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PubMed1993

Efficacy and safety of combination therapy with amiodarone and type I agents for treatment of inducible ventricular tachycardia.

In a prospective study the efficacy of amiodarone in combination with the three Class I drugs mexiletine, flecainide, or encainide was evaluated consecutively in 12 patients with recurrent ventricular tachycardias (VT) by programmed stimulation. None of the tested drug combinations suppressed induction of sustained VT. The combination of amiodarone with Class IC drugs flecainide and encainide prolonged the cycle length of VT significantly, whereas the combination with mexiletine did not have the same degree of slowing on the VT cycle length. Several proarrhythmic effects occurred during the combination therapy with encainide: (1) frequent, spontaneous recurrences of hemodynamically well tolerated VT in four patients; (2) enhanced inducibility of VT in three patients; (3) impaired termination of VT in three patients. Though a marked increase in QRS and QTc intervals was observed by combined treatment with encainide, no significant correlation could be established between aggravation of arrhythmia and plasma levels of encainide, degree of QRS widening, JT or QTc prolongation. The only predictor for the occurrence of proarrhythmic events was found in left ventricular ejection fraction. These findings suggest that in patients refractory to amiodarone alone or a combination with mexiletine, the combined treatment of amiodarone with other Class IC drugs prolongs the VT cycle length but does not suppress induction of VT during programmed stimulation. Combination therapy of amiodarone with encainide was associated with a high incidence of proarrhythmic effects.

Adult↗
PubMed1995

Time to arrhythmic, ischemic, and heart failure events: exploratory analyses to elucidate mechanisms of adverse drug effects in the Cardiac Arrhythmia Suppression Trial.

In this study we investigated the time to the first arrhythmic, ischemic, or failure event for encainide-flecainide and moricizine versus their respective placebo comparison groups in the Cardiac Arrhythmia Suppression Trial. The purpose was to explore possible mechanisms for the excessive deaths associated with active therapy that have been previously reported. Differences were noted between the active drugs. In particular, encainide-flecainide appeared to convert an ischemic event into death in more cases and more promptly than moricizine. However, the excessive deaths noted on encainide-flecainide were as likely to occur subsequent to a failure event as an ischemic event; for both encainide-flecainide and moricizine, the vast majority of excess deaths appeared to be the result of an increase in arrhythmia events without any protective effect of the drug. We were unable to identify any specific mechanism to explain the adverse effect of encainide and flecainide.

Anti-Arrhythmia Agents↗
PubMed1982

Antiarrhythmic drug combinations in the treatment of ventricular tachycardia.

Combinations of antiarrhythmic drugs are frequently used to treat refractory ventricular tachycardia (VT), but few scientific data support this practice. We examined the efficacy and electrophysiology of 110 antiarrhythmic drug combination trials at electrophysiologic study in 74 patients with recurrent ventricular tachycardia. Lidocaine was combined with quinidine in 33 trials, procainamide in 22 and encainide in 20. Propranolol was combined with quinidine in 17 trials, procainamide in 12 and encainide in six. All individual drugs tested (except propranolol, which was usually not tested individually) had failed at electrophysiologic study or clinically in the presence of usually accepted plasma concentrations. Lidocaine in combination with quinidine was effective in 3% of the trials, with procanamide in 5% and with encainide in none of the trials. Propranolol in combination with quinidine was effective in 18% of the trials, with procainamide in 17% and with encainide in none of the trials. The electrophysiologic effects of the tested drug combinations were dominated by the individual effects of the type 1 antiarrhythmic agents. We conclude that the tested antiarrhythmic drug combinations are infrequently effective in preventing VT induction at electrophysiologic study when each agent has failed individually. The addition of lidocaine or propranolol to quinidine, procainamide or encainide does not produce significant synergistic or new effects on the electrophysiologic variables analyzed.

Aged↗
PubMed1990

The Cardiac Arrhythmia Suppression Trial: background, interim results and implications.

