Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Propafenone”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 163 records · Page 9Linked to original sources
PubMed1992

Rate-dependent failure of ventricular capture in patients treated with oral propafenone.

The effects of propafenone on ventricular excitability were studied in 18 patients after 9 +/- 6 days on oral propafenone (900 mg/day). Late diastolic double threshold right ventricular stimulation was performed at variable rates. In five patients (28%, group I) an intermittent, rate-dependent failure of ventricular capture was reproducibly observed during stimulation at rates above the sinus rhythm but not exceeding 150 beats min-1. In four patients loss of capture was preceded by gradual prolongation of the interval between the stimulus artifact and the local right ventricular bipolar electrogram. Such findings were not observed in the remaining 13 patients (group II) on propafenone nor in 28 studies in the same patients on different antiarrhythmic agents. Group I vs group II patients were older (72 +/- 4 vs 53 +/- 18 years, P = 0.002), had longer right ventricular effective refractory periods on the baseline (P = 0.004) and on propafenone (P = 0.0003), and had longer QRS duration on propafenone. The increase produced by propafenone in sinus rhythm QRS duration, paced QRS duration and ventricular effective refractory period was greater in group I than in group II: 42 +/- 36 vs 14 +/- 12 ms, P = 0.01, 94 +/- 43 vs 34 +/- 26 ms, P = 0.0002, 88 +/- 64 vs 22 +/- 37 ms, P = 0.025, respectively. Thus propafenone can produce rate-dependent failure of ventricular capture which is associated with marked prolongation of refractoriness and QRS duration suggesting a marked use-dependent drug effect in selected patients.

Administration, Oral↗
PubMed1989

Electrophysiologic interactions between mexiletine and propafenone in guinea pig papillary muscles.

The effects of propafenone alone, mexiletine alone, and their combination at the sodium channel level were studied in isolated guinea pig papillary muscles. The maximum upstroke velocity (Vmax) was used as an indirect index of the magnitude of the sodium inward current. In muscles driven at 0.02 Hz, neither mexiletine (10(-5) M) nor propafenone (5 X 10(-6) M) had any effect on action potential characteristics, but their combination decreased Vmax. In the presence of mexiletine and propafenone, trains of stimuli at 1 Hz led to a use-dependent block (onset rate 0.11 +/- 0.008 and 0.19 +/- 0.02 per action potential, respectively). The combination of mexiletine plus propafenone increased the onset rate of the use-dependent Vmax block (0.32 +/- 0.04 per action potential), but did not modify the time-constant of recovery of Vmax block or the magnitude of the slow component of reactivation induced by propafenone. Moreover, the combination of both drugs was more effective in suppressing early test stimuli than either drug alone. We conclude that the combination of mexiletine and propafenone is a synergistic one that affects only the onset kinetics of use-dependent Vmax block without detracting from the characteristics of the propafenone.

Action Potentials↗
PubMed1994

New classification of moricizine and propafenone based on electrophysiologic and electrocardiographic data from isolated rabbit heart.

Because the classification of propafenone and moricizine is not clear, we measured in 20 specifically equipped isolated rabbit hearts QRS duration, QT interval, action potential duration at 90% of repolarization (APD90), effective refractory period (ERP), conduction time (CT), and rise velocity (Rv) of the monophasic action potentials (AP) during exposure to moricizine and propafenone in comparison with procainamide. Propafenone and procainamide prolonged APD90 and JT. All drugs increased ERP. Propafenone demonstrated marked tonic sodium channel block. Onset of use-dependent kinetics (tau on), defined as change in Rv as fraction per beat at 300 ms cycle length (CL), were 0.047 +/- 0.004/beat for procainamide, 0.050 +/- 0.004/beat for propafenone, and 0.022 +/- 0.003/beat for miricizine. Recovery kinetics, defined as recovery of Rv after cessation of pacing, had a time constant of 5.3 +/- 0.7 s for procainamide, 6.3 +/- 0.8 s for propafenone, and 25.0 +/- 1.3 s for moricizine. Based on these data, moricizine must be classified as a Ic agent, whereas propafenone demonstrates pronounced tonic sodium channel block, in addition to its phasic block, which is similar to class Ia kinetics.

