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At least 19 recordsLinked to original sources
PubMed1993

Modulation of flecainide's cardiac sodium channel blocking actions by extracellular sodium: a possible cellular mechanism for the action of sodium salts in flecainide cardiotoxicity.

Sodium salts reverse the clinical cardiotoxicity of class 1c antiarrhythmic agents, but the underlying mechanisms are unknown. We studied the modulation of flecainide's action by changes in extracellular sodium concentration ([Na+]e) produced by isotonic substitution of choline for sodium. Increasing [Na+]e by 25 mM attenuated the depressant effects of 3.2 microM flecainide of Vmax in canine cardiac Purkinje fibers, whereas decreasing [Na+]e enhanced drug action. The voltage dependence of Vmax was shifted by flecainide (activation potential for 50% decrease in Vmax, V50: -77.4 +/- 3.5 mV at 3.2 microM flecainide) compared to control (V50: -73.7 +/- 2.8 mV, mean +/- S.D., P < .05). Increasing [Na+]e in the presence of flecainide returned V50 toward control (-75.8 +/- 3.1 mV, P < .05 vs. flecainide at normal [Na+]e). Increased [Na+]e shifted the flecainide concentration-response curve to the right (EC50 19.0 microM) compared to normal (EC50 14.6 microM) and low (EC50 10.8 microM) [Na+]e. [Na+]e modulated the concentration-dependent displacement by flecainide of [3H]batrachotoxin-A-benzoate, with increased [Na+]e shifting the binding curve to the right and decreased [Na+]e shifting it to the left compared to normal [Na+]e. There was a strong linear correlation (r = 0.99) between flecainide's EC50 for Vmax depression and its IC50 for [3H]batrachotoxin-A-benzoate displacement at various [Na+]e. We conclude that [Na+]e modulates flecainide's interaction with the sodium channel. Sodium's ability to displace blocking drug from the sodium channel may underlie the efficacy of sodium salts in treating flecainide toxicity, and could play a similar role in antagonizing cardiotoxicity of other class 1 compounds.

Action Potentials↗
PubMed2003

Common molecular determinants of flecainide and lidocaine block of heart Na+ channels: evidence from experiments with neutral and quaternary flecainide analogues.

Flecainide (pKa 9.3, 99% charged at pH 7.4) and lidocaine (pKa 7.6-8.0, approximately 50% neutral at pH 7.4) have similar structures but markedly different effects on Na(+) channel activity. Both drugs cause well-characterized use-dependent block (UDB) of Na(+) channels due to stabilization of the inactivated state, but flecainide requires that channels first open before block develops, whereas lidocaine is believed to bind directly to the inactivated state. To test whether the charge on flecainide might determine its state specificity of Na(+) channel blockade, we developed two flecainide analogues, NU-FL (pKa 6.4), that is 90% neutral at pH 7.4, and a quaternary flecainide analogue, QX-FL, that is fully charged at physiological pH. We examined the effects of flecainide, NU-FL, QX-FL, and lidocaine on human cardiac Na(+) channels expressed in human embryonic kidney (HEK) 293 cells. At physiological pH, NU-FL, like lidocaine but not flecainide, interacts preferentially with inactivated channels without prerequisite channel opening, and causes minimal UDB. We find that UDB develops predominantly by the charged form of flecainide as evidenced by investigation of QX-FL at physiological pH and NU-FL investigated over a more acidic pH range where its charged fraction is increased. QX-FL is a potent blocker of channels when applied from inside the cell, but acts very weakly with external application. UDB by QX-FL, like flecainide, develops only after channels open. Once blocked, channels recover very slowly from QX-FL block, apparently without requisite channel opening. Our data strongly suggest that it is the difference in degree of ionization (pKa) between lidocaine and flecainide, rather than gross structural features, that determines distinction in block of cardiac Na(+) channels. The data also suggest that the two drugs share a common receptor but, consistent with the modulated receptor hypothesis, reach this receptor by distinct routes dictated by the degree of ionization of the drug molecules.

Anti-Arrhythmia Agents↗
PubMed1991

Flecainide acetate prevents recurrence of symptomatic paroxysmal supraventricular tachycardia. The Flecainide Supraventricular Tachycardia Study Group.

