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PubMed1984

Clinical efficacy and electrophysiologic effects of intravenous and oral encainide in patients with accessory atrioventricular pathways and supraventricular arrhythmias.

The electrophysiologic effects and clinical efficacy of intravenous (i.v.) and oral encainide were studied in 13 patients with accessory atrioventricular (AV) pathways (7 overt, 1 intermittent and 5 concealed) and drug-resistant supraventricular arrhythmias (5 paroxysmal atrial fibrillation, 1 atrial tachycardia and 7 with orthodromic circus movement tachycardia). Previously, therapy had failed with a mean of 3 conventional antiarrhythmic agents. In 5 patients, amiodarone administration had also been unsuccessful. All patients underwent programmed electrical stimulation of the heart before and after 1.5 mg/kg of i.v. encainide. Seven patients were restudied during oral encainide therapy (mean 155.8 +/- 54.2 mg/day) 3 days to 6 weeks (average 21 days) later. Anterograde conduction over the accessory AV pathway blocked in 4 of 7 patients after i.v. encainide. Oral encainide blocked anterograde conduction over the accessory pathway or prolonged the refractory period of the accessory pathway in 3 of 4 patients. This change in anterograde conduction was independent of the predrug value for the anterograde refractory period of the accessory AV pathway. Intravenous and oral encainide had minimal effects on retrograde conduction over the accessory AV pathway. The clinical effect of oral encainide was studied in 12 patients. Four patients responded to oral encainide and have been free of arrhythmia or side effects for 2 to 20 months (average 10.5). Encainide failed to prevent the clinical arrhythmia in 2 patients. In 4 patients with atrial arrhythmias, circus movement tachycardia developed during oral encainide therapy. In 1 patient the frequency of circus movement tachycardia increased with oral encainide treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1986

Encainide for ventricular arrhythmias: placebo-controlled and standard comparison trials.

Efficacy data obtained from the use of encainide in the treatment of patients with benign or potentially lethal ventricular arrhythmias are reviewed. These include an oral dose multicenter titration study involving 111 patients in whom encainide was given from 25 to 75 mg, 4 times/day, which was followed by a 3-center, reduced dose study in which 35 patients received a forced escalation of encainide from 10 to 30 mg, 4 times/day. Frequent Holter monitoring was used to judge efficacy. An 8-center, double-blind, parallel, placebo-controlled outpatient trial was conducted using encainide from 10 to 50 mg, 3 times/day, in 125 patients. This trial defined the lower end of the dose response curve for encainide to be 25 mg, 3 times/day. The data from all these trials show that when properly titrated, encainide is effective in decreasing ventricular premature complex frequency by at least 75% in about 80% of patients. A similar percentage will have abolition of ventricular tachycardia. When encainide was compared with quinidine in a 9-center placebo-controlled crossover study, encainide demonstrated more efficacy at 25 mg, 4 times/day, compared with quinidine at 200 mg, 4 times/day, in all arrhythmia parameters. Encainide was also better tolerated than quinidine and there was no statistically significant difference in the prevalence of asymptomatic proarrhythmia as detected by Holter monitoring between these 2 drugs. Long-term data in 220 patients over 36-month follow-up show continued encainide efficacy. Thus, encainide is a potent, effective class 1C antiarrhythmic agent and it has minimal negative inotropic effects and is well tolerated.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1990

Genetically determined steady-state interaction between encainide and quinidine in patients with arrhythmias.

