Efficacy Of Propafenone Research Articles

Efficacy of propafenone vs. amiodarone in pharmacological cardioversion of recent-onset atrial fibrillation to sinus rhythm: a pooled meta-analysis of 9 randomized controlled trials

Abstract Background Atrial fibrillation (AF) is the most common sustained cardiac dysrhythmia and is associated with substantial morbidity and mortality. It can be managed either through ventricular rate control or conversion to sinus rhythm while for the patients with recent onset of AF, the latter is the recommended choice of treatment. Purpose To determine crude rates and the likelihood of conversion to sinus rhythm from recent-onset AF and mean difference in time to do so with respect if pharmacological cardioversion with propafenone or amiodarone is utilized. Methods MEDLINE and EMBASE electronic databases were searched and after exclusion criteria were applied, a total of 94 potential studies were identified, while 9 randomized controlled trials (RCTs) were included in the meta-analysis. These RCTs were conducted from 1994 until 2019 and investigated the use of oral/intravenous propafenone vs. amiodarone to convert recent-onset AF to sinus rhythm. The main outcome measures were a) likelihood of sinus rhythm restoration and for this analysis, an odds ratio (OR) with 95% confidence interval (95% CI) was reported, and b) mean time to sinus rhythm conversion between two treatment groups and the outcome measure for this endpoint was a mean difference (MD, in minutes). In both instances, OpenMeta[Analyst] software was used to perform meta-analysis while random-effects model was used with a restricted maximum likelihood-REML correction factor. Heterogeneity between RCTs was examined by the I2 test. Results A total of 9 RCTs pooled 822 patients, 410 randomized to propafenone and 412 to amiodarone treatment. All trials reported conversion rates while 7 trials reported on the time needed to reach sinus rhythm. Of these, only trials measuring conversion time during 12 to 24 hours were considered. Seven trials monitored patients for conversion during the 24 hours, one trial up until 12 hours, and 1 trial up to 8 hours. In most trials, recent-onset AF was defined as lasting ≤48 hours, and most were designed to perform intravenous drug comparisons. On average, conversion to sinus rhythm was achieved in 76.1% cases treated with propafenone and 71.8% cases treated with amiodarone. Propafenone use was non-significantly associated with a higher likelihood of conversion to sinus rhythm compared to amiodarone (OR 1.26, 95% CI 0.825–1.912) and there was a low degree of heterogeneity observed between trials (I2=34.9%, P=0.139; Figure 1). On the other hand, treatment with propafenone was associated with a significantly shorter mean time to sinus rhythm conversion compared to amiodarone (MD −304 minutes, 95% CI −342 to −266) and there was no heterogeneity observed between included trials (I2=2.78%, P=0.440; Figure 2). Conclusion Propafenone and amiodarone are similarly efficacious in converting patients from recent-onset atrial fibrillation to sinus rhythm, however, propafenone acts significantly faster and cuts mean time to sinus rhythm for about 5 hours. Funding Acknowledgement Type of funding sources: None. Figure 1. Odds ratio for conversion to SRFigure 2. Mean difference in minutes to reach SR

