Flecainide supraventricular arrhythmias

Once the arrhythmia is controlled, it may be possible to reduce the dose, as necessary, to minimize side effects or effects on conduction. PSVT and PAF The recommended starting dose is 50 mg every 12 hours. Doses may be increased in increments of 50 mg twice daily every 4 days until efficacy is achieved. For PAF patients, a substantial increase in efficacy without a substantial increase in discontinuation for adverse experiences may be achieved by increasing the flecainide dose from 50 to 100 mg twice/day. The maximum recommended dose for patients with paroxysmal supraventricular arrhythmias is 300 mg/day. 

Approved indications for propafenone include treatment of supraventricular arrhythmias and life-threatening ventricular arrhythmias in the absence of structural heart disease. Propafenone has been shown to increase mortality in patients with structural heart disease, and so extreme caution must be used in this subset of patients. As with flecainide, the patient should be hospitalized for initiation of therapy. 

Flecainide is a potent blocker of sodium and potassium channels with slow unblocking kinetics. (Note that although it does block certain potassium channels, it does not prolong the action potential or the QT interval.) It is currently used for patients with otherwise normal hearts who have supraventricular arrhythmias. It has no antimuscarinic effects. 

Propafenone has some structural similarities to propranolol and possesses weak 3-blocking activity. Its spectrum of action is very similar to that of quinidine, but it does not prolong the action potential. Its sodium channel-blocking kinetics are similar to that of flecainide. Propafenone is metabolized in the liver, with an average half-life of 5-7 hours. The usual daily dosage of propafenone is 450-900 mg in three divided doses. The drug is used primarily for supraventricular arrhythmias. The most common adverse effects are a metallic taste and constipation arrhythmia exacerbation can also occur. 

Flecainide Sodium channel (INa) blockade Dissociates from channel with slow kinetics no change in action potential duration Supraventricular arrhythmias in patients with normal heart do not use in ischemic conditions (post-myocardial infarction) Oral hepatic, and kidney metabolism half life 20 h Toxicity Proarrhythmic... 

Hohnloser SH, Zabel M. Short- and long-term efficacy and safety of flecainide acetate for supraventricular arrhythmias. Am J Cardiol I 992 70(5) 3A-9A discussion 9A-I0A. 

International Symposinm on Supraventricular Arrhythmias Focus on Flecainide. October 23-26, 1987, Paradise Island, Nassau, Bahamas. Proceedings. Am I Cardiol 1988 62(6) D1-D67. 

Wehling M. Meta-analysis of flecainide safety in patients with supraventricular arrhythmias. Arzneimittelforschung 2002 52(7) 507-14. 

Class IC drugs Flecainide is effective in both atrial and ventricular arrhythmias but is approved only for refractory ventricular tachycardias that tend to progress to VF at unpredictable times, resulting in sudden death, and for certain intractable supraventricular arrhythmias. 

Fleca.inide, Elecainide acetate, a fluorobenzamide, is a derivative of procainamide, and has been reported to be efficacious in suppressing both supraventricular and ventricular arrhythmias (26—29). The dmg is generally reserved for patients with serious and life-threatening ventricular arrhythmias. Elecainide depresses phase 0 depolarization of the action potential, slows conduction throughout the heart, and significantly prolongs repolarization (30). The latter effect indicates flecainide may possess some Class III antiarrhythmic-type properties (31). 

Based on several studies flecainide appears to be beneficial in treating supraventricular and ventricular arrhythmias in children. Elimination half-life is shorter and volume of distribution is smaller. 

Clinical uses PVC, paroxysmal atrial tachycardia, AF, VT Documented life-threatening ventricular arrhythmias. Flecainide also may be used for AF and supraventricular tachycardias in patients without structural heart disease. Propafenone is also indicated for paroxysmal AF. 

Flecainide is absorbed well, has a long half-hfe of 3 to 5 days, is metabolized to -O-deaUcylated flecainide (active antiarrhythmic agent with less potency than flecainide) and to -0-deaUcylated lactam of flecainide, which is an inactive metabolite. A portion of flecainide is excreted unchanged. Flecainide, like other antiarrhythmic agents, can cause new or worsen supraventricular or ventricular arrhythmias. Ventricular proarrhythmic effects range from an increase in frequency of premature ventricular complexes (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. 

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