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At least 19 recordsLinked to original sources
PubMed1998

Comparison between propafenone and digoxin administered intravenously to patients with acute atrial fibrillation. PAFIT-3 Investigators. The Propafenone in Atrial Fibrillation Italian Trial.

In recent-onset atrial fibrillation, intravenous propafenone has been shown to effectively restore sinus rhythm, whereas the efficacy of intravenous digoxin has been questioned. We directly compared these 2 drugs and placebo in acute atrial fibrillation. One hundred twenty-three patients with atrial fibrillation lasting <72 hours were randomized to a 10-minute intravenous infusion of either propafenone (2 mg/kg, 41 patients) or digoxin (0.007 mg/kg, 40 patients) or placebo (42 patients). After 1 hour, nonconverted propafenone or digoxin patients were switched to the alternative drug, while nonconverted placebo patients were randomized to either propafenone or digoxin. The observation time ended 1 hour later. By 1 hour, conversion rates were 49% in the propafenone group, 32% in the digoxin group (p = 0.12), and 14% in placebo group (p <0.001 vs propafenone, p = 0.08 vs digoxin). After crossover, digoxin converted 5% of propafenone patients, while propafenone converted 48% of digoxin patients (p <0.05). In the 36 nonconverted placebo patients, sinus rhythm was obtained in 53% of cases with propafenone, and in 5% with digoxin (p < 0.05). Globally, among the 116 patients who received a drug as first treatment, 30 of 60 patients (50%) were converted by propafenone versus 14 of 56 (25%) by digoxin (p <0.01) (odds ratio 2.0, 95% confidence interval 1.19 to 3.36). In nonconverters, the ventricular rate reduction was faster (15 vs 45 minutes) and more prominent (-24% vs -14%) with propafenone than with digoxin. In conclusion, intravenous propafenone terminates atrial fibrillation more effectively than either placebo or intravenous digoxin. In addition, in nonconverted patients, it obtains a more rapid and marked control of the ventricular rate.

Acute Disease↗
PubMed1985

Electrophysiological effects of propafenone in untreated and propafenone-pretreated guinea-pig atrial and ventricular muscle fibres.

The electrophysiological effects of propafenone (10(-7) to 10(-4) M) were studied on guinea-pig isolated atrial and ventricular muscle fibres obtained from untreated animals and animals pretreated with propafenone, 3 and 10 mg kg-1, for 28 days. In untreated atria propafenone produced a dose-dependent decrease in the rate and maximum following frequency, prolonged the sinus node recovery time and reduced the maximum chronotropic responses to isoprenaline. In untreated atrial and ventricular muscle fibres propafenone depressed action potential amplitude and Vmax, reduced the resting membrane potential and prolonged the action potential duration (APD) and the effective refractory period, lengthening the effective refractory period relative to APD. Propafenone depressed the amplitude and Vmax and shortened the duration of the slow action potentials induced by isoprenaline and caffeine in K-depolarized papillary muscles. Pretreatment with propafenone reduced atrial rate, but did not modify the action potential characteristics compared to the values obtained in untreated atria. Further addition of propafenone produced similar but more marked changes in untreated atria. In ventricular muscle fibres pretreated with 3 mg kg-1, action potential characteristics before and after further addition of propafenone were similar to those obtained in untreated fibres. However, muscles pretreated with 10 mg kg-1 exhibited a significant prolongation of the APD compared to that in untreated muscles or those pretreated with 3 mg kg-1; further addition of propafenone shortened the APD even when this parameter was of similar value to those observed in the other two series of experiments. It is concluded that even though the effects of propafenone are similar to those of quinidine (class I antiarrhythmic), it also exhibited class II and class IV actions. In pretreated animals a prolongation of the APD (class III action) could also be involved in the antiarrhythmic effects of the drug.

Animals↗
PubMed1997

Propafenone for conversion and prophylaxis of atrial fibrillation. Propafenone Atrial Fibrillation Trial Investigators.

