Intravenous Flecainide Research Articles

Reversion of recent-onset atrial fibrillation to sinus rhythm by intravenous flecainide

Spontaneous reversion to sinus rhythm is a frequent occurrence in recent-onset atrial fibrillation (AF). In a randomized, double-blind, controlled study, intravenous flecainide (2 mg/kg, maximum dose 150 mg) was compared with placebo in the treatment of recent-onset AF (present for ≥30 minutes and ≤72 hours' duration and a ventricular response ≥120 beats/min). Intravenous digoxin (500 Mg) was administered concurrently to all patients in both groups who had not previously taken digoxin. The trial medication was administered over 30 minutes. Exclusion criteria included hemodynamic instability, severe heart failure, recent antiarrhythmic therapy, hypokalemia and pacemaker dependence. One hundred two consecutive patients with recent-onset AF were enrolled in the study. All patients underwent continuous electrocardiographic monitoring in the intensive care or coronary care unit. Twenty-nine (57%) patients given flecainide and digoxin, but only 7 (14%) given placebo and digoxin, reverted to sinus rhythm in ≤1 hour after starting the trial medication infusion and remained in stable sinus rhythm (chi-square 18.9, p = 0.000013; odds ratio 8.3, 95% confidence interval 2.9 to 24.8). At the end of the 6-hour monitoring period, 34 patients (67%) in the flecainide-digoxin group were in stable sinus rhythm, whereas only 18 patients (35%) in the placebo-digoxin group had reverted (chi-square 8.83, p = 0.003; odds ratio 3.67, 95% confidence interval 1.5 to 9.1). Severe hypotension, although transient, was more common in the flecainide-digoxin group. Flecainide is effective in reverting recent-onset AF, but should not be given to patients with severe left ventricular dysfunction because the risks may outweigh the potential benefits of reversion to sinus rhythm.

Flecainide

Efficacy of flecainide was investigated in 50 patients with sustained ventricular tachycardia (n = 38) or ventricular fibrillation (n = 12) during a 4-week in-hospital and 1-year follow-up period. