THE treatment of atrial fibrillation and the prevention of its complications are primarily pharmacologic problems. Treatment has two principal objectives. One is to use antiarrhythmic therapy to relieve symptoms; the other is to use prophylactic therapy to reduce the risk of stroke that accompanies atrial fibrillation. In planning the management of atrial fibrillation, it is useful to consider patients who are permanently in atrial fibrillation as having chronic atrial fibrillation and patients who have sinus rhythm punctuated by attacks of fibrillation as having paroxysmal atrial fibrillation. The two forms overlap, however, because many patients with chronic atrial fibrillation first present . . .

Management of atrial fibrillation.

Flecainide is a Class I antiarrhythmic drug of the local anaesthetic type. It can be given either intravenously or orally and its pharmacokinetic properties allow relatively long (12 hours) dosing intervals with oral administration. In several open and a few controlled therapeutic trials, orally administered flecainide has brought about a greater than 90% suppression of ventricular ectopic beats in about 80% of patients. A similar percentage of patients (83%) experienced at least an 80% suppression of their ventricular tachycardia in these trials. A slightly greater response rate was reported with intravenous infusion of flecainide. Initial results in arrhythmias complicating the Wolff-Parkinson-White syndrome have been favourable. Comparative trials are few in number but flecainide has proved to be more effective than quinidine, and possibly more effective than disopyramide, mexiletine, tocainide and propafenone, in suppressing ventricular ectopic activity. The most commonly reported extracardiac adverse effects have been dizziness and visual disturbances. Proarrhythmic effects have been reported in 7 to 8% of patients, with a higher incidence in patients with serious ventricular tachycardia and reduced myocardial function. The moderate negative inotropic effects of flecainide can become clinically significant in patients with impaired ventricular function. Thus flecainide, with its convenient dose schedule and apparently low incidence of serious side effects, would appear to be a useful addition to the antiarrhythmic agents available. Further studies are needed though, to confirm its long term tolerability when used prophylactically.

Flecainide. A preliminary review of its pharmacodynamic properties and therapeutic efficacy.

Flecainide acetate for resistant arrhythmias in the young: efficacy and pharmacokinetics.

The efficacy of flecainide acetate for conversion of atrial fibrillation into sinus rhythm was assessed in 69 patients (mean age of 63 ± 14 years). Mean duration of the arrhythmia was 49 ± 45 days. Mean cardiothoracic index was 0.49 ± 0.03. Flecainide treatment was started intravenously with a bolus of 2 mg/kg over 10 minutes, followed by oral treatment (200 to 300 mg/day) according to body weight.

Conversion to sinus rhythm was obtained in 49 patients (71%). The mean delay between initiation of treatment and restoration of sinus rhythm was 301 minutes (range 5 to 1,600). The left atrial diameter was smaller (40 ± 1 mm) in patients who had successful cardioversion than in those who did not (46 ± 1 mm) (p < 0.05). Patients with atrial fibrillation lasting for less than 10 days had a higher conversion rate (79%) than patients with longstanding atrial fibrillation, in whom the conversion rate was only 38% (p < 0.05). Conversion to sinus rhythm occurred in 33 patients during the first 5 minutes after injection. Adverse effects necessitated discontinuation of treatment in 4 patients (5.8%). Gastrointestinal disorders and dizziness occurred in 5 other patients but did not necessitate discontinuing treatment.

In conclusion, flecainide is an effective drug for converting atrial fibrillation into sinus rhythm. Unlike quinidine, flecainide can be administered intravenously. The conversion rate with flecainide is higher in patients with a shorter duration of atrial fibrillation and smaller atria.

Restoration of sinus rhythm with flecainide in patients with atrial fibrillation.

The electrophysiologic effects and therapeutic efficacy of intravenous and oral flecainide were studied in 15 patients with spontaneous and inducible sustained paroxysmal supraventricular tachycardia (SVT). Twelve patients had atrioventricular (AV) reentrance using an accessory pathway for retrograde conduction and 3 had AV nodal reentrance. Fourteen patients received intravenous flecainide (2 mg/kg body weight over 15 minutes) during an initial electrophysiologic study. Nine patients were restudied during oral flecainide administration (200 to 400 mg/day). After intravenous or oral flecainide therapy, reentrant SVT was noninducible in 6 patients with AV reentrance and in the 3 with AV nodal reentrance. In these 9 patients, intravenous flecainide prevented induction of reentrant SVT by depressing conduction over the retrograde limb of the reentry circuits. In the 6 patients with inducible sustained AV reentrant SVT before and after flecainide therapy, the cycle length of tachycardia increased significantly, mainly as the result of an increase in ventriculoatrial conduction time. There was concordance between the intravenous and the oral effects of flecainide on the mechanism of the SVT. Twelve patients continued oral flecainide treatment for a mean of 16 months (range 5 to 28). Tachycardia recurred in 3 of 4 patients whose arrhythmia remained inducible after flecainide therapy and in 1 of 8 patients whose SVT was suppressed. It is concluded that flecainide is an effective and convenient antiarrhythmic agent to treat patients who have AV nodal or AV reentrant SVT.

Treatment of paroxysmal reentrant supraventricular tachycardia with flecainide acetate.

The effect of flecainide in 12 patients with the Wolff-Parkinson-White syndrome was analyzed with respect to the anterograde and retrograde conduction properties of the accessory pathway, the modes of initiation and termination of circus movement tachycardias, and the ventricular response during induced atrial fibrillation. The principal effect of this drug was to depress both anterograde and retrograde conduction of the accessory pathway. In 8/9 cases circus movement tachycardia was terminated by prolongation of the retrograde effective refractory period of the accessory pathway. Flecainide increased the shortest and the mean cycle length during induced atrial fibrillation. It is concluded that the drug may be of potential benefit in patients with paroxysmal supraventricular tachycardias in patients with the Wolff-Parkinson-White syndrome.

Effects of flecainide on electrophysiological properties of accessory pathways in the Wolff-Parkinson-White syndrome

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Effects of flecainide on electrophysiological properties of accessory pathways in the Wolff-Parkinson-White syndrome