A genetically determined pharmacokinetic and pharmacodynamic interaction between quinidine and single doses of encainide in healthy volunteers has previously been described. In subjects with the extensive metabolizer phenotype, quinidine blunted encainide-induced QRS prolongation (a marker of sodium channel block) because it impaired encainide biotransformation to the potent active metabolites O-desmethyl encainide (ODE) and 3-methoxy-O-desmethyl encainide. Therefore, the purpose of this study was to test the hypothesis that quinidine would inhibit sodium channel block (and by inference arrhythmia suppression) during encainide therapy in patients with the extensive metabolizer phenotype. Surprisingly, however, in eight extensive metabolizer patients, the extent of QRS prolongation during chronic encainide therapy was unaltered by quinidine (139 +/- 21 vs. 139 +/- 22 msec) whereas arrhythmia suppression was enhanced (64 +/- 22 to 77 +/- 19%; P = .05). Plasma concentration data demonstrated that although encainide metabolism to ODE was partially impaired by quinidine, subsequent 3-methoxy-O-desmethyl encainide formation from ODE was virtually completely inhibited; thus steady-state plasma ODE remained unchanged whereas plasma encainide increased 10-fold (21 +/- 30 to 240 +/- 118 ng/ml; P less than .05). In contrast, no changes in disposition or in pharmacodynamics were observed in two poor metabolizers. It is concluded that the effect of this drug interaction in patients is determined by differential sensitivities to inhibition by quinidine of encainide O-demethylation and subsequent ODE 3-methoxylation. Evaluation of potential drug interactions should include assessment of possible genetic factors as well as of steady-state effects.

Aged↗
PubMed1989

Encainide.

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.

Anilides↗
PubMed1984

Electrophysiologic and clinical effects of intravenous and oral encainide in accessory atrioventricular pathway.

The effect of intravenous and oral encainide was studied in 12 patients with an accessory atrioventricular pathway (AP). Eight patients had Wolff-Parkinson-White syndrome and 4 had a concealed AP. Electrophysiologic studies were performed before and after intravenous encainide, 1.0 to 1.5 mg/kg, and 4 weeks after oral encainide, 75 to 200 mg/day. Mean follow-up was 19 +/- 6 months. During sinus rhythm, intravenous and oral encainide significantly prolonged the AH and HV intervals. In patients with Wolff-Parkinson-White syndrome, after intravenous encainide, anterograde conduction over the AP was blocked in 3 patients, and the anterograde effective refractory period (ERP) of the AP was markedly increased in 3. Five of these 6 patients had a control value of the anterograde AP ERP of less than 270 ms. Anterograde AP block was maintained in 2 patients after oral encainide therapy. Retrograde AP block or marked increase of retrograde AP ERP was seen in 4 of 9 patients after intravenous encainide and in 2 of 7 after oral therapy. Encainide either prevented induction of circus movement tachycardia (intravenous, 4 of 11 patients; oral, 2 of 7 patients) or significantly prolonged tachycardia cycle length (intravenous, 7 of 11 patients; oral, 5 of 7 patients). During long-term follow-up of 9 patients, 6 patients had no recurrences of tachyarrhythmia after individual adjustment of encainide dosage. One patient had worsening of supraventricular tachycardia after intravenous encainide therapy and 4 patients complained of visual blurring; in 1 patient it was so severe that it required withdrawal of the drug.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1988

Role of adrenergic stimulation by isoproterenol in reversal of effects of encainide in supraventricular tachycardia.

Reversal of the electrophysiologic effects of oral encainide with isoproterenol was evaluated in 16 patients with atrioventricular (AV) nodal reentry (group A) and in another 16 patients with Wolff-Parkinson-White syndrome (group B). Sustained AV nodal reentry was induced in all group A cases before administration of encainide, in 2 cases after oral encainide, and in 12 patients during infusion of isoproterenol. Among group B cases, 14 of 16 had sustained AV reentry during control, 6 of 16 after receiving encainide, and 8 of 16 with addition of isoproterenol. During a mean follow-up of 19 +/- 10 months in group A and 17 +/- 9 months in group B, clinical tachycardia recurred in 8 patients (4 from each group). These 8 patients were among the 20 patients who demonstrated (1) isoproterenol-induced reversibility of encainide-suppressed tachycardia, or (2) acceleration of tachycardia rate slowed by encainide. No recurrences were seen among any of the 12 cases in which isoproterenol failed to reverse the encainide-induced tachycardia suppression. Patients with clinical recurrences were controlled with a variety of means, which included beta blockers in 3 and nonpharmacologic methods in the remaining 5. In patients with AV junctional tachycardia treated with oral encainide, our findings suggest that lack of tachycardia inducibility with isoproterenol predicts freedom from clinical recurrences. Furthermore, addition of a beta blocker to oral encainide may prevent clinical recurrence in some who demonstrate adrenergic reversal of encainide effect.