Oral flecainide acetate was administered to 34 patients with documented symptomatic paroxysmal supraventricular tachycardia (PSVT) with a double-blind, placebo-controlled, 8-week crossover trial design. PSVT was defined as a regular tachycardia of at least 120 beats/min without evidence of atrioventricular dissociation. The study required considerable patient cooperation. Patients first entered a 4-week qualifying phase followed by a 3-week, open label, flecainide dose-ranging phase. They were then randomized in a blind fashion to receive either placebo or tolerated flecainide dose for an 8-week treatment period and then crossed over after four symptomatic documented episodes of PSVT or at the end of the treatment period. By all efficacy parameters analyzed, flecainide was superior to placebo. Flecainide was associated with an actuarial 79% freedom from symptomatic PSVT events compared with only 15% on placebo at 60 days (p less than 0.001). Of the 34 patients, 29 had recurrence of symptomatic PSVT at least once during the placebo phase; only eight patients had a recurrence during the flecainide phase (p less than 0.001). The median time to the first symptomatic PSVT event was 11 days in the placebo group and greater than 55 days in the flecainide group (p less than 0.001). Likewise, the interval between attacks was a median of 12 days on placebo compared with more than 55 days on flecainide (p less than 0.001). Finally, the flecainide slowed symptomatic PSVT heart rates to 143 +/- 12 beats/min from 178 +/- 12 on placebo (p less than 0.02) in the seven patients who had events in the placebo and flecainide treatment phases.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1987

Chronic flecainide therapy selected by electrophysiology testing of intravenous flecainide.

The utility of flecainide acetate was evaluated in 93 patients by means of electrophysiologic studies before and after intravenous flecainide administration to determine long-term efficacy. Twenty patients had a prior history of at least one cardiac arrest and 73 patients had sustained ventricular tachycardia (VT). The mean radionuclear ejection fraction was 32 +/- 5%. Flecainide was evaluated in 93 patients, with 44 patients no longer having VT following flecainide (47% efficacy). Procainamide was evaluated in 69 patients; 24 patients had an adverse reaction to reaction to procainamide and 28 of the 69 patients were protected on procainamide (40% efficacy). The mean serum concentration of flecainide achieved in the protected group was 298 +/- 36 ng/ml and 4.3 micrograms/ml for procainamide. Both flecainide and procainamide significantly prolonged refractoriness, lengthened QRS duration, while only procainamide increased the QT interval. All 93 patients were discharged on antiarrhythmic therapy, 42 on flecainide, 27 on other antiarrhythmic therapy guided by electrophysiologic testing, and 24 on amiodarone (when all other agents failed). Six of the 42 patients on flecainide complained of adverse side effects, but none were severe enough to warrant stopping therapy. Of the 42 patients on flecainide, four (9%) died suddenly over 18 +/- 4 months. Twenty-seven patients were on other therapy; eight of these have died, three suddenly (11%), four with myocardial infarctions, and one due to congestive heart failure. Twenty-four patients started amiodarone; 11 have died, five (21%) suddenly, four of congestive heart failure, one of pulmonary fibrosis, and one with myocardial infarction.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1996

Comparison of the safety and efficacy of flecainide versus propafenone in hospital out-patients with symptomatic paroxysmal atrial fibrillation/flutter. The Flecainide AF French Study Group.

