMINISTRATION.)

The relatively high frequency of proarrhythmic events in patients with sustainedVT and serious underlying heart disease, and the need for careful titration and monitoring, requires that therapy of patients with sustainedVT be started in the hospital. (See DOSAGE AND ADMINISTRATION.)

HEART FAILURE

Flecainide acetate has a negative inotropic effect and may cause or worsen CHF, particularly in patients with cardiomyopathy, preexisting severe heart failure (NYHA functional class III or IV) or low ejection fractions (less than 30%). In patients with supraventricular arrhythmias new or worsened CHF developed in 0.4% (1/225) of patients. In patients with sustainedventricular tachycardia during a mean duration of 7.9 months of flecainide acetate therapy, 6.3% (20/317) developed new CHF. In patients with sustainedventricular tachycardia and a history of CHF, during a mean duration of 5.4 months of flecainide acetate therapy, 25.7% (78/304) developed worsened CHF. Exacerbation of preexisting CHF occurred more commonly in studies which included patients with class III or IV failure than in studies which excluded such patients. Flecainide acetate should be used cautiously in patients who are known to have a history of CHF or myocardial dysfunction. The initial dosage in such patients should be no more than 100 mg bid (see DOSAGE AND ADMINISTRATION) and patients should be monitored carefully. Close attention must be given to maintenance of cardiac function, including optimization of digitalis, diuretic, or other therapy. In cases where CHF has developed or worsened during treatment with flecainide acetate, the time of onset has ranged from a few hours to several months after starting therapy. Some patients who develop evidence of reduced myocardial function while on flecainide acetate can continue on flecainide acetate with adjustment of digitalis or diuretics, others may require dosage reduction or discontinuation of flecainide acetate. When feasible, it is recommended that plasma flecainide levels be monitored. Attempts should be made to keep trough plasma levels below 0.7 to 1 mcg/mL.

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