Action Potentials↗
PubMed1988

Propafenone versus disopyramide for treatment of chronic symptomatic ventricular arrhythmias. A multicenter study.

The efficacy and safety of propafenone, 150 mg four times daily, were compared with those of disopyramide, 100 mg four times daily, in a randomized single-blind, cross-over study in 38 patients with symptomatic premature ventricular complexes (PVCs). The 24-hour ambulatory ECG, employed for assessing antiarrhythmic efficacy, was analyzed blindly. The median reduction in the number of PVCs was higher with propafenone than with disopyramide (91.4% vs. 63.5%, respectively, p less than 0.01). A reduction of at least 80% was achieved by propafenone in 22 (59%) and by disopyramide in 16 patients (43%) (NS). Ventricular tachycardias (VTs) were abolished by propafenone in eight out of 11, and by disopyramide in five out of nine patients with VTs (NS) a possible proarrhythmic effect was seen in three patients during disopyramide and in one patient during propafenone treatment. Micturition disturbances (p less than 0.001) and a dry mouth (p less than 0.01) were more commonly associated with disopyramide than with propafenone. In conclusion, in the given dosages, propafenone was superior to disopyramide in suppressing PVCs and had fewer side-effects.

Adult↗
PubMed1989

Genetically-determined interaction between propafenone and low dose quinidine: role of active metabolites in modulating net drug effect.

1. Quinidine is a potent inhibitor of the genetically-determined debrisoquine 4-hydroxylation. Oxidation reactions of several other drugs, including the 5-hydroxylation of the new antiarrhythmic drug propafenone, depend on the isozyme responsible for debrisoquine 4-hydroxylation. 2. The effect of quinidine on the debrisoquine phenotype-dependent 5-hydroxylation and the pharmacological activity of propafenone was studied in seven 'extensive' metabolizers and two 'poor' metabolizers of the drug receiving propafenone for the treatment of ventricular arrhythmias. 3. In patients with the extensive metabolizer phenotype, quinidine increased mean steady-state plasma propafenone concentrations more than two fold, from 408 +/- 351 (mean +/- s.d.) to 1096 +/- 644 ng ml-1 (P less than 0.001), decreased 5-hydroxypropafenone concentrations from 242 +/- 196 to 125 +/- 97 ng ml-1 (P less than 0.02) and reduced propafenone oral clearance by 58 +/- 23%. 4. Despite these changes in plasma concentrations, electrocardiographic intervals and arrhythmia frequency were unaltered by quinidine coadministration, indicating that 5-hydroxypropafenone contributes to the pharmacologic effects of propafenone therapy in extensive metabolizers. 5. In contrasts, plasma concentrations of propafenone and 5-hydroxypropafenone remained unchanged in the two patients with the poor metabolizer phenotype. 6. Biotransformation of substrates for the debrisoquine pathway can be markedly perturbed by even low doses of quinidine; interindividual variability in drug interactions may have a genetic component.

Adult↗
PubMed1989

Effects of propafenone on electrical and mechanical activities of single ventricular myocytes isolated from guinea-pig hearts.

1. The effects of propafenone on the transmembrane action potential and sarcomere shortening during twitch contraction were investigated in single ventricular myocytes isolated from guinea-pig hearts. 2. Propafenone at low concentrations (3-5 x 10(-7) M) slightly lengthened action potential duration (APD), but shortened it at higher concentrations. The shortening of APD was accompanied by an attenuation of sarcomere shortening during twitch contraction. 3. Propafenone (greater than 10(-6) M) caused a concentration-dependent decrease in the maximum upstroke velocity (Vmax) of the action potential. In the presence of propafenone (3 x 10(-6) M), trains of stimuli led to an exponential decline in Vmax. A time constant for the recovery of Vmax from the use-dependent block was 4.8 s. 4. In myocytes treated with propafenone (3 x 10(-6) M), the Vmax of test action potentials preceded by the conditioning clamp pulses to 0 mV was progressively decreased by increasing the duration of single clamp pulse or by increasing the number of multiple brief clamp pulses. 5. These findings suggest that propafenone has use-dependent inhibitory action on the sodium channel by binding to the channel during both activated and inactivated states, and that the unbinding rate is comparable to that of Class-I antiarrhythmic drugs with intermediate kinetics. Propafenone may also have an inhibitory action on calcium and potassium channels.