To assess the cardiac and extracardiac safety and efficacy of flecainide versus propafenone in patients suffering from episodes of paroxysmal atrial fibrillation (AF) or atrial flutter, 97 patients were enrolled in a randomized, open-label, long-term, parallel, comparative multicenter study. The diagnosis of paroxysmal AF or atrial flutter had to be fully documented prior to inclusion in the study. Of the 97 patients enrolled in the study, 48 patients (25 men, 23 women, mean age 62.4 +/- 12.3 years) received flecainide; 49 patients (26 men, 23 women, mean age 63.6 +/- 12.2 years) received propafenone. The initial dose of flecainide was 50 mg twice daily, and this could be increased in steps of 50 mg twice daily every 4 days to a maximum of 300 mg/day. The initial dose of propafenone was 300 mg twice daily and this could be increased in steps of 300 mg every 4 days to a maximum of 1200 mg/day. At each visit, medical events, vital sign measurements (blood pressure, pulse rate), concomitant medications, adverse experiences, and study drug dosage changes were evaluated. Routine clinical laboratory tests were evaluated at the month 6 visit, and a 24-hr Holter recording was obtained at the month 1 visit. Almost half (45) of the patients were discontinued from the study before completing 1 year of therapy. The probability of successful treatment versus time--i.e., the proportion of patients who remained on therapy over the course of 1 year therapy--was 0.619 for the flecainide group and 0.469 for the propafenone group (p = 0.079; difference not significant). The difference is largely attributed to the higher proportion of patients in the propafenone group (9) than in the flecainide group (2) who experienced side effects important enough to stop the treatment. (The incidence of side effects was not statistically different between treatment groups, although it was higher in the propafenone group.) The proportion of patients who discontinued treatment due to inadequate response was similar in the 2 groups: 11 patients (22.9%) in the flecainide group and 12 patients (24.4%) in the propafenone group withdrew from the study, primarily because of an inadequate response, i.e., they experienced an increase in duration, frequency, and severity of attacks of AF or atrial flutter. Neurologic signs, central and peripheral, were mostly encountered in the flecainide group (8.5%), and, gastrointestinal effects were more often reported in the propafenone group (16.7%). In paroxysmal AF and paroxysmal atrial flutter, flecainide and propafenone are equally effective. However, in this study the probability of a patient's staying on flecainide after 1 year had a tendency to be higher than the probability of staying on propafenone, due to a greater proportion of secondary effects with propafenone.

Adult↗
PubMed1996

A randomized comparison of flecainide versus verapamil in paroxysmal supraventricular tachycardia. The Flecainide Multicenter Investigators Group.

Reentrant paroxysmal supraventricular tachycardia (PSVT) are frequently encountered in clinical practice. Verapamil and flecainide have both been successfully used as chronic oral therapy to prevent PSVT recurrences. This open-label, randomized, multicenter study was designed to compare the efficacy and adverse effects of verapamil (median dose, 240 mg/day) versus flecainide (median dose, 200 mg/day) in patients with frequent and symptomatic attacks of PSVT (other than atrial fibrillation or flutter). A total of 121 patients receiving flecainide (n = 63) or verapamil (n = 58) were followed for 8.1 +/- 5.1 and 7.5 +/- 5.4 months, respectively. Response was judged clinically as effective or not by the treating physician. By life table analysis, 11% discontinued flecainide and 19% discontinued verapamil for inefficacy at 1 year (difference not significant). Both groups showed a marked reduction in the frequency of attacks of PSVT. Before therapy, 71% of flecainide patients and 73% of verapamil patients had > or = 2 attacks per month. During therapy, 86% of all flecainide patient-months and 73% of all verapamil patient-months occurred with 0 or 1 attack; 19 (30%) patients on flecainide completed the trial ( > 270 days) without symptomatic attacks versus 7 (13%) of the patients on verapamil (p = 0.026). Both drugs were well tolerated; 19% of the flecainide group discontinued primarily because of adverse effects, compared with 24% discontinuing verapamil for this reason (difference not significant). Both flecainide and verapamil are effective and well tolerated for the prevention of recurrences of PSVT. For patients in whom radiofrequency ablation procedures cannot be performed or are not indicated, either therapy is a reasonable choice for long-term prophylaxis.

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↗
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↗
PubMed1996

Prospective comparison of flecainide versus quinidine for the treatment of paroxysmal atrial fibrillation/flutter. The Flecainide Multicenter Atrial Fibrillation Study Group.