ANTIARRHYTHMIC EFFICACY OF PROPAFENONE IN PATIENTS WITH PERSISTENT ATRIAL FIBRILLATION

Aim. To assess propafenone antiarrhythmic efficacy and optimal timing of the drug administration for relief of persistent atrial fibrillation (PAF). Material and methods. 24 patients (19 men, 5 women, aged 53,8±13,3) with PAF (duration is more than 7 days) were included in the study. PAF was confirmed clinically as well as by ECG and daily ECG monitoring. Indications for sinus rhythm recovery by propafenone were defined in according to the ACC/AHA/ESC recommendations (2006). 12-lead ECG was performed before the fist administration and 2, 4, 8, 12, 24 hours and some next days after propafenone therapy start. Echocardiography and thyroid hormone tests were also performed. Propafenone was administered additionally to standard treatment of the underlying disease and oral anticoagulants. The first dose of propafenone was 300 mg, after 4 hours patients received next dose of 300 mg if atrial fibrillation persisted and no side effects were observed, then doses of 300 mg were administered every 6-8 hours (but not more than 900-1200 mg per day) during 5 days. Maintenance propafenone dose of 450-600 mg daily was used in case of sinus rhythm recovery. Results. Sinus rhythm was restored in 41,6% of patients taking propafenone, and time of sinus rhythm recovery was 53,1±28,9 hours after therapy start. Propafenone antiarrhythmic efficacy in the loading dose (300 mg) was 4,2%. Propafenone efficacy during the first 24 hours (dose of 700±282,8 mg) was 12,5%. The maximum rate of sinus rhythm recovery was observed during the first 2-3 days of propafenone receiving (60% of all patients with rhythm recovery). Patients with unrecovered sinus rhythm had longer duration of PAF in comparison with this in effectively treated patients, 105,8±89,0 vs 39,7±38,9 days (p<0,05), respectively, as well as the more prominent basal pulse deficit, 24,6±15,0 vs 13,56±5,7 beats per minute (p<0,05), respectively. Cardiac and transient noncardiac side effects were registered in 8,6 and 4,3% of patients taking propafenone in dose of 900-1200 mg/day, respectively. Side effects did not require propafenone therapy cessation. Conclusion. Propafenone (900-1200 mg/day) antiarrhythmic efficacy in PAF was 41,6%. The probability of sinus rhythm recovery was maximal during the first 2-3 days. Ineffectively treated patients had longer duration of PAF last episode and more prominent basal pulse deficit in comparison with these in effectively treated patients. Transient side effects not requiring propafenone (900-1200 mg/day) withdrawal were observed in 12,6% of patients.

Propafenone for the Prevention of Atrial Tachyarrhythmias After Cardiac Surgery: A Randomized, Double-blind Placebo-controlled Trial

We studied the efficacy of propafenone in preventing atrial tachyarrhythmias after cardiac surgery, and the possible relationships between CYP2D6 polymorphism and the efficacy, pharmacokinetics, and tolerability of propafenone. One hundred and sixty patients were randomized (double blind) to receive propafenone (n= 78) or placebo (n= 82) for 1 week after cardiac surgery. The patients who were assigned to the propafenone group received 1 mg/kg infused in 1 h, followed by a continuous infusion at a rate of 4 mg/kg/24 h until the following morning, and subsequently 450 mg/day orally until the sixth postoperative day. Thirty-seven patients completed the trial in the propafenone group and 45 in the placebo group. The frequency of occurrence of atrial tachyarrhythmia was lower in the propafenone group than in the placebo group (29.7% vs. 53.3%, P< 0.05; relative risk, 0.56). Plasma propafenone concentrations were markedly influenced by CYP2D6 genotype-derived phenotype.

Efficacy of propafenone in paramyotonia congenita

Paramyotonia congenita (PC) is an autosomal dominant condition with high penetrance linked to SCN4A .1 It is characterized by myotonic stiffness that paradoxically worsens with repeated contractions and with exposure to cold and by episodes of spontaneous or cold-induced paralysis. Pharmacologic treatment of PC is directed toward reducing myotonia and preventing episodes of weakness.2 We tested the clinical and electrophysiologic responses of both myotonia and paralysis to propafenone hydrochloride (PH). PH was chosen as a single-drug treatment for both symptoms on theoretical grounds of its pharmacologic properties.3,4 We studied a 42-year-old man belonging to a large family with several affected members including his two sons. Since early childhood, he had been experiencing muscle stiffness and disabling episodes of paralysis. He had received mexiletine, 200 mg three times daily. A reduction in muscle stiffness was observed, but the appearance of nausea, vomiting, constipation, and confusion required discontinuation of the drug. Therefore, we decided to …

555 Efficacy of propafenone as single oral loading dose in pharmacology converting recent-onset atrial fibrillation and atrial flutter