The Cardiac Arrhythmia Suppression Trial (CAST) was designed to test the hypothesis that suppression of ventricular premature complexes (VPCs) in survivors of acute myocardial infarction would reduce arrhythmic death risk. Instead, a preliminary finding from the CAST was that the encainide and flecainide groups had a 3.6-fold increase in arrhythmic death compared with their placebo group. These unfortunate results were especially surprising in that the CAST population represented patients in whom the risk of arrhythmic death was only moderate and the risk of proarrhythmia was thought to be low. In contrast, the arrhythmic death rate of the CAST placebo group was unusually low, to the extent that it paralleled the arrhythmic death rate in previous clinical trials of patients surviving myocardial infarction with no ventricular arrhythmia. The excessive arrhythmic death rate in patients taking encainide and flecainide occurred over the duration of the CAST, implying a proarrhythmic effect that may be due to mechanisms that are unique in this population, and thus challenging traditional concepts of proarrhythmia. The existing knowledge regarding the proarrhythmic and negative inotropic effects of encainide and flecainide are reviewed. The previous pharmaceutical database experience with these 2 antiarrhythmic drugs exceeded 3,000 patients; however, there was no indication of this serious proarrhythmic effect. In contrast, the CAST population taking encainide and flecainide totaled only 725 patients who were followed for 10 months and had an extremely high proarrhythmic event rate. The reasons for this discrepancy are discussed. The results of the CAST emphasize the power of a randomized, placebo-controlled clinical trial to uncover previously unsuspected benefits or liabilities of traditional therapies.

Anilides↗
PubMed1999

Safety of antiarrhythmics during pregnancy: case report and review of the literature.

A young woman is reported with intractable sustained ventricular tachycardia thought to originate in the right ventricle, which was treated successfully with encainide after failure to respond to beta-blockers and several class IA antiarrhythmic agents. She became pregnant twice while on encainide and gave birth to two healthy children. This is the first report of pregnancy during treatment with encainide. A literature review showed no other reported case of encainide taken during pregnancy, but several reports of the safe use of flecainide, a similar class IC drug, during pregnancy. Other antiarrhythmics are also reviewed.

Adolescent↗
PubMed1991

Significance of classifying antiarrhythmic actions since the cardiac arrhythmia suppression trial.

The Cardiac Antiarrhythmic Suppression Trial (CAST) showed flecainide and encainide induced excess mortality compared with placebo. Labeling drugs as Class 1C is based on clinical observations, comprising measurements of the electrocardiographic parameters QRS. H-V and J-T intervals and of effective refractory period (ERP) as follows: 1--(QRS) wide, 2--(HV) long, 3--(ERP) unchanged, 4--(JT) unchanged. In vitro electrophysiology helped to explain the clinical findings. Flecainide and encainide rendered Na channels as nonconducting, but F and E were only slowly released from the channels after repolarization. At any given drug concentration, a proportion of total channels were eliminated, and the steady-state proportion increased at rising heart rate. It is not proven that the properties that lead to classification of a drug as 1C were those that caused excess deaths in the CAST. The proarrhythmic tendency of 1C drugs can be reduced by beta-blockade, and the mechanisms of adrenergic arrhythmogenicity are discussed. Propafenone is both a 1C drug and a beta-blocker, and its pharmacologic profile is reviewed to illustrate how it resembles and differs from flecainide and encainide. Some features of the CAST are assessed with particular reference to the extent to which conclusions drawn from the results may be justifiably extrapolated to other drugs classified as 1C.

Anilides↗
PubMed1991

Events in the cardiac arrhythmia suppression trial: baseline predictors of mortality in placebo-treated patients.

Patients randomized to placebo in the encainide and flecainide arms of the Cardiac Arrhythmia Suppression Trial (CAST) have been found to have a relatively low 1-year mortality rate of 3.9% in comparison with previous studies of patients in the postmyocardial infarction period. To determine the comparability of CAST with previous studies, baseline variables were examined in the 743 patients randomized to placebo in the flecainide and encainide arms of CAST. Twenty-three baseline characteristics were correlated with major outcome events: arrhythmic death (16 events), total mortality (26 events) and congestive heart failure (51 events). On multivariate analysis the risk of new or worsening congestive heart failure was significantly associated with diuretic use, diabetes, high New York Heart Association functional class, age, prolonged QRS duration and low ejection fraction. The risk of arrhythmic death or resuscitated cardiac arrest was significantly associated with an index Q wave myocardial infarction, history of heart failure, use of digitalis, diabetes and prolonged QRS duration. Total mortality or resuscitated cardiac arrest was significantly associated with an index Q wave myocardial infarction, diabetes, ST segment depression, high functional class, prolonged QRS duration and low ejection fraction. The variables at baseline associated with mortality from all causes or arrhythmic death or resuscitated cardiac arrest and heart failure in the CAST placebo-treated patients are similar to those identified in previous postmyocardial infarction studies. Thus, the observation of increased mortality in CAST associated with the administration of encainide and flecainide for suppression of ventricular premature depolarizations is probably applicable to any comparably defined group of patients in the postmyocardial infarction period.