In order to compare the efficacy and long-term tolerability of flecainide acetate versus quinidine, 239 patients with paroxysmal atrial fibrillation were prospectively treated with flecainide (n = 122) or quinidine (n = 117) in an open-label, randomized trial. All patients were followed for 1 year after initiation of therapy unless their antiarrhythmic drug was discontinued due to an inadequate therapeutic response or intolerable side effects. Although both drugs were equally effective in adequately controlling recurrences of atrial fibrillation (difference, p = 0.282; not significant), fewer flecainide patients had to have their therapy discontinued due to adverse experiences (p = 0.012). Based on both endpoints (efficacy and tolerability), an estimated 70.5% of flecainide versus 55.4% of quinidine patients would remain effectively treated at the end of 1 year on therapy (p < or = 0.007). The findings of this prospective study suggest that in the treatment of paroxysmal atrial fibrillation (1) flecainide and quinidine are equally effective in the acceptable suppression of symptomatic paroxysmal atrial fibrillation; (2) flecainide is better tolerated than quinidine and is less likely to be discontinued due to adverse effects; and (3) given the overall endpoint of efficacy and tolerability, more patients are likely to continue long-term therapy with flecainide than with quinidine.

Administration, Oral↗
PubMed1996

Safety and utility of flecainide acetate in the routine care of patients with supraventricular tachyarrhythmias: results of a multicenter trial. The Flecainide Supraventricular Tachycardia Study Group.

Patients with supraventricular arrhythmias have been safely and effectively treated with flecainide. We conducted an open-label, 20-center trial to define further the safety and efficacy profile of oral flecainide in patients with supraventricular arrhythmias, including atrial tachycardias (ectopic or multifocal), atrial-ventricular tachycardias (reentrant), paroxysmal atrial fibrillation/flutter (PAF), and chronic atrial fibrillation (CAF). Our study population of 151 patients with documented supraventricular arrhythmias requiring treatment included 67 with paroxysmal supraventricular tachycardia (PSVT), 67 with PAF (symptoms < 15 days), and 17 with CAF (symptoms > of = 15 days)> The initial flecainide dose of 100 mg twice daily could be increased by 50 mg bid every 4 days to a maximum of 200 mg twice daily. Patients who were effectively treated could receive flecainide for 1 year. The study was terminated April 26, 1989, in response to interim results reported by the Cardiac Arrhythmia Suppression Trial (CAST). All patients were removed from the study by August 1989. At study termination 87% of PSVT, 73% of PAF, and 56% of CAF patients had improved symptomatically while on flecainide therapy. Eleven patients experienced cardiac adverse experiences: proarrhythmic events (3 patients), new or worsened congestive heart failure (7 patients), sinus pauses (1 patient). Cardiac side effects appeared to be more frequent in patients in the CAF group (5/17 patients), all of whom had structural heart disease. Overall, 45 (67%) PSVT, 43 (64%) PAF, and 9 (56%) CAF patients reported at least 1 noncardiac adverse experience; the most common were abnormal vision, dizziness, and headaches. One patient from the CAF group died; the death was considered to be unrelated to flecainide. Flecainide appears to be safe and effective treatment for patients with supraventricular arrhythmias of a variety of mechanisms and appears particularly effective for patients with PSVT. The efficacy is lowest and side effects most frequent in patients with CAF, as seen with other trials of antiarrhythmic medication in these patients. In the context of the CAST experience and other trials of antiarrhythmic drugs in patients with CAF, the balance of risk and benefit of therapy should be considered carefully before initiating treatment.

Administration, Oral↗
PubMed1988

[Concentrations of amiodarone and flecainide in plasma and saliva--indications for the active transport of flecainide].

UNLABELLED: Only the free protein-unbound drug concentration in plasma is pharmacologically active. The concentration of some drugs in saliva is equal to the free drug level. We compared concentrations (in plasma before, 30 and 60 min after the morning dose, in saliva before, 30, 60, 90 and 120 min after the morning dose) of amiodarone (n = 8, 2 x 200 mg orally per day) and flecainide (n = 16, 2 x 100 mg) administered as chronic antiarrhythmic treatment. Drug levels were measured by "high performance liquid chromatography". RESULTS: Just prior to the first morning dose, amiodarone concentrations in plasma were 1.0-2.9 (2.0 +/- 0.6) micrograms/ml, in saliva 0.02-0.25 micrograms/ml; flecainide in plasma 80-560 (316 +/- 163) ng/ml, in saliva 630-3700 (1749 +/- 963) ng/ml. After the morning dose we found maximal flecainide plasma levels of 462 +/- 203 and saliva levels of 3218 +/- 2857 ng/ml. The highest flecainide concentrations in the saliva (13,400 and 11,300 ng/ml) were found in two patients 30 and 60 min after the morning dose. Flecainide, but not amiodarone, is excreted actively in the saliva, probably indicating an enteroenteric circulation. This should be considered to reduce life-threatening flecainide intoxications by gastric and intestinal lavage and suction. The concentration of flecainide in the saliva does not represent the non-protein-bound free drug level in the plasma.