Administration, Oral↗
PubMed1991

Genetically determined stereoselective excretion of encainide in humans and electrophysiologic effects of its enantiomers in canine cardiac Purkinje fibers.

Encainide metabolism is mediated by the polymorphically distributed cytochrome P450IID6, which displays stereoselectivity for some substrates. In this study we found that urinary recovery during steady-state encainide in three poor metabolizers was high (49% to 80%), consisted mainly of unchanged encainide, was nonstereoselective (+/- ratio, 0.985 to 1.049), and was unchanged by quinidine, a potent inhibitor of P450IID6. In contrast, in seven extensive metabolizers the +/- urinary ratios were 1.20 +/- 0.06 for encainide and 0.81 +/- 0.06 (both p less than 0.01) for the cytochrome P450IID6 products O-desmethylencainide plus 3-methoxy-O-desmethylencainide; with quinidine the total percentage recovery rose from 4% +/- 4% to 37% +/- 9% because of increased recovery of unchanged encainide and became non-stereoselective (+/- ratio, 0.84 +/- 0.08 [encainide alone] versus 0.97 +/- 0.05 [encainide plus quinidine]). In vitro, encainide enantiomers depressed the maximum rate of metabolism with similar frequency and concentration dependence. We conclude that (-)-encainide undergoes preferential metabolism by cytochrome P450IID6; however, this genetically determined stereoselective disposition is unlikely to play a major role in mediating the clinical actions of encainide.

Action Potentials↗
PubMedDate not supplied

Response to encainide of refractory ventricular tachycardia: clinical application of assays for parent drug and metabolites.

To assess the response to encainide in patients with malignant arrhythmias, we treated 22 patients with recurrent ventricular tachycardia (VT) or fibrillation (VF) refractory to an average of 5.7 drugs. Thirteen patients (59%) showed a favorable in-hospital response, and 11 of 22 (50%) maintained a favorable antiarrhythmic response during a median follow-up of 13.5 months (range 0.3--25.5). Encainide was well tolerated. Six (46%) of 13 patients responded to intravenous encainide with suppression of VT by programmed ventricular stimulation or continuous monitoring; oral encainide has maintained arrhythmia control. In six of seven others, cycle length of VT was lengthened. Initial therapy with oral drug yielded five complete and two partial responses, assessed by monitoring, among nine other patients. Of three outpatient failures, only one was an inpatient responder. Proarrhythmic responses were also noted and included spontaneous increases in ectopy (three patients), easier induction of VT spontaneously or at programmed stimulation (three patients), facilitation of exercise VT (one patient), and syncope due to VT/VF (one patient). After intravenous therapy, plasma encainide concentration averaged 773 ng/ml (range 476--1,279, n = 4), with low or negligible metabolites. During chronic oral therapy, encainide concentrations were low and variable, averaging 67.5 ng/ml (less than 10--585; n = 23, 10 patients); metabolite levels were higher and less variable: O-demethyl encainide, mean 198 ng/ml (61--882); 3-methoxy-o-demethyl encainide, mean 128 ng/ml (39--379). Active metabolites(s) may thus be more important than parent drug during chronic therapy. In summary, encainide may provide successful therapy in approximately half of patients with malignant, refractory ventricular arrhythmias. Inpatient response predicts outpatient results. Encainide, like other antiarrhythmics, has proarrhythmic potential, suggesting a carefully monitored initial approach.

Adult↗
PubMed1993

Demonstration of proarrhythmic activity with the class IC antiarrhythmic agent encainide in a canine model of previous myocardial infarction.