Action Potentials↗
PubMed1991

Effects of propafenone on 45Ca movements and contractile responses in vascular smooth muscle.

1. In rat isolated aorta the class Ic antiarrhythmic drug, propafenone, dose-dependently inhibited the contractile responses induced by high K (80 mM) and noradrenaline (NA, 10(-5) M), the IC50s being 2.5 +/- 0.7 x 10(-6) M and 8.7 +/- 0.8 x 10(-6) M, respectively. These inhibitory actions were also observed with propafenone added after the induced contractions. 2. Contractile responses induced by addition of Ca to 0 Ca high-K solution were also inhibited by propafenone (IC50 = 2.5 +/- 0.8 x 10(-6) M). Moreover, propafenone inhibited the contractile responses elicited by NA in strips incubated in 0 Ca (IC50 = 1.9 +/- 0.9 x 10(-6) M). 3. Propafenone also inhibited (IC50 = 1.2 +/- 0.4 x 10(-5) M) the development of spontaneous mechanical activity in portal vein segments. 4. Propafenone, 5 x 10(-6) M and 10(-5) M, inhibited 45Ca uptake stimulated by high K or NA without altering 45Ca uptake in resting strips. 5. These results indicated that in rat isolated aortae and portal veins propafenone inhibited Ca entry through voltage-operated channels and NA-induced Ca uptake as well as Ca release from intracellular stores. As a consequence it would reduce the concentration of intracellular free Ca available at the contractile apparatus for vascular smooth muscle contraction.

Animals↗
PubMed1991

The effects of the stereoisomers of propafenone and diprafenone in guinea-pig heart.

1. Optically pure enantiomers of propafenone and diprafenone were prepared from their racemic mixtures and tested for their ability to block beta-adrenoceptors and to prolong functional refractory period in the guinea-pig heart. beta-Adrenoceptor affinity of the enantiomers was determined by the radioligand binding technique and in functional experiments. 2. Propafenone and diprafenone inhibited specific binding of the beta-adrenoceptor antagonist (-)-[3H]-CGP-12177 to guinea-pig myocardial membranes. beta-Adrenoceptor affinities of diprafenone enantiomers exceeded those of corresponding propafenone enantiomers by one order of magnitude. Displacement of (-)-[3H]-CGP-12177 by both antiarrhythmics was highly stereoselective, in that the (S)-enantiomers were 40-60 fold, i.e. 1.6-1.8 log units more potent than the (R)-enantiomers. 3. Propafenone and diprafenone antagonized the positive inotropic action of isoprenaline in isolated atria. beta-Adrenoceptor antagonist potencies of diprafenone enantiomers were about one order of magnitude higher than those of corresponding propafenone enantiomers. For both drugs the (S)-enantiomer was found to be considerably more potent (14-40 fold) than the (R)-enantiomer. 4. Propafenone and diprafenone prolonged functional refractory period of isolated auricles with equal potency and no difference in the antiarrhythmic activity of purified enantiomers was found. 5. It is concluded that the enantiomers of propafenone and diprafenone exert comparable antiarrhythmic activity, whereas only (S)-enantiomers block cardiac beta-adrenoceptors with high affinity, which explains the beta-adrenoceptor antagonist effects of the racemic drugs.

Adrenergic beta-Antagonists↗
PubMed1993

Effects of propafenone on calcium current in guinea-pig ventricular myocytes.

