Encainide is a class IC antiarrhythmic agent having little or no effect on action-potential duration or maximum diastolic potential but decreasing the maximum rate of phase O depolarization as well as increasing atrial and ventricular effective refractory periods. In intact animals or humans, encainide increases the AH, PR, QRS, and H-V intervals while not affecting the sinus node cycle length or JT interval. QT interval increases only by the concomitant increase in the QRS interval. Encainide is metabolized to O-demethyl encainide (ODE) and 3-methoxy-ODE (MODE), both of which are also antiarrhythmics with similar pharmacology to encainide. Encainide and its metabolites have little negative inotropic activity and ancillary pharmacology. Consequently, encainide has little or no effect on hemodynamic variables in patients with either normal or compromised cardiac function. The drug is well tolerated, with side effects being mainly those associated with its local anesthetic activity such as blurred vision and dizziness. Encainide is particularly effective in patients with excessive premature ventricular complexes (PVCs) and less so in patients with sustained ventricular tachycardia (VT). Like all antiarrhythmics, encainide may aggravate or precipitate new arrhythmias (proarrhythmia). The overall incidence of proarrhythmia is about 10%, with less occurring in patients with PVCs and more in those with sustained VT; also, the incidence of proarrhythmia is higher in patients with underlying heart disease. Encainide is also effective for the treatment of supra-ventricular arrhythmias, including atrial fibrillation, PSVT (both PAF as well as reentry of the nodal or W-P-W type), and ectopic atrial tachycardia. Its dosage and role in antiarrhythmic therapy are discussed.
Encainide (MJ 9067) was given intravenously at 1, 2, or 5 mg/kg and orally at 1, 2.5, 5, or 10 mg/kg to conscious dogs 18--23 h after two-stage ligation of the left anterior descending coronary artery. Heart rate and ventricular ectopic rate were lowered in a dose-related manner by 40--70 and 55--158 beats/min, respectively, following drug administration. Ventricular arrhythmia was frequently abolished with doses of 2 mg/kg and above. The onset of antiarrhythmic activity was 1--2 min after intravenous injection and 15--30 min after oral ingestion. The duration of effect was 6--7 h or longer following either route of drug administration. Emesis occurred in 1 of 10 and 1 of 6 dogs, respectively, at the 2 and 5 mg/kg intravenous dose levels. Brief ataxia was also observed in one dog given the latter dose.
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