555 Efficacy of propafenone as single oral loading dose in pharmacology converting recent-onset atrial fibrillation and atrial flutter

555 Efficacy of propafenone as single oral loading dose in pharmacology converting recent-onset atrial fibrillation and atrial flutter

555 Efficacy of propafenone as single oral loading dose in pharmacology converting recent-onset atrial fibrillation and atrial flutter

Efficacy of propafenone for maintaining sinus rhythm in patients with recent onset or persistent atrial fibrillation after conversion: a randomized, placebo-controlled study

Objective — The aim of this study was to investigate the efficacy and safety of propafenone in the prevention of atrial fibrillation (AF) relapse after restoration of sinus rhythm.Methods — This study consisted of 110 consecutive patients with recent onset and persistent AF. After restoration of sinus rhythm, patients were randomized to propafenone (n: 58, age: 60 ± 12 years) or placebo (n: 52, age: 62 ± 10 years).There were 11 withdrawals (7 in the propafenone and 4 in the placebo group) during follow-up. Follow-up evalutations were conducted at the first, 3rd and then at an interval of three months during 15 months. The clinical characteristics in both groups were comparable.The AF relapse was analysed by the Kaplan-Meier method.Results — At 15-month follow-up, AF relapsed in 20 (39%) and 31 (65%) patients in the propafenone and placebo groups, respectively (p = 0.015). In subgroup analysis, AF recurrence was significantly lower in the propafenone group than in the placebo group only in the recent onset AF patients with spontaneous conversion (21% vs. 61%, p = 0.01). However, the AF relapse rates were similar in patients with persistent AF and with recent AF who converted to sinus rhythm pharmacologically or electrically in the propafenone and placebo groups. Four patients on propafenone and one on placebo had adverse effects necessitating discontinuation of the drug (p = 0.36).Conclusion — At 15 months, propafenone seems to be superior to placebo for maintaining sinus rhythm in patients with recent onset or peristent AF. This superiority originates mainly from patients with recent onset AF in whom sinus rhythm occurred spontaneously. Its adverse effects are similar to placebo. (Acta Cardiol 2004; 59(3): 255-261)

P2750 Efficacy of propafenone for maintaining sinus rhythm in patients with recent onset or persistent atrial fibrillation after conversion: a randomized, placebo-controlled study

P2750 Efficacy of propafenone for maintaining sinus rhythm in patients with recent onset or persistent atrial fibrillation after conversion: a randomized, placebo-controlled study

Permanent pacing following repeat cardiac valve surgery

sient hypotension, and 2 had a significant QRS widening with induction of a transient complete left bundle branch block in I. Electrocardiographic QRS intervals measured immediately after conversion to sinus rhythm were unchanged compared with baseline for placebo, but for flecainide and propafenone a mean lengthening of 25% and 21% occurred, respectively. The efficacy of propafenone and flecainide in converting recent-onset AF to sinus rhythm has been studied, but no direct comparison between these 2 drugs administered as acute, oral loading doses in a placebocontrolled study has been previously reported. The present study confirms that acute oral antiarrhythmic drug loading is simple and effective. Because spontaneous conversion of AF to sinus rhythm may occur in 39% to 48% of patients within 8 hours,3 we believe a placebo group is essential to assess drug efficacy. The use of class 1C antiarrhythmic drugs like propafenone or flecainide carries the risk of inducing atria1 flutter with a fast ventricular response,5,6 and we observed this. However, spontaneous atria1 flutter with 22: 1 AV conduction ratio and a heart rate of 1150 beats/min occurs relatively often, even with placebo, especially during the time preceding conversion to sinus rhythm. The negative inotropic effect of class 1C drugs mandates that patients with heart failure or significant cardiac dysfunction are not treated with these agents. The negative chronotropic response (long pause at the time of conversion from AF to sinus rhythm) was observed with both drugs but was not associated with an adverse outcome.

Clinical experience with propafenone for cardiac arrhythmias in the young.

Seventy-two children were treated with propafenone between 1980 and 1990. The mean age was 34 months (range 0-192). Arrhythmias included atrioventricular re-entry tachycardia in 32 patients (44%), atrial flutter in 16 (22%), atrial or junctional ectopic tachycardia in 10 (14%), atrial re-entry tachycardias in three (4%) and ventricular arrhythmias in 11 patients (16%). The efficacy of oral treatment was good in patients with atrio-ventricular re-entry tachycardia (80%), atrial flutter (71%) and atrial ectopic tachycardia (83%); it was poor in ventricular arrhythmias (40%). The mean oral dose was 13.5 mg.kg-1. day-1. Dosage and serum levels of propafenone did not differ whether the patients were treated successfully or not. No correlation between dosage and serum level was observed. Intravenous propafenone administration was only partially successful in suppressing supraventricular tachycardias (6 of 11 patients). The presence of a congenital heart defect and the time of onset of the arrhythmias had a significant influence on the efficacy of propafenone. Better results were observed in patients with normal hearts and in whom onset of arrhythmia was pre-natal (success 80%) as well as in patients with arrhythmias seen early after surgery for congenital heart defects (success 87%). Success (65%) was also observed in patients without congenital heart defects and postnatal onset of supraventricular arrhythmias. Patients with ventricular or supraventricular arrhythmias late after corrective surgery showed the poorest response (31%).

Drug therapy of supraventricular tachyarrhythmias--based on efficacy or futility?

The clinical spectrum of supraventricular tachyarrhythmias ranges from infrequent, brief and well tolerated episodes of arrhythmia to attacks resulting in cardiovascular collapse. Many patients have such infrequent episodes that prophylactic or ablative therapy is not indicated. In those with more troublesome symptoms, an initial trial of medical therapy is common unless the arrhythmia has major prognostic or vocational importance. Thus despite the recent advances in catheter ablation techniques, there remains a place for antiarrhythmic drug therapy in supraventricular tachyarrhythmias. Furthermore, ablation therapy in atrial fibrillation is currently unable to control arrhythmias except by destruction of the normal conduction system. In contrast to the therapy goals in ventricular tachyarrhythmias, safety considerations far outweigh those of efficacy in the drug management of supraventricular tachycardias. Many patients with supraventricular tachyarrhythmias are young and have no serious underlying heart disease. Although symptomatic recurrences of arrhythmia are troublesome, these should be regarded as acceptable if the alternative is serious drug-related toxicity. There are relatively few well conducted clinical trials of the efficacy of drug therapy in supraventricular tachycardia. Existing study data and new trial information on the efficacy of propafenone are reviewed.

The use of propafenone in the treatment of tachyarrhythmias in children.

Propafenone was given to 60 children (mean age 4.5 years) with paroxysmal re-entrant supraventricular tachycardia (rSVT: 41 cases), postoperative automatic junctional tachycardia (JET: eight cases), automatic atrial tachycardia (AT:four cases), ventricular tachycardia (VT:four cases) and atrial flutter (AF: three cases). In acute cases (29) propafenone was administered intravenously (mean dose 1.3 +/- 0.5 mg.kg-1) chronic oral treatment (mean dose of either 11 +/- 3.3 mg.kg.day-1 or 265 +/- 78 mg.m-2 x day-1) was given to 48 children, in 2-3 divided doses. Overall efficacy was 76% for acute and 69% for chronic treatment, with best results in paroxysmal rSVT. It was effective in 89% acutely of those treated acutely and in 69% of those administered chronically. The efficacy of propafenone in the prevention of rSVT was strictly related to the incidence of attacks before treatment:propafenone was indeed inefficacious in 6/11, 6/14 and 0/12 of patients with daily, weekly and monthly attacks respectively. Side effects were observed in 25% of patients: 6% required suspension of therapy due to pro-arrhythmic effects in one patient on intravenous administration, peripheral neuropathy in one case and hypotension in two postoperative JET patients. In conclusion, its efficacy and limited side effects make propafenone a relatively safe and very useful drug in the treatment of various tachyarrhythmias. However, risk of unpredictable toxic levels requires careful use of the drug especially in the first days of treatment, when a daily monitoring of ECG is strongly recommended.

Efficacy and safety of propafenone in congenital junctional ectopic tachycardia

Objectives. Class 1C anliarrhythmic drugs have recently been shown to be effective in some patients with atrial ectopic tachycardia. We therefore studied the efficacy of these drugs in patients with congenital junctional ectopic tachycardia.Background. Follow-up data on patients with Junctional eclopic tachycardia suggest that this potentially lethal arrhythmia may cease spontaneously in a significant proportion af affected children. Therefore, temporary antiarrhythmic treatment appears to be the therapy of choice.Methods. The efficacy of propafenone was prospectively assessed in four infants with Junctional ectopic tachycardia (ventricular rate 180, 185, 210 and 320 beats/min, respectively). The diagnosis of Junctional ectopic tachycardia was established before the age of 2 months in all four infants. Propafenone was given orally in a mean dose of 350 (300 to 500) mg/m2body surface area per day. Success of therapy was determised by serial electrocardiograms (ECGs) and Holler ambulatory ECG monitoring.Results. In two patients, junctional ectopic tachycardia was completely suppressed. In the remaining two patients, the tachycardia rate decreased to < 150 beats/min. Serum propafenone levels did not correlate with efficacy of treatment. The mean duration of therapy was 18 months (range 3 to 36). No chemical or clinical side effects were noted.Conclusions. Because of its effectiveness, safety and lack of side effects, propafenone appears to be a valuable drug in the treatment of Junctional ectopic tachycardia in newborns and infants.

Acute and long-term efficacy of propafenone in patients with sustained ventricular tachyarrhythmias: assessment with programmed ventricular stimulation

To determine the electrophysiological properties of oral propafenone, 50 patients (39 male and 11 female, aged 31 to 80 years) with sustained ventricular tachycardia or ventricular fibrillation underwent serial electrophysiological drug testing, using propafenone (750 to 900 mg daily) as the anti-arrhythmic regimen of first choice. During baseline study, all patients had inducible sustained ventricular tachyarrhythmias. After oral loading of propafenone, 37 patients (74%) remained inducible whereas 13 were rendered non-inducible. Among the still inducible patients, the mean VT rate decreased from 223 +/- 38 b.min-1 (baseline) to 172 +/- 32 b.min +/- 1 (P less than 0.001). Four patients showed an increase of VT rate during propafenone compared to the VT rate at control. Non-inducible patients were discharged on propafenone. During a mean follow-up period of 20 +/- 15 months, there were three non-fatal VT recurrences among the responders, two of them due to non-compliance. Thus, propafenone used as the anti-arrhythmic agent of first choice among patients undergoing serial electrophysiological drug testing for ventricular tachyarrhythmias proved effective in suppressing VT induction in 26%. With regard to arrhythmic events, these patients have a favourable outcome.

Clinical Pharmacology and ??-Blocking Efficacy of Propafenone

Propafenone, like encainide and flecainide, is an antiarrhythmic drug characterized by slow kinetics of interaction with cardiac sodium channels. In addition, it shares structural similarities with propranolol and has been shown to exert consistent beta-blocking action in vitro. On the other hand, the extent of beta-blockade noted after oral administration of propafenone in vivo has been reported to range from undetectable to clinically significant. Although the explanation for this discrepancy was initially unclear, recent work has convincingly demonstrated that the degree of beta-blockade during propafenone therapy reflects genetically determined variations in the metabolism of the parent drug, which has greater beta-blocking potency than do its metabolites. At lower dosages, beta-blockade is significantly greater and more likely to be clinically noticeable in the small percentage of patients who have poor metabolism and in whom deficient 5-hydroxylation is associated with higher plasma propafenone concentrations. Because this metabolic pathway is saturable, at the usual highest clinical dosage (900 mg/24 h) plasma propafenone concentration rises disproportionately in patients with normal 5-hydroxylation, and more comparable degrees of beta-blockade are noted in both metabolizer types. Beta-blockade during propafenone therapy, which can contribute both to the genesis of side effects and to the suppression of arrhythmias, is a potentially important drug effect that can largely be predicted by genetic variations in the metabolism of the drug.

Efficacy of propafenone in preventing ventricular tachycardia: Inverse correlation with rate-related prolongation of conduction time

The efficacy of propafenone in preventing induction of ventricular tachycardia was evaluated in 25 consecutive patients (mean age 62 ± 8 years) with remote myocardial infarction who underwent programmed electrical stimulation for ventricular arrhythmia using up to three extrastimuli after basic drive at the right ventricular apex. In nine patients (Group A), propafenone prevented induction of sustained ventricular tachycardia (noninducible in four, nonsustained [<30 s] in five). In the other 16 patients (Group B), sustained ventricular tachycardia was still inducible; in 11 of the 16, the tachycardia configuration was unchanged but the cycle length was significantly longer (431 ± 99 versus 284 ± 44 ms, p < 0.001).Propafenone did not significantly affect either sinus cycle length or AH and HV intervals. However, it prolonged QRS duration during sinus rhythm equally in both groups of patients. With ventricular pacing, propafenone also prolonged right ventricular effective and functional refractory periods and surface QRS duration. There was greater lengthening of the paced surface QRS duration when drug therapy was ineffective (for example, +35 ± 12 ms in Group A versus +69 ± 23 ms in Group B at a basic drive of 400 ms, p < 0.01). Drag-induced prolongation of a paced QRS complex >40 ms had a 94% positive predictive value for drug failure to prevent induction of ventricular tachycardia. Drug-induced percent prolongation of ventricular tachycardia cycle length in Group B did not correlate well with percent QRS prolongation. Rather, the best correlation was with percent prolongation of right ventricular effective (r = 0.72, p < 0.02) and functional (r = 0.73, p < 0.02) refractory periods at a basic drive of 400 ms.These observations suggest that excessive prolongation of conduction time in presumably normal tissue reduces the ability of propafenone to prevent ventricular tachycardia induction. It is speculated that effects of a drug on conduction time in partially refractory abnormal tissue forming the reentrant circuit may play a role in determining the tachycardia cycle length in the presence of that drug.

Propafenone in Wolff-Parkinson-White syndrome at risk

We present our experience on the efficacy of propafenone in ten symptomatic patients with Wolff-Parkinson-White syndrome. The symptoms were dizziness in seven patients and syncope in three patients. While experiencing the symptoms, three of them presented an episode of atrial fibrillation, the shortest preexcited RR intervals being 140, 190, and 200 ms. In the other seven patients, the ECG was not recorded during the symptoms, but an episode of atrial fibrillation was subsequently induced by transesophageal pacing. The shortest preexcited RR intervals during induced atrial fibrillation were 180, 200, 270, 240, 230, 250, and 200 ms. Seven patients had both atrial fibrillation and supraventricular tachycardia. Propafenone (1-2 mg/kg) administered IV in only the patients with sustained atrial fibrillation (spontaneous in two and induced in one patient) prolonged the shortest preexcited RR intervals from 190, 200, and 180 ms to 340, 335, and 340 ms. In the other seven patients, propafenone was not given IV because atrial fibrillation rapidly deteriorated into ventricular fibrillation (one patient) or spontaneously reverted within 1-2 minutes to sinus rhythm (six patients). After oral propafenone, serial trans-esophageal pacing studies reinduced atrial fibrillation in 4 of 6 patients (the shortest preexcited RR intervals increased from 190, 180, 200, and 270 ms to 420, 320, 340, and 380 ms); only in one patient was it possible after propafenone to induce an atrial flutter without preexcitation. After propafenone therapy in 4 of 7 patients, supraventricular tachycardia was not inducible.(ABSTRACT TRUNCATED AT 250 WORDS)

Oral Propafenone Therapy for Patients with Paroxysmal Supraventricular Tachyarrhythmia

P ropafenone, a class IC antiarrhythmic drug with sodium-channel blocking properties along with weak calcium-channel and �3-blocking activity, has been shown to be effective for a variety of supraventricular and ventricular arrhythmias. ‘‘#{176} To assess its effect on paroxysmal supraventricular tachyarrhythmia, we evaluated 16 patients with paroxysmal atrial fibrillation (eight), atrioventncular (AV) nodal reentry (five), or intra-atrial tachycardia (three). There were seven men and nine women, aged 30 to 82 (mean 59) years, who had paroxysms of tachyarrhythmia for a mean of 8. 6 years and had not improved with a mean of 3.4 prior antiarrhythmic drugs. Propafenone was initiated at a dose of 150 mg every 8 h and therapy titrated upward at intervals of at least 48 h to efficacy, intolerable side effects, or a maximum of 1,050 mg/day. Four patients continued to receive �3blockers for hypertension, and two received digoxin therapy to control the ventricular response during the study. Baseline arrhythmia frequency was assessed by patient interview. The efficacy of propafenone was assessed by follow-up interview and 24-h ambulatory ECG monitoring. Successful oral therapy was defined as complete absence or a marked reduction of symptomatic arrhythmia compared with baseline measurements. Long-term oral therapy with propafenone was successful in treating five of eight (63 percent) patients with atrial fibrillation and four of eight (50 percent) patients with either AV nodal reentry or intra-atrial tachycardia as judged by history and follow-up 24-h

Efficacy of Propafenone When Used in Combination Antiarrhythmic Therapy

Propafenone is a new antiarrhythmic agent that has been classified as a type IC agent. Combination therapy using propafenone with either procainamide or quinidine was undertaken in this study. The addition of propafenone to procainamide or quinidine in 30 patients with more than 30 VPDs per hour resulted in a mean suppression of VPD frequency of 80%; 8 of 11 patients with runs of ventricular tachycardia had greater than 90% reduction of these events during combination therapy. During combination therapy, only two patients had proarrhythmic effects. Thus, this study demonstrates that combination of propafenone with either quinidine or procainamide is effective in suppressing ventricular arrhythmias.

Efficacy of propafenone in Wolff-Parkinson-White syndrome: Electrophysiologic findings and long-term follow-up

The efficacy and safety of intravenous propafenone was studied in 10 patients with Wolff-Parkinson-White syndrome and in 2 patients with a concealed accessory pathway. During electrophysiologic study, the effect of propafenone on the effective refractory period of the accessory pathway was determined, as well as its effect during orthodromic atrioventricular (AV) reentrant tachycardia and atrial fibrillation. Propafenone caused significant increases in the accessory pathway refractory period, both in the anterograde direction (290 +/- 19 versus 474 +/- 50 ms, p less than 0.05) and in the retrograde direction (238 +/- 15 versus 408 +/- 44 ms, p less than 0.05). Complete anterograde accessory pathway conduction block occurred in four patients. Sustained AV reentrant tachycardia was inducible in 11 patients before administration of propafenone. Drug infusion during AV reentrant tachycardia promptly terminated arrhythmia in 10 of these 11 patients and caused slowing of AV reentrant tachycardia in the remaining patient. Before propafenone, sustained atrial fibrillation was inducible in six patients and nonsustained atrial fibrillation in four patients. After propafenone, no patient had inducible sustained atrial fibrillation. Furthermore, propafenone caused a marked decrease in peak ventricular rate during atrial fibrillation. Eight patients have been treated with oral propafenone and followed up for 12 +/- 2 months. All have remained virtually free of recurrent arrhythmia and none has developed significant side effects. Propafenone is a very promising agent for emergency intravenous therapy as well as long-term oral therapy in patients with Wolff-Parkinson-White syndrome.