1. The modulation of L-type voltage-sensitive calcium channels in guinea-pig isolated ventricular myocytes by propafenone was examined by the whole cell voltage-clamp technique. 2. Propafenone, 10(-7) -5 x 10(-5) M, produced a concentration-dependent inhibition of Ca current (ICa) without any significant change in the current-voltage relation. Half-blocking concentration (IC50) of propafenone for the peak ICa at +10 mV was 5 x 10(-6) M. 3. The voltage-dependence of ICa inactivation was shifted in the hyperpolarizing direction in the presence of 5 x 10(-6) M propafenone. 4. A frequency-dependent relative block by propafenone was observed after repetitive depolarizing test pulses at a frequency of 0.5 and 1 Hz. The recovery of ICa from inactivation was prolonged by propafenone and the reactivation exhibited an additional exponential component attributed to the slow release from drug block of Ca channels. 5. These results suggest that propafenone, at therapeutic concentrations exhibits Ca channel blocking properties that may be involved in its antiarrhythmic mechanism.

Animals↗
PubMed2003

Molecular site of action of the antiarrhythmic drug propafenone at the voltage-operated potassium channel Kv2.1.

The effects of the antiarrhythmic drug propafenone at Kv2.1 channels were studied with wild-type and mutated channels expressed in Xenopus laevis oocytes. Propafenone decreased the Kv2.1 currents in a time- and voltage-dependent manner (decrease of the time constants of current rise, increase of block with the duration of voltage steps starting from a block of less than 19%, increase of block with the amplitude of depolarization yielding a fractional electrical distance delta of 0.11 to 0.16). Block of Kv2.1 appeared with application to the intracellular, but not the extracellular, side of membrane patches. In mutagenesis experiments, all parts of the Kv2.1 channel were successively exchanged with those of the Kv1.2 channel, which is much more sensitive to propafenone. The intracellular amino and carboxyl terminus and the intracellular linker S4-S5 reduced the blocking effect of propafenone, whereas the linker S5-S6, as well as the segment S6 of the Kv1.2 channel, abolished it to the value of the Kv1.2 channel. In the linker S5-S6, this effect could be narrowed down to two groups of amino acids (groups 372 to 374 and 383 to 384), which also affected the sensitivity to tetraethylammonium. In segment S6, several amino acids in the intracellularly directed part of the helix significantly reduced propafenone sensitivity. The results suggest that propafenone blocks the Kv2.1 channel in the open state from the intracellular side by entering the inner vestibule of the channel. These results are consistent with a direct interaction of propafenone with the lower part of the pore helix and/or residues of segment S6.

Amino Acid Sequence↗
PubMed1992

Short-term and long-term treatment with propafenone: determinants of arrhythmia suppression, persistence of efficacy, arrhythmogenesis, and side effects in patients with symptoms.

OBJECTIVE: To assess the clinical criteria predicting the short and long-term efficacy of propafenone, an agent with class IC antiarrhythmic activity and a broad pharmacological profile. DESIGNS: Prospective study of propafenone at doses of 450 to 900 mg/day during a six week dose titration period (including a placebo phase with two separate 24 Holter recordings). Responders to treatment were followed for one year. PATIENTS: One hundred patients with frequent ventricular arrhythmias (greater than 30 extrasystoles/h) of Lown class III and IVA/B and without evidence of myocardial infarction within the past six months. ANALYSIS: Multivariate regression analysis of spontaneous arrhythmia variability and of different clinical variables to determine the short and long-term efficacy and safety of propafenone. MEASUREMENTS AND MAIN RESULTS: Propafenone 450 mg/day was effective in 30/100 patients (30%), and at 600 mg/day another 14 responded. The efficacy of propafenone correlated with a low spontaneous arrhythmia variability and, as shown by multivariate analysis, with a lower patient age (p less than 0.05). When the dose was increased to 900 mg/day a further six (12%) patients responded. However, with increasing doses of propafenone, the one year probability of effective treatment decreased from 86% (450 mg/day) to 67% (600 mg/day) and to 44% (900 mg/day). After restudying the patients at three, six, and 12 months and after dose adjustment in 11/44 patients (25%), 31 patients (70%) remained responders. Loss of permanent antiarrhythmic efficacy was best predicted by the initial dose that achieved a response. No patient died suddenly or had arrhythmogenic effects during Holter monitoring. Side effects occurred in 36% of patients but these rarely limited long-term treatment. CONCLUSIONS: A younger age, low spontaneous arrhythmia variability, and particularly a low titration dose were the best predictors of the short and long term efficacy of propafenone. All other responders should have repeated Holter recordings during the first year of treatment.

