Flecainide (Tambocor) is a fluorinated aromatic hy-drocarbon examined initially for its local anesthetic action and subsequently found to have antiarrhythmic effects. Flecainide inhibits the sodium channel, leading to conduction slowing in all parts of the heart, but most notably in the His-Purkinje system and ventricu-lar myocardium. It has relatively minor effects on re-polarization. Flecainide also inhibits abnormal auto-maticity.
Flecainide decreases the sinus cycle length but re-sults in a clinically insignificant decrease in heart rate.
Flecainide decreases the maximal rate of depolar-ization in atrial tissue and shifts the membrane respon-siveness curve to the right.
The atrioventricular conduction time, measured as the A–H interval, is prolonged by flecainide as is the His-Purkinje or H–V interval.
Flecainide slows conduction in the His-Purkinje system and ventricular muscle to a greater degree than in the atrium. Flecainide may also cause block in acces-sory A-V connections, which is the principal mecha-nism for its effectiveness in treating A-V reentrant tachycardia.
Flecainide increases the PR, QRS, and to a lesser ex-tent, QTc intervals. The rate of ventricular repolariza-tion is not affected, and the QT interval prolongation is caused by the increase in the QRS duration.
Flecainide produces modest negative inotropic effects that may become significant in the subset of patients with compromised left ventricular function.
The pharmacokinetic characteristics of flecainide:
Oral bioavailability : 85–90%
Onset of action : 1–2 hours
Peak response : 1.5–6 hours
Duration of action : 1–2 days
Plasma half-life : 12–30 hours
Primary route of metabolism:Hepatic
Primary route of excretion: 10–50% renal; 5% fecal
Therapeutic serum concentration: 0.2–1.0 μg /mL
Flecainide is effective in treating most types of atrial ar-rhythmias. It is also used for life-threatening ventricular arrhythmias. However, flecainide should be used with ex-treme caution in any patient with structural heart disease. Flecainide crosses the placenta, with fetal levels reaching approximately 70% of maternal levels. In many centers, it is the second-line drug after digoxin for therapy of fe-tal arrhythmias. Because of the high incidence of proar-rhythmia, initiation of therapy or significant increases in dosing should be performed only on inpatients.
Most adverse effects occur within a few days of initial drug administration. The most frequently reported ef-fects are dizziness, light-headedness, faintness, unsteadi-ness, visual disturbances, blurred vision (e.g., spots be-fore the eyes, difficulty in focusing), nausea, headache, and dyspnea.
Worsening of heart failure and prolongation of the PR and QRS intervals are likely to occur with flecainide, and an increased risk of proarrhythmia has been reported.
Flecainide is contraindicated in patients with preexist-ing second- or third-degree heart block or with bundle branch block unless a pacemaker is present to maintain ventricular rhythm. It should not be used in patients with cardiogenic shock.
In patients whose condition has been stabilized by fle-cainide, the addition of cimetidine may reduce the rate of flecainide’s hepatic metabolism, increasing the po-tential for toxicity. Flecainide may increase digoxin con-centrations on concurrent administration.