Pharmacologic therapy is widely used for restoration of sinus rhythm and prevention of recurrences of atrial fibrillation. Because concerns have been raised about their potential proarrhythmic effects, therapeutic regimens should be evaluated by placebo-controlled studies to determine their efficacy and safety. One hundred thirty-six patients with persistent atrial fibrillation were randomized to receive propafenone 2 mg/kg over 30 minutes, followed by oral propafenone 150 mg 3 times daily or matching placebo. Nonresponders to intravenous therapy underwent direct-current cardioversion. Both responders to intravenous therapy and converters to sinus rhythm after direct-current cardioversion were followed for 6 months in a double-blind oral treatment period of propafenone 150 mg 3 times daily or matching placebo. Pharmacologic conversion to sinus rhythm was achieved in 29% of the patients taking propafenone and in 17% of patients taking placebo (p > or = 0.10). Subsequent direct-current cardioversion in nonresponders was equally successful (70%) in both groups (p > or = 0.10). The proportion of patients free from recurrent symptomatic arrhythmia at 6 months was 67% for the propafenone and 35% for the placebo group (p < 0.01). Time to atrial fibrillation relapse was more favorable with propafenone than with placebo (p < 0.001). The incidence of drug-related side effects was 10% in the propafenone group and 14% in the placebo group. Thus, "slow" infusion of propafenone seems to be of limited value for terminating atrial fibrillation. Oral propafenone at a low dosage 150 mg 3 times daily is well tolerated and effective in maintaining sinus rhythm for 6 months after pharmacologic or electrical restoration of sinus rhythm.

Administration, Oral↗
PubMed1995

Safety of flecainide versus propafenone for the long-term management of symptomatic paroxysmal supraventricular tachyarrhythmias. Report from the Flecainide and Propafenone Italian Study (FAPIS) Group.

In order to compare the long-term safety of flecainide and propafenone, an open label, randomized, parallel group study was performed in 335 patients with paroxysmal atrial fibrillation (n = 200) or paroxysmal supraventricular tachycardia (n = 135), and no history of heart disease. Patients were treated with an initial daily dose of flecainide 100 mg (n = 72) or propafenone 450 mg (n = 63) for paroxysmal supraventricular tachycardia and flecainide 200 mg (n = 97) or propafenone 450 mg (n = 103) for paroxysmal atrial fibrillation. Dose escalations were permitted after > or = 2 attacks, up to a maximum of flecainide 300 mg or propafenone 900 mg.day-1.Follow-up duration was 12 months, or when patients stopped the treatment as a result of inadequate efficacy or adverse experiences. Twelve patients on flecainide reported 16 cardiac adverse experiences, of whom six discontinued the treatment. Seven propafenone patients had eight cardiac adverse experiences, of whom five discontinued the treatment. Serious proarrhythmic events were infrequent: one case of ventricular tachycardia on propafenone: two cases of atrial fibrillation with rapid ventricular response on flecainide, associated in one patient with pulmonary oedema. An intention-to-treat analysis showed that the probability of 12 months' safe and effective treatment of paroxysmal supraventricular tachycardia was 93% for flecainide and 86% for propafenone (P = 0.24), whereas in paroxysmal atrial fibrillation it was 77% for flecainide and 75% for propafenone (P = 0.72). In conclusion, flecainide and propafenone were safe in the long-term treatment of patients with paroxysmal supraventricular tachyarrhythmias and without evidence of clinically significant heart disease.

Adolescent↗
PubMed1986

[Digoxin-propafenone interaction: values and limitations of plasma determination of the 2 drugs. Anti-arrhythmia effectiveness of propafenone].

Propafenon's influence on the pharmacokinetic and actions of digitalis and viceversa have been evaluated in 27 patients (25 with ventricular hyperkinetic arrhythmias and 2 with paroxismal atrial fibrillation). Patients were divided in two groups according to whether the drug firstly administered were digoxin or propafenon. Plasmatic digoxin and/or propafenon's concentrations, these last performed only in 12 patients, were determined before and during the association and after propafenon's interruption at 7.55-9-11 and at 3-8 p.m. During drug's association area under the plasmatic digoxin concentration curve (AUC 12h) increased on the average by 13.8% (from 19.27 +/- 6.002 ng hours/ml to 21.94 +/- 6.198 ng hours/ml: P less than 0.05) and by 19% at the first hour. Neverthless individual behaviour was not homogeneous since the plasmatic digoxin concentration (PDC) increased in 22 cases (81.4%) and decreased in 5 (18.6%). In 6 patients mean increase was 38.8% (from 16.72 +/- 3.0 ng hours/ml to 23.21 +/- 5.44 ng hours/ml) without signs of digoxin intoxication. Another patient with congestive heart failure and basal PDC 1.87 ng/ml experienced digoxin poisoning with fatal ventricular fibrillation after propafenon. Digoxin administration in the second group's patients produced a not significant increase of plasmatic propafenon concentration (PPC). There was a good correlation among propafenon's absolute amount and plasmatic concentration and antiarrhythmic effect and no correlation among PPC and body-weight related dose. Propafenon's to digitalis association induced, in propafenon's steady state, significant P-R longation from 170 to 190 ms (P less than 0.01) but HR, QRS and QTc didn't show any important change (P greater than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

A randomized, placebo-controlled trial of propafenone in the prophylaxis of paroxysmal supraventricular tachycardia and paroxysmal atrial fibrillation. UK Propafenone PSVT Study Group.

BACKGROUND: Few antiarrhythmic agents have been shown in randomized controlled trials to be effective and well tolerated in the prophylaxis of paroxysmal supraventricular tachycardia or paroxysmal atrial fibrillation. Propafenone, a class IC anti-arrhythmic agent with weak beta-adrenoceptor antagonist properties, has shown promise in preliminary clinical studies. METHODS AND RESULTS: A double-blind, placebo-controlled trial of the efficacy and tolerability of propafenone was undertaken in 100 patients with paroxysmal supraventricular tachycardia ([PSVT] n = 52) or atrial fibrillation/flutter ([PAF] n = 48) who had recorded two or more symptomatic arrhythmia recurrences by transtelephonic ECG monitoring during a 3-month drug-free observation period. Patients were randomized into two consecutive crossover periods of propafenone (300 mg BID) versus placebo followed by 300 mg TID propafenone versus placebo. Analysis was based on the time to treatment failure, defined as the interval from treatment onset to the occurrence of either ECG-documented arrhythmia or an intolerable adverse event. With a proportional-hazards model, we determined the relative risk (95% confidence interval) of treatment failure after the achievement of steady-state drug levels for placebo compared with propafenone 300 mg BID to be 6.8 (2.2 to 21.2, P < .001, n = 45) for PSVT and 6.0 (1.8 to 20.0, P = .004, n = 30) for PAF. Due to a greater incidence of adverse events on high-dose propafenone, the relative risks of receiving placebo rather than propafenone 300 TID were only 2.2 (0.9 to 5.3, P = .1, n = 34) for PSVT and 1.9 (0.7 to 4.7, P = .2, n = 25) for PAF. However, if adverse events were excluded in the high-dose comparison, relative risks for arrhythmia recurrence were 15.0 (2.0 to 113, P = .009) for PSVT and incalculable (no preferences for placebo, P = .0002) for PAF. One episode of wide-complex tachycardia was documented during propafenone therapy. CONCLUSIONS: Propafenone is of value in the prophylaxis of both PSVT and PAF. A dose of 300 mg BID is effective and well tolerated. A larger dose of 300 mg TID causes more adverse effects but may be more effective in those who can tolerate it.

Adolescent↗
PubMed2003

Efficacy and safety of sustained-release propafenone (propafenone SR) for patients with atrial fibrillation.

The objective of this randomized, double-blind, placebo-controlled clinical trial was to test the efficacy and safety of a new sustained-release preparation of the antiarrhythmic drug propafenone (propafenone SR) in reducing the frequency of symptomatic arrhythmia recurrences in patients with atrial fibrillation (AF). Patients with a history of symptomatic AF who were in sinus rhythm were randomly assigned to receive placebo or propafenone SR 425, 325, or 225 mg, all twice daily. Recurrent symptomatic arrhythmias were documented using transtelephone electrocardiographic monitoring. Electrocardiograms were reviewed by an event committee that was blinded to treatment assignment. In the primary efficacy analysis, propafenone SR significantly lengthened the time to first symptomatic atrial arrhythmia recurrence at all 3 doses compared with placebo as assessed by log-rank test: propafenone SR 425 mg twice daily versus placebo twice daily, p <0.001; 325 mg twice daily versus placebo twice daily, p <0.001; and 225 mg twice daily versus placebo twice daily, p = 0.014. The median time to recurrence was 41 days in the placebo twice daily group, >300 days in the propafenone SR 425-mg group, 291 days in the 325-mg group, and 112 days in the 225-mg group. Adverse effects leading to withdrawal were higher in the propafenone SR 425-mg twice daily group than in any other group. Thus, propafenone SR has important and statistically significant antiarrhythmic effects in patients with AF.

Adult↗
PubMed1996

Safety of long-term flecainide and propafenone in the management of patients with symptomatic paroxysmal atrial fibrillation: report from the Flecainide and Propafenone Italian Study Investigators.

To compare the relative safety of flecainide acetate to propafenone HCl during long-term treatment (12 months), we conducted a randomized, open-label, comparative, parallel, multicenter trial in 200 patients with paroxysmal atrial fibrillation (AF) and no history of heart disease. Initial daily doses were flecainide 200 mg (n = 97) or propafenone 450 mg (n = 103). Dose escalations up to a maximum of flecainide 300 mg/day or propafenone 900 mg/day were permitted after > or = 2 attacks of paroxysmal AF. Patients were assessed for safety and drug tolerance at designated intervals over the 12-month study unless discontinued for adverse experience or inadequate response. Ten patients on flecainide reported 14 cardiac adverse experiences; 4 discontinued the drug. Seven propafenone patients reported 8 cardiac adverse experiences; 5 discontinued the drug. Three proarrhythmic events occurred: 1 propafenone patient developed ventricular tachycardia and 2 flecainide patients experienced AF with a rapid ventricular response. An intention-to-treat analysis showed that the probability of safe and effective treatment after 12 months was 77% for flecainide-treated patients and 75% for the propafenone-treated patients. There was an acceptable risk-benefit profile in patients with paroxysmal AF and no evidence of clinically significant heart disease who were treated with flecainide or propafenone for 12 months. Further, there was no statistically significant difference in safety or efficacy between flecainide and propafenone in this study.

Adolescent↗
PubMed1989

Pharmacokinetic and pharmacodynamic evaluation of propafenone in patients with ventricular arrhythmia. Propafenone Research Group.

Propafenone, a class IC antiarrhythmic agent, is metabolized into two active metabolites: 5-hydroxypropafenone (5-OHP) and N-depropylpropafenone (NDPP). In a placebo-controlled, double-blind study, we examined trough plasma concentrations of propafenone and its two metabolites in 169 subjects. Patients were randomized to one of five parallel treatment groups: placebo and 337.5, 450, 675, or 900 mg/day propafenone with 24-hour ambulatory ECG monitorings, 12-lead ECGs, and plasma samples obtained at frequent intervals. Nonlinear kinetics were noted for propafenone and NDPP but not for 5-OHP. The ratio of NDPP to propafenone was about 10% at all doses, but the ratio of 5-OHP to propafenone decreased from 33% at 337.5 mg/day to 18% at 900 mg/day. Propafenone suppression of ventricular ectopy was dependent on concentration, with pairs and VT beats selectively suppressed at lower concentrations than VPBs. The PR interval and QRS duration increased significantly at propafenone concentrations above 100 ng/ml, while minimal heart rate slowing was noted at concentrations above 1,000 ng/ml.

Adult↗
PubMed1996

Effects of oral propafenone on defibrillation and pacing thresholds in patients receiving implantable cardioverter-defibrillators. Propafenone Defibrillation Threshold Investigators.

OBJECTIVES: The effects of propafenone, a predominantly class IC antiarrhythmic drug, on defibrillation and pacing thresholds were evaluated in patients undergoing cardioverter-defibrillator implantation. BACKGROUND: Previous studies have shown that the class IC agents encainide and flecainide may increase the energy requirements for pacing and defibrillation. Animal studies with propafenone have shown inconsistent results regarding its effect on defibrillation energy requirements. This report investigated the effects of propafenone on defibrillation and pacing thresholds in humans. METHODS: After cardioverter-defibrillator implantation, 47 patients were enrolled in a double-blind, three-way parallel, randomized trial of 450 mg/day (Group 1) or 675 mg/day (Group 2) of oral propafenone or placebo (Group 3) for 3 to 7 days. Predischarge defibrillation and pacing thresholds after treatment were compared with baseline thresholds obtained at implantation. RESULTS: There was no statistically significant difference between implantation and predischarge defibrillation thresholds in the three groups (Group 1: [mean +/- SE] 11.0 +/- 1.3 vs. 12.1 +/- 1.5 J; Group 2: 11.5 +/- 1.1 vs. 13.6 +/- 1.3 J; Group 3: 12.5 +/- 1.2 vs. 13.3 +/- 1.6 J), and no significant difference between treatment groups was found with a 0.86 power to detect a 5-J difference between groups. Paired pulse width pacing thresholds at 2.8 V were compared in 14 patients. A small increase of 0.02 ms was noted at predischarge testing in patients treated with propafenone and placebo. CONCLUSIONS: Short-term oral propafenone (450 and 675 mg/day) does not significantly affect defibrillation or pacing thresholds. Concomitant use of propafenone in patients with implantable cardioverter-defibrillators with recurrent ventricular or atrial tachyarrhythmias should not interfere with proper device function.

Administration, Oral↗
PubMed1998

Effects of propafenone and 5-hydroxy-propafenone on hKv1.5 channels.

1. The goal of this study was to analyse the effects of propafenone and its major metabolite, 5-hydroxy-propafenone, on a human cardiac K+ channel (hKv1.5) stably expressed in Ltk- cells and using the whole-cell configuration of the patch-clamp technique. 2. Propafenone and 5-hydroxy-propafenone inhibited in a concentration-dependent manner the hKv1.5 current with K(D) values of 4.4+/-0.3 microM and 9.2+/-1.6 microM, respectively. 3. Block induced by both drugs was voltage-dependent consistent with a value of electrical distance (referenced to the cytoplasmic side) of 0.17+/-0.55 (n=10) and 0.16+/-0.81 (n=16). 4. The apparent association (k) and dissociation (l) rate constants for propafenone were (8.9+/-0.9) x 10(6) M(-1) s(-1) and 39.5+/-4.2 s(-1), respectively. For 5-hydroxy-propafenone these values averaged (2.3+/-0.3) x 10(6) M(-1) s(-1) and 21.4+/-3.1 s(-1), respectively. 5. Both drugs reduced the tail current amplitude recorded at -40 mV after 250 ms depolarizing pulses to +60 mV, and slowed the deactivation time course resulting in a 'crossover' phenomenon when the tail currents recorded under control conditions and in the presence of each drug were superimposed. 6. Both compounds induced a small but statistically significant use-dependent block when trains of depolarizations at frequencies between 0.5 and 3 Hz were applied. 7. These results indicate that propafenone and its metabolite block hKv1.5 channels in a concentration-, voltage-, time- and use-dependent manner and the concentrations needed to observe these effects are in the therapeutical range.

Adrenergic beta-Antagonists↗
PubMed1990

Minimal effective concentration values of propafenone and 5-hydroxy-propafenone in acute and chronic therapy.

We evaluated the antiarrhythmic efficacy and the minimal effective concentrations of propafenone and its metabolite 5-hydroxy-propafenone during a) acute intravenous infusion (1.5 mg/kg in bolus followed by 45 minutes infusion), b) an acute oral single-dose test (450 mg), and c) 14-day chronic therapy (300 mg tid) followed by a washout. Oxidative metabolism was assessed by a debrisoquine oral test in every patient. Eleven patients with stable ventricular premature beats (VPBs) greater than or equal to 300/hr and Lown class greater than or equal to 3 completed the study. The main results emphasized a certain discrepancy between the clinical effect of the acute intravenous infusion (efficacy in 5 out of 11 patients) and of the acute oral test and chronic therapy (efficacy in 11/11), with a time lag of the ECG changes during the acute intravenous infusion. The minimal effective concentrations were lower after acute oral administration compared with chronic treatment both for propafenone (200 +/- 189 ng/ml vs. 492 +/- 530 ng/ml; p less than 0.05) and for 5-hydroxy-propafenone (82 +/- 40 ng/ml vs. 149 +/- 80 ng/ml; p less than 0.02). A linear correlation was demonstrated between drug/metabolite ratios of propafenone and debrisoquine, either after acute oral (r = 0.91) or after chronic administration (r = 0.84). The pharmacokinetics of propafenone was nonlinear and showed wide interindividual variations.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1996

Safety and tolerability of long-term propafenone therapy for supraventricular tachyarrhythmias. The Propafenone Multicenter Study Group.

An important issue regarding the long-term use of antiarrhythmic drugs concerns the safety of these agents, particularly with regard to cardiac toxicity. Propafenone is an effective drug for preventing supraventricular tachyarrhythmia, but the incidence of side effects during longterm therapy in patients with such arrhythmias has not been adequately reported. A total of 480 patients received oral propafenone as therapy for symptomatic atrial fibrillation, atrial flutter, or supraventricular tachycardia. During the follow-up (mean 14.4 months), 290 patients (60%) discontinued propafenone therapy, but in only 70 patients (15%) was the reason for discontinuation an adverse drug reaction. Overall, 284 patients (59%) experienced at least 1 adverse reaction, and the incidence was related to dose and age >65 years. The overall incidence of side effects was not related to structural heart disease; however, cardiovascular toxicity including arrhythmia aggravation, congestive heart failure, and serious conduction disturbances occurred more often in those with heart disease (20% vs 13%). Sixteen patients died during drug therapy, but in only 1 case was the drug considered contributory. For patients with a supraventricular arrhythmia, propafenone was well tolerated and was infrequently discontinued because of side effects. The incidence of serious cardiac toxicity when propafenone was used to treat supraventricular arrhythmia was low, and these side effects were more frequent in patients with structural heart disease.

Administration, Oral↗
PubMed1994

Rapid determination of CYP2D6 phenotype during propafenone therapy by analysing urinary excretion of propafenone glucuronides.

Metabolism of the antiarrhythmic, propafenone, cosegregates with the sparteine/debrisoquine polymorphism. Patients devoid of CYP2D6 activity have a higher incidence of adverse effects than those with normal enzyme function. In this paper we present a method for rapid assignment of CYP2D6 phenotype using urinary excretion of intact glucuronides of propafenone (PPFG). After establishing an HPLC assay, urinary excretion of PPFG was quantified during one dosage interval and related to individual CYP2D6 activity as determined by phenotyping. We observed a close correlation of urinary excretion of PPFG with individual CYP2D6 activity (r = 0.84, P < 0.01) and conclude that this method is suitable for rapid assignment of phenotype during propafenone therapy.

Aged↗
PubMed1989

Comparative electrophysiological effects of propafenone, 5-hydroxy-propafenone, and N-depropylpropafenone on guinea pig ventricular muscle fibers.

Propafenone (Pf) is a class I antiarrhythmic drug that can be given both orally and intravenously. In order to examine whether its two major metabolites [5-hydroxypropafenone (5-OH-Pf) and N-depropylpropafenone (N-DP-Pf)] possess pharmacodynamical properties, we compared their electrophysiological effects to those of the parent drug on papillary muscle fibers from guinea pig ventricular myocardium. After baseline action potential and refractory period characteristics were measured at different pacing rates, the tissue preparations were superfused with either Pf, 5-OH-Pf, or N-DP-Pf at five different concentrations and electrophysiological characteristics were studied again. The maximal rate of depolarization (Vmax) was depressed by the three compounds only at the highest concentration, although the effect of N-DP-Pf was slightly less than the other two. Refractory periods were altered only by the highest concentration of 5-OH-Pf. Propafenone and N-DP-Pf exhibited equally slow on-set/off-set kinetics of the sodium channel block, whereas those of 5-OH-Pf were twice as long, which seems to suggest a slower rate of dissociation of the latter from the inactivated sodium channels. Thus, 5-OH-Pf and N-DP-Pf comply with the definition of the class IC antiarrhythmic drugs. The cumulative in vivo effects of the two metabolites and of the parent drug could have far reaching clinical implications, especially in the genetically predisposed extensive metabolizing subject.

Action Potentials↗
PubMed2001

The influence of CYP2D6 polymorphism on the antiarrhythmic efficacy of propafenone in patients with paroxysmal atrial fibrillation during 3 months propafenone prophylactic treatment.

OBJECTIVE: Propafenone (PPF) is an antiarrhythmic, Class Ic agent. Its metabolism is genetically controlled by a cytochrome P450 isoenzyme named CYP2D6, which shows polymorphism in human population. The aim of this paper was to determine the correlation between the antiarrhythmic efficacy of PPF and the oxidation phenotype. SUBJECTS AND MATERIAL: The study group consisted of 42 patients, aged 36 to 75 years, suffering from paroxysmal atrial fibrillation (AF). The oxidation phenotype was described by the metabolic ratio (MR) of sparteine. The MR value separated the group of poor metabolizers (MR > 20) from the group of extensive metabolizers (MR < 20) with the subgroup of very extensive metabolizers (MR < 1). METHOD: The study was conducted during a 3-month PPF therapy for the prophylaxis of paroxysmal atrial fibrillation. PPF was given orally, 300-450 mg/day. The oxidation phenotype was checked prior to the administration of PPF. Serum concentration of PPF at 7, 11 days and the end of PPF therapy were determined. Statistical analysis of data was performed with the chi2 test and the Pearson's correlation methods. RESULTS: In the group of 42 patients, PPF therapy was 100% effective in poor metabolizers (PM). In extensive metabolizers (EM), 61% efficacy was observed with efficacy 0% in very extensive metabolizers (VEM). The correlation between oxidation phenotype and the ability to maintain sinus rhythm (SR) was statistically significant (r = 0.414, p < 0.05). CONCLUSIONS: The antiarrhythmic efficacy of propafenone depends on the oxidation phenotype; 100% efficacy occurred in the group of poor metabolizers whereas PPF, at the dose tested, was ineffective in very extensive metabolizers.

Administration, Oral↗