Aged↗
PubMed1991

Events in the Cardiac Arrhythmia Suppression Trial (CAST): mortality in the entire population enrolled.

To test the hypothesis that suppression of ventricular arrhythmias by antiarrhythmic drugs after myocardial infarction improves survival, the Cardiac Arrhythmia Suppression Trial (CAST) was initiated. Suppression was evaluated before randomization during an open label titration period. Patients whose arrhythmias were suppressed were randomized in the main study and those whose arrhythmias were partially suppressed were randomized in a substudy. Overall survival and survival free of arrhythmic death or cardiac arrest were lower [corrected] in patients treated with encainide or flecainide than in patients treated with placebo. However, the death rate in patients randomized to placebo therapy was lower than expected. This report describes the survival experience of all patients enrolled in CAST and compares it with mortality in other studies of patients with ventricular arrhythmias after myocardial infarction. As of April 18, 1989, 2,371 patients had enrolled in CAST and entered prerandomization, open label titration: 1,913 (81%) were randomized to double-blind, placebo-controlled therapy (1,775 patients whose arrhythmias were suppressed and 138 patients whose arrhythmias were partially suppressed during open label titration); and 458 patients (19%) were not randomized because they were still in titration, had died during titration or had withdrawn. Including all patients who enrolled in CAST, the actuarial (Kaplan-Meier) estimate of 1-year mortality was 10.3%. To estimate the "natural" mortality rate of patients enrolled in CAST, an analysis was done that adjusted for deaths that might be attributable to encainide or flecainide treatment either during prerandomization, open label drug titration or after randomization. Because the censoring procedure excluded patients treated with encainide or flecainide after randomization, the mortality estimate will be less than the unadjusted mortality estimate of 10.3%.(ABSTRACT TRUNCATED AT 250 WORDS)

Anilides↗
PubMed1991

A prospective comparison of class IA, B, and C antiarrhythmic agents in combination with amiodarone in patients with inducible, sustained ventricular tachycardia.

BACKGROUND: Clinical experience suggests that combinations of antiarrhythmic agents provide more effective control of ventricular tachyarrhythmias than does therapy with single agents. METHODS AND RESULTS: Antiarrhythmic and electrophysiological effects of three class I antiarrhythmic agents, one from each subclass A, B, and C, were assessed in single use and in combination with amiodarone in patients with inducible, sustained ventricular tachycardia that was not suppressed by monotherapy with these agents. Thirty-one patients underwent an electrophysiology test on four occasions: at baseline; after 2-4 days of treatment with quinidine, mexiletine, or encainide; after 2 weeks of treatment with 1,200 mg/day amiodarone; and last, after 2-4 days of treatment with both amiodarone and the previously tested class I agent. The combination of a class I agent and amiodarone prevented the induction of sustained ventricular tachycardia in only one of 31 (3%) patients. Ventricular tachycardia became hemodynamically stable in 11 of 31 (34%) patients because of a marked prolongation in the tachycardia cycle length. It increased from 323 +/- 39 to 423 +/- 84 msec (n = 11, p less than 0.01) by adding encainide to amiodarone therapy, and it showed a tendency to lengthen when quinidine was added to amiodarone (from 373 +/- 77 to 425 +/- 58 msec; n = 10, NS). Each class I agent increased amiodarone-induced depression in myocardial conduction, but the extent of the additional depression seemed to differ among the three subclasses. Ventricular refractoriness was increased by all class I agents when used in combination with amiodarone, although not by mexiletine or encainide when used alone. CONCLUSIONS: Class I antiarrhythmic agents slow ventricular conduction and increase ventricular refractoriness when used in combination with amiodarone. When amiodarone and class I drugs by themselves do not suppress the induction of ventricular tachycardia, the combination of amiodarone and a class I agent seldom results in noninducibility; however, it often lengthens the ventricular tachycardia cycle length and may render the ventricular tachycardia hemodynamically stable.

Amiodarone↗
PubMed1987

Antiarrhythmic agents for chronic ventricular arrhythmias.