Adult↗
PubMed1991

Usefulness of flecainide for prevention of paroxysmal atrial fibrillation and flutter. Danish-Norwegian Flecainide Multicenter Study Group.

To evaluate the efficacy of flecainide acetate in the prevention of paroxysmal atrial fibrillation and flutter, 43 patients (23 men) (mean age 53 years) were randomized blindly to receive either placebo or 150 mg of flecainide twice per day for consecutive periods of 3 months. Attacks were verified by a minielectrocardiogram event recorder. If intolerable symptoms developed, the protocol allowed patients to cross over between treatments before the end of the first 3-month period. Four patients crossed over prematurely, between 1 week and 1 month, and 15 between 1 month and 3 months. The remaining 24 patients completed both 3-month periods. In all 3 treatment intervals, there was a significant reduction in the number of attacks during flecainide treatment (p less than 0.002). Complete suppression was seen in 15 of 43 patients (35%) treated with flecainide for 1 week, in 18 of 39 (46%) treated for 1 month and in 12 of 24 (50%) completing all 3 months in each period. Adverse effects were reported in 32 of the 43 patients (74%) treated with flecainide, but only 2 were withdrawals. One patient died suddenly. In comparison, 3 of 43 patients (7%) reported adverse effects in the placebo group. In conclusion, flecainide significantly suppressed the number of attacks of paroxysmal atrial fibrillation and flutter. Adverse effects were frequent but were mostly tolerable.

Adult↗
PubMed1987

[Treatment of recurrent supraventricular tachyarrhythmias with flecainide or a flecainide and amiodarone combination].

The acute electrophysiologic effects and therapeutic efficacy of intravenous and oral flecainide were assessed in 18 patients with recurrent supraventricular tachyarrhythmias, resistant to conventional antiarrhythmic agents. They were 22 to 76 years old (mean 50). Twelve patients underwent electrophysiologic study for the investigation of tachyarrhythmias. Of the whole four patients had functional longitudinal AH dissociation (dual AV pathways). These patients had provocable intra-AV nodal reentrant tachycardia (Group I). Six patients had a direct accessory AV pathway, that showed bidirectional conduction in 5 and retrograde conduction alone in 1 (Group II). These patients had provocable atrioventricular reentrant tachycardia using the accessory pathway as the retrograde limb of the tachycardia circuit. Two patients suffered from automatic supraventricular tachycardia (Group III). Group IV included patients with paroxysmal atrial flutter or fibrillation. The patients of this group did not discontinue chronic treatment with amiodarone. After baseline electrophysiologic evaluation, intravenous flecainide (2 mg/Kg body weight over 5 minutes) was given to patients of I and II group during induced reentrant tachycardia. Flecainide was administered to other patients during spontaneous episodes of tachyarrhythmias. Flecainide resulted in tachycardia termination in all patients of group I and in 4 patients of group II (66%). Tachycardia termination was due to block in the retrograde limb of the circuit. Before termination tachycardia cycle length increased significantly, mainly as the result of an increase in ventriculo-atrial conduction time. After intravenous flecainide therapy, reentrant SVT was non inducible in the patients of group I and in 4 patients of group II. Flecainide was successful in the acute termination of 100% of automatic supraventricular tachycardia and 75% of fibrillation. The patients with atrial flutter developed a faster ventricular rate.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1986

Treatment of resistant ventricular tachycardia with flecainide acetate. Flecainide Ventricular Tachycardia Study Group.