The antiarrhythmic efficacy and proarrhythmic potential of the class IC antiarrhythmic agent encainide were assessed in subacute and chronic postinfarction canine models, respectively. In conscious dogs with spontaneous premature ventricular complexes (PVCs) at 48 h after anterior myocardial infarction (MI), cumulative intravenous (i.v.) administration of 1.0 and 3 mg/kg encainide significantly reduced PVC frequency. However, in anesthetized dogs studied more chronically after anterior MI (range 8-44 days), i.v. administration of 0.3-3 mg/kg encainide resulted in induction of new ventricular tachyarrhythmias by programmed ventricular stimulation in 6 of 10 dogs with no inducible arrhythmias prior to encainide. Newly induced arrhythmias after encainide administration included unimorphic and polymorphic ventricular tachycardia (VT) as well as VT degenerating rapidly into ventricular fibrillation (VF). The incidences of new arrhythmia induction after cumulative i.v. administration of encainide were 3 of 9 after 0.3 mg/kg i.v. encainide, 4 of 9 after 1.0 mg/kg i.v. encainide, and 5 of 10 after 3.0 mg/kg i.v. encainide. Time elapsed between MI and electrophysiologic testing tended to predict proarrhythmic response to encainide, with the six preparations with newly induced arrhythmias tested earlier than the four preparations that remained nonresponsive to postencainide programmed stimulation (13.2 +/- 3.1 vs. 26.5 +/- 6.5 days postinfarction, respectively, p = 0.07). There was also a trend toward larger underlying anterior MIs in the six preparations with newly induced arrhythmias as compared with the four preparations that remained nonresponsive to postencainide programmed stimulation (13.2 +/- 2.9 vs. 7.5 +/- 2.1% of left ventricle, respectively, p = 0.19).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Polymorphism of dextromethorphan metabolism: relationships between phenotype, genotype and response to the administration of encainide in humans.

The polymorphism of dextromethorphan and encainide metabolism is genetically determined and is related to the activity of hepatic CYP2D6. In order to examine the relations between CYP2D6 phenotype, genotype and the electrocardiographic response to the oral administration of encainide, 110 healthy subjects were studied. Metabolic ratios were calculated in urine after oral administration of 40 mg of dextromethorphan and in plasma obtained 2.5 h after oral administration of 50 mg of encainide. Encainide-induced electrocardiographic changes were measured 2.5 h after oral administration of the drug. Genotype was determined in 52 subjects. Results showed that phenotype, either extensive or poor metabolizer, for CYP2D6-dependent metabolism could be identified from the dextromethorphan metabolic ratio calculated in urine, from the encainide metabolic ratio calculated in plasma and from the genotype. However, despite the fact that the changes in atrioventricular (PR) and intraventricular (QRS) conduction times produced by encainide were different in extensive and poor metabolizer subjects and correlated with CYP2D6 activity, the electrocardiographic response was never 100% specific and sensitive for the identification of either phenotype. Moreover, genotypic identification of heterozygous and homozygous extensive metabolizer subjects did not predict CYP2D6 activity, as determined by dextromethorphan and encainide metabolic ratios, or encainide response, as determined by intraventricular and atrioventricular changes. Thus, CYP2D6 activity does not fully predict the electrocardiographic effects of encainide, and genotype, as determined in our study, cannot replace the determination of metabolic ratio in predicting CYP2D6 activity and encainide response in extensive metabolizer subjects.

Adult↗
PubMedDate not supplied

Structural characterization of urinary metabolites of the antiarrhythmic drug encainide in human subjects.