A vast array of new antiarrhythmic agents have joined the old agents among the clinician's available resources. While treatment of ventricular arrhythmias is completely justifiable for patients with symptoms, their use to prevent sudden cardiac death has not yet been established. Because of their potential risks, the benefit/risk ratio must always be kept in mind. If we elect to treat patients who have benign or potentially lethal ventricular arrhythmias (usually to eliminate refractory symptoms) we typically begin with either a beta blocker or one of the new potent class IC antiarrhythmic agents such as flecainide or encainide. These drugs cause few side effects, no organ toxicity, and in the case of encainide or flecainide, have marked potency. Few important proarrhythmic effects are seen with these potent drugs in this group of patients. If these fail, one can try either a class IA or IB agent or a combination of a IA and IB agent. We always avoid amiodarone. In patients with lethal ventricular arrhythmias, one should choose a drug without negative inotropic potential such as quinidine or encainide as initial therapy. The combination of IA and IB agents should also be considered early in therapy. In patients with overt congestive heart failure with markedly depressed left ventricular function in the setting of lethal arrhythmias, disopyramide, beta blockers, and flecainide should be avoided. Amiodarone is used in this population only when the other available agents have proven to be ineffective or badly tolerated.

Amiodarone↗
PubMed1987

Assessment of drug effects on spontaneous and induced ventricular arrhythmias in a 24-h canine infarction model.

The antiarrhythmic efficacy of encainide, sotalol, flecainide and disopyramide was evaluated in anesthetized dogs subjected to 2-stage total occlusion of the left anterior descending coronary artery. Utilization of this canine model, while anesthetized, permitted the assessment of drug effects not only on uni- and/or multi-focal ectopic ventricular arrhythmias, but also on dysrhythmias associated with aberrant conduction or reentrant excitation pathways. The former was assessed by quantification of ectopic-to-total beat ratios while the later was determined by subjecting the animal to provocative stimuli which produced repetitive ventricular responses. At the cumulative i.v. doses studied, encainide (0.5-4 mg/kg), flecainide (1-8 mg/kg) and disopyramide (0.3-10 mg/kg), but not sotalol (2-8 mg/kg), effectively suppressed ventricular ectopic activity in a dose-related manner. In contrast, sotalol was highly effective in preventing the induction of reentrant ventricular tachyarrhythmias. Disopyramide was only modestly active, while flecainide and encainide had the least favorable profiles of effect in suppressing re-entry arrhythmias in this model. Based on these observations, the anesthetized Harris dog appears to represent a useful two-faceted in vivo model for use in the evaluation of potential antiarrhythmic agents.

Anilides↗
PubMed1995

Acute intravenous conversion of canine atrial flutter: comparison of antiarrhythmic agents.

We studied the acute intravenous (i.v.) effects of the antiarrhythmic agents ibutilide, sematilide, lidocaine, and encainide in a canine Y-shaped right atrial incision model of atrial flutter. After baseline determination of atrial effective refractory period (AERP), sustained atrial flutter (AFL) was initiated by atrial pacing in 25 dogs. Each dog then received placebo, followed by sequential doses of a particular agent every 5 min until AFL was terminated or the highest dose was administered. Ibutilide increased AFL cycle length (CL: 26 +/- 6 ms) before termination of AFL in 8 of 8 dogs in 1 min after the effective dose (6 +/- 1 micrograms/kg). AERP determined immediately after termination of AFL was significantly increased (44 +/- 7 ms). AFL could not be reinitiated after termination with ibutilide. Sematilide increased AFL CL 12 +/- 6 ms, significantly increased AERP 25 +/- 6 ms, and terminated AFL in 4 of 8 dogs (0.6 +/- 0.2 mg/kg). After sematilide or pacing-induced termination, AFL was reinducible in only 1 dog. Lidocaine terminated AFL in 2 of 5 dogs (2.0 +/- 0.5 mg/kg). AERP was unchanged in both animals, and AFL CL increased by 37 +/- 3 ms. AFL was reinducible in all 5 lidocaine-treated dogs after AFL was terminated. Encainide terminated AFL in 3 of 4 dogs after a dose of 3.0 +/- 0.0 mg/kg. AERP was significantly increased 77 +/- 10 ms, and AFL CL was markedly increased by 226 +/- 11 ms. AFL could not be reinitiated after termination of AFL by encainide.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2002

Impact of stereoselectivity on the pharmacokinetics and pharmacodynamics of antiarrhythmic drugs.

Many antiarrhythmic drugs introduced into the market during the past three decades have a chiral centre in their structure and are marketed as racemates. Most of these agents, including disopyramide, encainide, flecainide, mexiletine, propafenone and tocainide, belong to class I antiarrhythmics, whereas verapamil is a class IV antiarrhythmic agent. Except for encainide and flecainide, there is substantial stereoselectivity in one or more of the pharmacological actions of chiral antiarrhythmics, with the activity of enantiomers differing by as much as 100-fold or more for some of these drugs. The absorption of chiral antiarrhythmics appears to be nonstereoselective. However, their distribution, metabolism and renal excretion usually favour one enantiomer versus the other. In terms of distribution, plasma protein binding is stereoselective for most of these drugs, resulting in up to two-fold differences between the enantiomers in their unbound fractions in plasma and volume of distribution. For disopyramide, stereoselective plasma protein binding is further complicated by nonlinearity in the binding at therapeutic concentrations. Hepatic metabolism plays a significant role in the elimination of these antiarrhythmics, accounting for >90% of the elimination of mexiletine, propafenone and verapamil. Additionally, in most cases, significant stereoselectivity is observed in different pathways of metabolism of these drugs. For some drugs, such as propafenone and verapamil, the stereoselectivity in metabolism is further complicated by nonlinearity in one or more of the metabolic pathways. Further, the metabolism of a number of chiral antiarrhythmics, such as mexiletine, propafenone, encainide and flecainide, cosegregates with debrisoquine/sparteine hydroxylation phenotype. Therefore, it is not surprising that a wide interindividual variability exists in the metabolism of these drugs. Excretion of the unchanged enantiomers in urine is an important pathway for the elimination of disopyramide, flecainide and tocainide. The renal clearances of both disopyramide and flecainide exceed the filtration rate for these drugs, suggesting the involvement of active tubular secretion. However, the stereoselectivity in the renal clearance of these drugs, if any, is minimal. Similarly, there is no stereoselectivity in the renal clearance of tocainide, a drug that undergoes tubular reabsorption in addition to glomerular filtration. Overall, substantial stereoselectivity has been observed in both the pharmacokinetics and pharmacodynamics of chiral antiarrhythmic agents. Because the effects of these drugs are related to their plasma concentrations, this information is of special clinical relevance.

Absorption↗
PubMed1990

Lack of effect of hypertonic sodium bicarbonate on QRS duration in patients taking therapeutic doses of class IC antiarrhythmic drugs.

Hypertonic sodium bicarbonate (HSB) has been reported to reduce the toxicity of Class IC antiarrhythmic agents in rats and, anecdotally, in patients. A pilot study was conducted of the safety and efficacy of HSB for reversing the electrocardiographic effects of therapeutic doses of encainide or flecainide in ten patients taking these drugs for chronic ventricular arrhythmias. Patients had a mean drug-induced QRS prolongation before treatment of 27.6 +/- 8.8%. Each patient received a single dose of HSB 100 mEq or normal saline IV over 5 minutes on two separate occasions. The administration of treatments was blinded and balanced. There were no important side effects of HSB. Venous blood pH, CO2 content and sodium concentration were all significantly increased by HSB in comparison to saline. No differences were found during the 2-hour observation period in the primary endpoint, QRS duration, the PR or QT intervals, or the frequency of premature ventricular beats. It was concluded that HSB 100 mEq does not reduce QRS duration in patients taking therapeutic doses of flecainide or encainide. Because HSB was well tolerated, investigation of its use in higher doses or in patients with overt toxicity due to Class IC drugs is feasible.

Aged↗
PubMed1990

Recasting the approach to the treatment of potentially malignant ventricular arrhythmias after the CAST study.

The best therapeutic approach to the therapy of potentially malignant ventricular arrhythmias is still unknown, particularly in view of the increased mortality with flecainide and encainide shown in the CAST study. Various ongoing studies, particularly with amiodarone, will show whether better results can be obtained with other agents. Flecainide and encainide do, however, have a restricted place when other agents cannot be used. Low-dose amiodarone with low-dose flecainide may be worth trying.

Anilides↗
PubMed1982

Drug conversion of nonsustained ventricular tachycardia to sustained ventricular tachycardia during serial electrophysiologic studies: identification of drugs that exacerbate tachycardia and potential mechanisms.