Ninety-four patients with ventricular tachycardia (VT), 49 with sustained and 45 with nonsustained VT, who had been refractory to or intolerant of other antiarrhythmic agents were treated in a multicenter, open-label study with flecainide acetate. Most had serious cardiac disorders associated with their arrhythmia: 49 patients (52%) had 1 or more conduction disorders on electrocardiography; 43 (46%) had congestive heart failure; 30 (33%) had left ventricular ejection fractions of 30% or less. Patients were initially treated orally in the hospital with 100 mg twice daily; dosage was titrated upward as needed at 4-day intervals to a maximal dose of 200 mg twice daily. Flecainide plasma level monitoring was performed to ensure plasma levels remained in the therapeutic range of 0.2 to 1.0 micrograms/ml. Patients were discharged with flecainide therapy if investigators judged it to be safe and effective. Minimum efficacy requirements included elimination of sustained VT and reduction of other ventricular arrhythmias as determined by 1 or more of the following: 24-hour electrocardiographic monitoring, programmed electrical stimulation, exercise testing and in-hospital monitoring. Sixty-eight patients (72%) were discharged with flecainide therapy. After a mean follow-up of 8 months, 45 patients (48%) were still taking flecainide, including 22 of 49 (45%) with sustained and 23 of 45 (51%) with nonsustained VT. Nine patients with sustained VT and 1 patient with nonsustained VT had aggravation of arrhythmia. Two patients had third-degree heart block. Nine patients died after discharge from the hospital: 6 from out-of-hospital sudden death and 3 from acute myocardial infarctions.(ABSTRACT TRUNCATED AT 250 WORDS)

Arrhythmias, Cardiac↗
PubMed2006

[Flecainide acetate utilisation review among general practitioners and hospital or office-based cardiologists in France. Obepine: observational study of flecainide].

A pharmacoepidemiological cross-sectional observational study was performed among a representative sample of French general practitioners and cardiologists. The aim of this study was to describe the prescription modalities of flecainide acetate, an Ic class antiarrhythmic, and how these modalities match the marketing authorization and the current summary of product characteristics. A total of 941 physicians participated in the study, 496 GPs and 445 cardiologists, and 1116 patients treated with flecainide for more than one month were included. On average, the patients were 68.7-years-old and 54% of them were women. Most of the initial flecainide prescriptions came from cardiologists (96%) and the check-up included an electrocardiogram (98%), a Holter monitoring (56%) and/or an echocardiography (71%). The preferred indication was supraventricular rhythm disorders (95%) and mostly atrial fibrillation (63%). A small proportion of coronary patients (7%) and of patient suffering from cardiac insufficiency (4%) was found. Flecainide was prescribed with a median posology of 150 mg per day, mostly as LP form (64%). Overall, the indications specified in the summary of product characteristics were respected in 90% of the cases, the contraindications in 91% of the cases and the patient follow-up was appropriate in 99% of the cases. In conclusion, the study showed that the prescription's conditions of flecainide in France complied with the summary of product characteristics data for most of the prescribing physicians with a respect of the indications, contraindications and management recommendations in 84% of the cases.

Aged↗
PubMed1991

Flecainide acetate treatment of paroxysmal supraventricular tachycardia and paroxysmal atrial fibrillation: dose-response studies. The Flecainide Supraventricular Tachycardia Study Group.

The dose-response relations for efficacy and tolerance of the antiarrhythmic drug flecainide acetate were studied in 28 patients with paroxysmal supraventricular tachycardia (Group 1) and 45 patients with paroxysmal atrial fibrillation or flutter (Group 2). Recurrent symptomatic tachycardia was documented with use of transtelephonic electrocardiographic recording. Patients received flecainide in doses of 25, 50, 100 and 150 mg twice daily and placebo for 1 month treatment periods. Among 14 patients in Group 1 who qualified for efficacy analysis, 4 (29%) had no tachycardia while taking placebo. The number with no tachycardia increased with progressively larger flecainide doses; with the 150 mg twice daily dose, 12 (86%) of 14 patients had no tachycardia (p less than 0.01 for overall differences among all treatments). Among 28 patients in Group 2, 2 (7%) had no tachycardia while taking placebo. The number with no tachycardia also increased with progressively larger flecainide doses; with the 150 mg twice daily dose, 17 (61%) of 28 patients had no tachycardia (p less than 0.01 for overall differences among all treatments). Noncardiac adverse experiences were the leading cause of premature study discontinuation during flecainide treatment periods (five patients in Group 1 and six patients in Group 2).

Adult↗
PubMed1996

Flecainide and the electrophysiologic matrix: the effects of flecainide acetate on the determinants of cardiac excitability in sheep Purkinje fibers.