Metabolism of the antiarrhythmic drug encainide was studied in human subjects after a single 50-mg oral dose. Encainide labeled on the carbonyl carbon with 14C and at the benzylic (2'-1-ethyl) carbon with 13C was administered to four normal healthy male subjects. A large proportion of the radioactive dose (42%) was excreted in the urine in the first 24 hr. The total urinary excretion was 47.0 +/- 4.6% and total fecal excretion was 38.7 +/- 5.7% over 5 days. The conjugated metabolites excreted in the urine were hydrolyzed with beta-glucuronidase/arylsulfatase, and were isolated and purified by HPLC. Structural characterization was carried out by a combination of fast atom bombardment-mass spectrometry, gas chromatography/electron impact mass spectrometry, and 1H-NMR spectroscopy. Structures of the metabolites were confirmed by co-elution on HPLC with authentic standards when available. Six metabolites of encainide were identified from the hydrolyzed urine together with unchanged drug. In addition to already known metabolites O-demethyl-encainide, 3-methoxy-O-demethyl-encainide, and N,O-di-demethyl-encainide, three new metabolites were identified: N-demethyl-3-methoxy-O-demethyl-encainide, 3-hydroxy-encainide, and O-demethyl-encainide-lactam. These metabolites accounted for greater than 90% of the radioactivity excreted in the urine. Four major routes of metabolism were identified: first, O-demethylation of the aromatic methyl ether; second, formation of methylated catechol derivatives; third, N-demethylation of the piperidyl nitrogen; and fourth, oxidation at carbon alpha to the piperidyl nitrogen. A plausible scheme for the metabolism of encainide in human subjects is proposed.

Anilides↗
PubMed1982

Antiarrhythmic activity of the O-demethyl metabolite of encainide.

Clinical trials of the new antiarrhythmic agent encainide have demonstrated a high degree of efficacy in association with marked slowing of intracardiac conduction (prolongation of QRS). Indirect evidence has strongly suggested that at least some of these effects are mediated by the O-demethyl metabolite. The activity of a series of dosages of O-demethyl encainide, encainide and procainamide were compared against aconitine-induced ventricular arrhythmias in rats. Effective dosages were lowest for O-demethyl encainide and highest for procainamide: a 25% increase in the time to aconitine-induced ventricular tachycardia was produced by 0.02, 0.46 and 13 microM/kg of O-demethyl encainide, encainide and procainamide, respectively. QRS prolongation correlated well (r greater than 0.7, p less than .001) with enhanced survivorship for each agent tested and the cycle length of the ventricular tachycardia induced was lengthened in a dose-related fashion. Post-mortem plasma analysis showed that concentrations of the metabolite usually associated with pharmacological activity were present after encainide administration. However, encainide itself produced antiarrhythmic and electrocardiographic effects even when its metabolism was blocked. We conclude that both O-demethyl encainide and encainide exert antiarrhythmic actions in this model, but the metabolite is active at much lower dosages.

Aconitine↗
PubMed1992

Impact of food on the bioavailability of encainide.

The bioavailability of drugs that undergo extensive presystemic hepatic metabolism may be increased by concomitant ingestion with food. The effect of food on the bioavailability of encainide, a class IC antiarrhythmic agent, was evaluated in 14 healthy subjects in this randomized crossover study. The subjects received encainide 35 mg every 8 hours for 7 days and were randomized to receive their test dose of encainide with food or after an overnight fast. Encainide area-under-the-concentration versus time curve (AUCs) were detectable in 3 of 14 subjects after fasting and in 7 of 14 after feeding. Although food increased the mean encainide AUC by more than threefold, this increase did not reach statistical significance because of the large number of subjects with indeterminate encainide AUCs. Food did significantly increase the AUC of O-demethyl-encainide (ODE), but not the AUC of methoxy-O-demethyl-encainide (MODE). Despite the increase in ODE AUC, no significant effect on the surface electrocardiogram 2 hours after dose administration could be detected. Food may increase the bioavailability of encainide and one of its active metabolites (ODE). The clinical relevance of this pharmacodynamic effect warrants further evaluation.

Adult↗
PubMed1987

Electrophysiologic and antiarrhythmic effects of oral encainide in patients with atrioventricular nodal reentry or nodoventricular reentry.