Adult↗
PubMed2001

Evaluation of CYP2D6 oxidation of dextromethorphan and propafenone in a Chinese population with atrial fibrillation.

The objective of this study was to determine the percentage of patients with paroxysmal atrial fibrillation who were poor metabolizers of CYP2D6 in a Chinese population from Hong Kong and to assess the relationship between the dextromethorphan/dextrorphan ratio and the propafenone/5-hydroxypropafenone ratio or the steady-state propafenone concentration. Patients (n = 60) were recruited from the Arrhythmia Clinic at the University of Hong Kong and given dextromethorphan 30 mg. The dextromethorphan and dextrorphan concentrations in urine over the next 8 hours were used to determine metabolizer status. If the metabolic ratio was greater than 0.3, the patient was determined to be a poor metabolizer. In phase 2, patients (n = 38) were given propafenone 150 mg twice daily, and at steady state, the propafenone and 5-OH propafenone plasma concentrations were determined. It was found that 15% of the patients were poor metabolizers of dextromethorphan. There was a significant correlation between the metabolic ratios of dextromethorphan/dextrorphan and propafenone/5-OH propafenone (r = 0.49, p = 0.0019) and between the dextromethorphan/dextrorphan ratio and the concentration of propafenone (r = 0.32, p = 0.05). No correlations were found in the extensive or poor metabolizer subgroups. It was concluded that the percentage of poor metabolizers in atrial fibrillation patients from Hong Kong was much larger than in previous studies of Chinese patients who were not from Hong Kong. The ability to metabolize dextromethorphan to dextrorphan is related to the ability to metabolize propafenone to 5-hydroxypropafenone.

Anti-Arrhythmia Agents↗
PubMed1987

Hemodynamic and electrophysiologic effects of combined infusion of lidocaine and propafenone in humans.

The hemodynamic and electrophysiologic effect of a combined intravenous infusion of lidocaine (100 mg bolus followed by 2 mg/min infusion) and propafenone (1 or 2 mg/kg) in patients with a history of ventricular arrhythmia was studied. Lidocaine infusion alone significantly increased the mean pulmonary artery (+28%) and pulmonary capillary wedge (+17%) pressure, with no effect on cardiac index. Lidocaine alone produced no consistent change in any measured electrophysiologic parameter, except slight QTc shortening (-2%, P less than .05). Propafenone alone, particularly at the higher dose (2 mg/kg), produced significant increases in mean blood pressure (+14%), right atrial pressure (+78%), pulmonary artery pressure (+50%), pulmonary capillary wedge pressure (+65%), systemic vascular resistance (+29%), and pulmonary vascular resistance (+61%) and a decrease in cardiac index (-12%). Significant prolongation of PR (+9%), AH (+29%), and HV (+23%) intervals, atrial functional refractory period (+12%), ventricular effective (+7%) and functional (+6%) refractory period, and Wenckebach cycle length (+13%) also occurred after the administration of propafenone alone. Only the effects on atrioventricular (AV) node were observed at the lower dose of propafenone (1 mg/kg). Combined infusion of lidocaine with propafenone produced a mild, statistically insignificant additional negative inotropic effect but reversed the prolongation in atrial and ventricular refractoriness produced by propafenone alone. Thus, the data show that lidocaine attenuates certain electrophysiologic effects of propafenone, which might alter its antiarrhythmic efficacy, while producing mild additive negative inotropic effects that may be of hemodynamic significance.

Adult↗
PubMed1989

Propafenone: a novel type Ic antiarrhythmic agent.

Propafenone is an investigational type Ic anti-arrhythmic agent that markedly slows conduction velocity in all cardiac tissues. Propafenone also possesses weak beta- and calcium-channel blocking properties. The bioavailability of propafenone is dose-dependent. Hepatic metabolism of this agent is polymorphic and appears to correlate with the ability of the liver to oxidize debrisoquin sulfate. Propafenone is effective in suppressing spontaneous ventricular ectopy; however, the drug may be less effective in patients with sustained ventricular tachycardia or ventricular fibrillation when evaluated using programmed stimulation. Propafenone is also useful in the treatment of supraventricular tachycardias including atrioventricular (AV) nodal reentrant tachycardia, AV reentrant tachycardia associated with the Wolff-Parkinson-White syndrome, and atrial fibrillation. Adverse reactions seen with propafenone affect the gastrointestinal, central nervous, and cardiovascular systems. Comparative studies with currently available type Ic agents are needed to better define propafenone's place in therapy.

Animals↗
PubMed1993

Effects of flecainide and propafenone on systolic performance in subjects with normal cardiac function.

Flecainide and propafenone are effective in suppressing both ventricular and supraventricular tachyarrhythmias, but their efficacy is often limited by dose-related side effects. This study was performed to evaluate noninvasively the effects of intravenous flecainide and propafenone on left ventricular systolic function indices in a selected population of 40 subjects (28 men and 12 women; mean age, 25 years) with normal cardiac structure and performance. Echocardiographic indexes of global systolic pump function (ejection fraction [EF] and percentage of fractional shortening [percent FS]) as well as monodimensional parameters of the intraventricular septum (IVS) and left ventricular posterior wall (PW) contractility (percent systolic thickening [percent th] and systolic excursion [ex]) were assessed in all subjects at baseline, immediately after, and in the early recovery (15 min) after randomized injection of either flecainide or propafenone. Heart rate and blood pressure did not significantly change after both drugs. A significant increase (p < 0.001) in left ventricular systolic internal diameter was observed after both flecainide and propafenone; simultaneously a significant decrease of percent FS (p < 0.001), EF (p < 0.001), PW percent thickening (th) (p < 0.001), and PWex (p < 0.001 after flecainide and p < 0.01 after propafenone) was recorded. These changes were comparable and promptly reversible. In analyzing individual data, a marked systolic dysfunction was observed in two patients after intravenous flecainide (percent FS from 37 percent to 17 percent and from 42 percent to 13 percent; EF from 55 percent to 40 percent and from 65 percent to 35 percent, respectively) and in one patient after intravenous propafenone (percent FS from 30 percent to 15 percent; EF from 58 percent to 35 percent). We conclude that both intravenous flecainide and propafenone exhibit mild negative inotropic effects leading to a moderate and reversible reduction of left ventricular systolic performance; however, in some cases, a dramatic impairment of systolic pump function may occur, suggesting careful use of both drugs as first-line agents also in normal subjects; finally, the true incidence of this deleterious effect is still unknown.

Adolescent↗
PubMed1994

Clinical course of recent-onset atrial fibrillation treated with oral propafenone.

Atrial fibrillation (AF) is one of the most common cardiac arrhythmias in the adult population. Propafenone is a class 1c antiarrhythmic agent that has an electrophysiologic profile suggesting that it might be potentially effective in recent-onset AF. The present study was undertaken, therefore, to examine the time course as well as the frequency of successful conversion in patients with recent-onset AF treated with propafenone administered orally. Fifty patients with recent-onset AF were recruited into 2 groups: 25 patients were given propafenone, 150 mg every 4 h, and 25 patients served as a control group and received verapamil (a drug known to slow the ventricular response but not to restore sinus rhythm) 40 mg, every 4 h and up to 48 h or until conversion to sinus rhythm occurred. Of the 50 patients, 2 refused to continue the study and another 2 were excluded because of left heart failure. Conversion to sinus rhythm occurred in 21 of 24 patients (87 percent) in the propafenone group as compared with 9 of 22 (41 percent) in the verapamil group (p < 0.001). In 10 patients in the propafenone group, conversion occurred within 12 h, within 24 h in another 9 patients, and between 24 and 48 h in the remaining 2 patients. There was no correlation between the duration of AF prior to entry into the study and the subsequent incidence of and time to conversion with propafenone. With respect to cause of AF, all groups showed a high incidence of conversion. Two patients developed heart failure during treatment and one patient (in the verapamil group) developed embolic stroke while still having atrial fibrillation. We conclude that in patients with AF, the prognosis for conversion to sinus rhythm within 48 h, with propafenone, is excellent (87 percent) and safe.