Flecainide was associated with excess mortality distributed virtually equally throughout the period of the Cardiac Arrhythmia Suppression Trial, suggesting the intersection of two events, drug effect and perhaps ischemia. Flecainide's effect on active properties has been studied extensively, but nothing is known of its effects on passive properties or on the balance among active and passive cellular properties that determines cardiac excitability. The multiple microelectrode method of intracellular current application and transmembrane voltage recording was used in sheep Purkinje fibers to determines strength- and charge-duration as well as constant current-voltage relationships and to estimate active properties, liminal length, and cable properties at a normal [K+]o and in a setting of hyperkalemia analogous to that of ischemia. A computer tracked in time the alterations in the active and passive properties relevant to excitability. Flecainide slightly decreased excitability at a normal [K+]o, primarily by depressing the sodium system with some contributory effect of passive properties. At high [K+]o, flecainide caused a frequency-dependent decrease in excitability and conduction, the latter best interpreted as a failure of the fiber to attain the liminal length requirements to produce a local action potential due primarily to an effect on sodium conductance. Together, the observations suggest that the action potential is the local phenomenon and that the propagated event is the sequential fulfillment of liminal length requirements. The data were interpreted in terms of the electrophysiologic matrix first proposed in detail in this Journal, which indicated that the electrophysiologic universe moved as a system in response to the drug and a change in [K+]o, the presumed antiarrhythmic and proarrhythmic electrophysiologic matrices for flecainide were quite similar, and the matrical configuration shared characteristics with the matrices of other drugs with known proarrhythmic potential.

Action Potentials↗
PubMed1989

Prevention of symptomatic recurrences of paroxysmal atrial fibrillation in patients initially tolerating antiarrhythmic therapy. A multicenter, double-blind, crossover study of flecainide and placebo with transtelephonic monitoring. Flecainide Supraventricular Tachycardia Study Group.

Paroxysmal atrial fibrillation (PAF) is a problematic clinical arrhythmia that is usually symptomatic. Unfortunately, few adequate trials and trial methods are available for assessment of the value of therapy, and traditional treatment has often been ineffective or associated with unacceptable side effects. Transtelephonic monitoring is a new method that allows evaluation of paroxysmal arrhythmias and arrhythmia-related symptoms in outpatients. We used a patient-initiated transtelephonic monitor system to evaluate the potential of flecainide, a class 1C antiarrhythmic, in prevention of symptomatic recurrences of PAF. Sixty-four patients qualified for the study (two or more PAF attacks documented within a 4-week baseline period) and entered a dose-finding phase to determine drug tolerance. Dose was incremented at weekly intervals from 200-300 and finally to 400 mg/day. The largest dose that was well tolerated was selected for the 4-month, double-blind, randomized, crossover comparison with placebo. Fifty-five patients entered and 53 received both treatments in the double-blind phase; 48 of these patients without protocol violations were evaluable for efficacy comparisons. Evaluable patients had undergone an average of 3.8 previous drug trials (range, 1-8); 30 were men, 18 had hypertension, and 14 had ischemic heart disease. The study demonstrated a highly significant correlation (p less than 0.0001) between perceived symptoms and documented PAF by transtelephonic monitoring. The rate of symptoms and PAF attacks was also significantly reduced by therapy (median dose, 300 mg/day). The first PAF attack occurred after a median of 3 days on placebo versus 14.5 days on flecainide (p less than 0.001) therapy. Similarly, the time interval between attacks was lengthened, from a median of 6.2 days on placebo to 27.0 days on flecainide (p less than 0.001) therapy. PAF was prevented in 15 patients (31%) during flecainide and four (9%) during placebo therapy (p = 0.013). However, during the study, 13 patients dropped out, seven because of adverse effects (five cardiac), five for other reasons, and one because of cardiac arrest/death. Adverse cardiac events occurred in a total of seven patients (11%) during flecainide therapy. Thus, transtelephonic monitoring is a useful method for documentation of the occurrence of paroxysmal arrhythmias such as PAF and its related symptoms during daily living and for assessment of new therapies in an outpatient setting.

Atrial Fibrillation↗