Three patients with drug-resistant atrioventricular (AV) nodal reentrant tachycardia and two patients with reciprocating tachycardia associated with nodoventricular pathways received oral encainide after a control drug-free electrophysiologic study. In one patient with AV nodal reentry, encainide prolonged anterograde AV nodal conduction, produced complete ventriculoatrial (VA) block, and prevented tachycardia induction. Encainide had no effect on AV or VA conduction in the second patient with AV nodal reentry, and tachycardia with similar cycle length was still induced. The third patient was not studied while receiving encainide, but spontaneous AV nodal reentrant tachycardia occurring multiple times daily was abolished. In both patients with nodoventricular pathways, anterograde AV nodal and VA conduction were prolonged by encainide and tachycardia was no longer inducible. Two patients with AV nodal reentry were given long-term encainide therapy and have been free of recurrent arrhythmias for 16 and 30 months. One patient with a nodoventricular pathway has been without arrhythmia recurrence after 73 months of encainide therapy; the other patient required addition of propranolol to encainide because of recurrent tachycardia. We conclude that encainide can prolong anterograde AV nodal and VA conduction and prevent induced and spontaneous tachycardia in some patients with drug-resistant and highly symptomatic AV nodal or nodoventricular reentry.

Administration, Oral↗
PubMed1986

Electrophysiology, hemodynamic and arrhythmia efficacy model studies on encainide.

Encainide is a class IC agent possessing a broad spectrum of antiarrhythmic actions in a variety of animal models. It increases the ventricular fibrillation threshold of the perfused rabbit heart and in situ dog myocardium. Encainide suppresses atrial fibrillation resulting from topical application of aconitine in the anesthetized dog and ventricular fibrillation induced by chloroform asphyxiation in the mouse. In these latter 2 models, encainide is approximately 7 to 11 and 16 to 18 times more potent, respectively, on a milligram basis than quinidine. In anesthetized dogs encainide converts ouabain-induced tachyarrhythmias to normal sinus rhythm at a mean intravenous dose of 0.67 mg/kg. Single doses of 0.5 mg/kg intravenously or 1 mg/kg orally significantly reduced ventricular ectopy in conscious dogs 18 to 22 hours after 2-stage ligation of the left coronary artery. At doses and plasma concentrations exceeding efficacious therapeutic levels, encainide has no major negative inotropic effects and does not compromise cardiac function or hemodynamics. It is devoid of peripheral autonomic or mediator-evoked responses and, in particular, lacks anticholinergic actions. Encainide is rapidly absorbed by all routes of administration and extensively metabolized by the liver. The major metabolites, O-demethyl encainide and 3-methoxy-O-demethyl encainide, have been shown to have quantitatively different, but qualitatively similar, profiles of pharmacodynamic effects. Subacute and chronic administration of encainide at doses representing 11 times an effective oral human dose have produced no distinct or consistent toxicologic findings. Carcinogenicity and mutagenicity studies were negative.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1988

Efficacy and electrophysiologic effects of encainide for atrioventricular nodal reentrant tachycardia.

To prospectively determine the clinical efficacy and electrophysiologic effects of encainide in atrioventricular nodal reentrant tachycardia (AVNRT), 49 patients refractory to 2.7 +/- 1.5 previous antiarrhythmic drug trials underwent electrophysiologic study before and 47 did so after administration of oral encainide (75 to 240 mg/day). Encainide prolonged the minimum atrial pacing cycle length maintaining 1:1 atrioventricular (AV) nodal conduction from 334 +/- 55 to 391 +/- 55 ms (p = 0.0001). Encainide induced ventriculoatrial (VA) block in 12 patients (25%) and slowed the minimum ventricular pacing cycle length maintaining 1:1 VA conduction from 315 +/- 46 to 485 +/- 89 ms (p = 0.0001) in the remaining 35 patients. After encainide, AVNRT was not inducible in 32 of 47 patients (68%) primarily because of the effects on retrograde AV nodal conduction. In the remaining 15 (32%) patients, AVNRT remained inducible; however, the tachycardia cycle length slowed from 397 +/- 86 to 492 +/- 90 ms (p = 0.0001). There was no significant difference in the baseline minimum ventricular pacing cycle length maintaining 1:1 VA conduction in patients whose inducible tachycardia was or was not suppressed. Forty-seven patients were treated for 18.9 +/- 12.9 months (range 1 to 50) with oral encainide. Encainide was completely effective in eliminating recurrences of supraventricular tachycardia in 26 of 47 patients (55%) and partially effective in an additional 42%. Recurrences of arrhythmia occurred in 15 of 32 patients (47%) whose inducible tachycardia was suppressed by encainide and 7 of 15 patients (47%) whose inducible tachycardia was not suppressed by encainide (p = not significant).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Encainide for resistant supraventricular tachycardia in children: follow-up report.

Forty-one children (26 weeks gestational age to 20 years) with drug-resistant supraventricular tachycardia were treated with oral encainide, and 29 were followed for 3 to 34 months (mean 15). Diagnoses obtained by electrocardiographic criteria (23 patients) or electrophysiologic testing (18 patients) included permanent junctional reciprocating tachycardia in 15 children, paroxysmal atrioventricular reciprocating tachycardias (AVRT) in 13, atrial ectopic tachycardia in 4, atrial flutter in 1, chaotic atrial tachycardia in 5 and junctional ectopic tachycardia in 3. Encainide was completely effective in 54% (22 of 41 study patients) and partially effective in an additional 24% (10 of 41 patients), when combined with propranolol or verapamil. Within 1 month, 13 (32%) discontinued encainide for inefficacy or intolerance. Encainide was most effective in the treatment of permanent junctional reciprocating tachycardia (60% effective) and AVRT (69% effective). It controlled only 40% of primary atrial tachycardias. Encainide was well tolerated on a long-term basis in patients not experiencing symptoms during initiation. In study infants younger than age 6 months, encainide was associated with excessive QRS aberrancy during initiation in 4 of 13 (31%), compared with 3 of 28 (11%) in older children. Ventricular proarrhythmia occurred in 2 children and 1 died suddenly. Mean effective encainide dose was 3.5 mg/kg/day or 86 mg/m2/day. In 4 children who had nonextensive metabolism of encainide, the drug was ineffective. Encainide is effective in the treatment of some resistant forms of permanent junctional reciprocating tachycardia and AVRT in otherwise healthy children. Children younger than age 6 months and those with either previous proarrhythmic events or severe cardiac dysfunction appear to have a high incidence of adverse effects.

Administration, Oral↗
PubMed1988

Comparison of encainide and quinidine for supraventricular tachyarrhythmias.

The antiarrhythmic efficacy and tolerability of encainide and quinidine were compared in an open-design study in which 50 patients with recurrent supraventricular tachyarrhythmias received intravenous encainide in an initial phase and oral encainide and quinidine in a subsequent, randomized crossover phase. Oral encainide (75 to 200 mg/day), administered to 47 patients for an average of 4.7 months, was effective in 77%, and oral quinidine (1,200 mg/day), administered to 44 patients for an average of 3.2 months, was effective in 66% of the patients (difference not significant). When the duration of therapy at each crossover period was compared, the percentage of patients who continued to take encainide was consistently higher than the percentage who continued to take quinidine (p less than 0.01). Twenty-nine percent of the patients discontinued encainide treatment, 23% because of clinical inefficacy and 6% because of adverse effects. Fifty-nine percent of the patients discontinued quinidine treatment, 20% because of inefficacy and 39% because of adverse effects. Based on antiarrhythmic efficacy, encainide is at least as effective as quinidine in the treatment of patients with supraventricular tachyarrhythmias. However, because of encainide's much greater tolerability, it was distinctly superior in terms of clinical use. This study was an open-design, randomized crossover trial to compare the efficacy and tolerability of encainide with those of quinidine in the treatment of supraventricular tachyarrhythmias.

Administration, Oral↗