Administration, Oral↗
PubMed1995

Guidelines for the use of propafenone in treating supraventricular arrhythmias.

Propafenone is a sodium channel blocking agent with a mild beta- and calcium channel-blocking activity. Several controlled and noncomparative studies have documented its efficacy in a variety of supraventricular arrhythmias in both adults and children. Propafenone is comparable with other Vaughan-William class I antiarrhythmic drugs for acute conversion of atrial fibrillation. It is also comparable with other drugs for prevention of recurrences in paroxysmal atrial fibrillation and for maintenance of sinus rhythm following successful cardioversion of chronic atrial fibrillation. Although propafenone is effective in the acute management of junctional reentrant tachycardias, the availability of safer drugs precludes its routine use for these arrhythmias. It may, however, be preferred for the acute management of haemodynamically well tolerated pre-excited atrial fibrillation in patients with the Wolff-Parkinson-White (WPW) syndrome. It also has documented efficacy in the long term therapy of patients with junctional tachycardias, and is a useful first-line drug in the management of arrhythmias in patients with the WPW syndrome, particularly when there is a short anterograde refractory period of the accessory pathway. Noncomparative studies were confirmed good efficacy and tolerability of propafenone in the short and long term management of paediatric supraventricular arrhythmias. It seems to be particularly effective for the treatment of ectopic atrial and junctional tachycardias, which are generally difficult arrhythmias to manage. Propafenone appears to have an acceptable adverse effect profile during both short and long term therapy. As with most other antiarrhythmic agents, there is a proarrhythmic potential. This has also been observed in children. There is a theoretical possibility that the beta-blocking properties of propafenone may protect against its proarrhythmic potential. However, this has not been confirmed in clinical studies. In conclusion, propafenone appears to be effective in the management of a wide spectrum of supraventricular arrhythmias. It should be considered among the first line drugs for management of these arrhythmias in patients without structural heart disease.

Adult↗
PubMed2002

Oral loading with propafenone for conversion of recent-onset atrial fibrillation: a review on in-hospital treatment.

Atrial fibrillation (AF) is a very common arrhythmia. In order to treat acute AF rapidly, effective drug regimens are required. Propafenone is a class IC antiarrhythmic agent that is suitable for oral loading as it reaches peak plasma concentrations within 2 to 4 hours of administration. The use of propafenone loading in patients with AF must be based on appropriate patient selection in view of the negative inotropic effect and the potential proarrhythmic effects of the drug. A series of controlled trials in patients with recent-onset AF without heart failure who were hospitalised with enforced bed rest has shown that orally loaded propafenone (450 to 600 mg as single dose) exerts a relatively quick effect (within 3 to 4 hours) and a high rate of efficacy (72 to 78% within 8 hours). A potentially harmful effect of class IC agents is the risk of transforming AF into atrial flutter (3.5 to 5% of patients). However, atrial flutter with 1 : 1 atrioventricular response was observed in only two of 709 patients receiving propafenone (0.3% incidence). Nevertheless, the potential negative inotropic effect of propafenone demands careful patient selection, with systematic exclusion of patients with left ventricular dysfunction or congestive heart failure. Oral loading with propafenone can be considered as an episodic treatment in patients with AF recurrences, as has been proposed for other drugs in the past. However, the safety of oral loading with propafenone as an outpatient treatment in appropriately selected patients has to be assessed by appropriately designed prospective studies.

Administration, Oral↗