Eleven of 83 patients who had ventricular tachycardia (VT) and underwent serial electrophysiologic study (EPS) had a more severe VT induced while receiving a particular antiarrhythmic drug as compared to control study. For all patients only nonsustained VT was initiated during control study, while sustained VT occurred during drug testing with disopyramide (2 patients), quinidine (2 patients), amiodarone (4 patients), and encainide (7 patients), although spontaneous arrhythmias appeared well-controlled prior to repeat testing. Pacing techniques used to induce sustained VT were the same as those used in the control study in eight patients and "less aggressive" in three patients. Almost all episodes of sustained VT resulted in substantial hypotension, especially in patients who were taking encainide. Drugs associated with sustained VT increased the median tachycardia cycle length by 112 msec (p less than 0.005) but increased the median ventricular effective refractory period by only 30 msec (p less than 0.02). Assuming re-entry was responsible for VT, we postulate that drugs facilitated initiation of sustained VT by prolonging activation time but only minimally increasing refractoriness of the tachycardia circuit.

Adult↗
PubMed1988

Efficacy and safety of class IC antiarrhythmic agents for the treatment of coexisting supraventricular and ventricular tachycardia.

Thirty-three patients with concurrent supraventricular (SVT) and ventricular tachycardia (VT) were treated with class IC antiarrhythmic agents. Twenty-two patients had atrial fibrillation (17 with paroxysmal and 5 with chronic fibrillation), 1 patient had ectopic atrial tachycardia and 11 patients had reentrant paroxysmal SVT (8 with atrioventricular node reentrant tachycardia, 3 with atrioventricular reentrant tachycardia). Of 5 patients with Wolff-Parkinson-White syndrome, 2 had only atrial fibrillation. Six patients had sustained VT and 27 had nonsustained VT. Twenty-nine patients had organic heart disease (16 with coronary artery disease, 8 with cardiomyopathy and 5 with valvular heart disease) and 4 had primary electrical disease. The mean ejection fraction was 40 +/- 14% (range 15 to 66%). The study population's arrhythmias were not controlled despite having received 2 to 5 (mean 3.1) previous drug trials. Eighteen patients were referred for treatment of SVT and 15 were referred for treatment of VT (mean symptom duration 107 months). Efficacy was determined in 13 of 33 patients with sustained SVT or VT by programmed electrical stimulation and in 20 of 33 by telemetry and 24-hour Holter response. Twenty-two flecainide and 15 encainide trials were conducted in the 33 patients. Four patients underwent trials with both drugs. Of 33 patients with coexisting SVT and VT, 15 (45%) were controlled with an IC agent alone and 3 continued therapy with an IC agent plus additional therapy (2 drugs, 1 antitachycardia pacing). During the follow-up period (mean 10.4 months), flecainide produced a complete response in 9 patients and encainide in 9 patients. SVT was not controlled in 7 patients and VT was not controlled in 7 patients. One patient had neither arrhythmia controlled. Atrial or ventricular proarrhythmia was seen in 9 of 33 patients (27%) (5 with ventricular and 4 with atrial arrhythmia). Noncardiac side effects were uncommon. Oral class IC agents may be effective therapy for some patients with coexisting VT and SVT of different mechanisms. Patients with such complex arrhythmias should be evaluated carefully because there is a potential for both atrial and ventricular proarrhythmia.

Anilides↗
PubMed1990

Comparisons of efficacy and tolerance of moricizine with other antiarrhythmic agents in the treatment of chronic ventricular arrhythmias.

Comparative trials of a new drug with standard antiarrhythmic agents are important for establishing relative efficacy and tolerance. For moricizine, such trials have included comparisons with propranolol, disopyramide and quinidine. Furthermore, the Cardiac Arrhythmia Pilot Study compared moricizine in postinfarction patients with encainide and flecainide. These trials show moricizine to be superior in efficacy to a beta blocker (propranolol) and disopyramide and equivalent to quinidine. Although the class IC drugs (encainide and flecainide) showed somewhat greater efficacy in the Cardiac Arrhythmic Pilot Study, they are now known to increase the risk of mortality in postinfarction patients. Moricizine was also shown to be well tolerated in these trials and associated with fewer discontinuations than propranolol, disopyramide and quinidine. Thus, moricizine is a promising new agent when profiled against other drugs frequently used for therapy of chronic ventricular arrhythmias.

Anilides↗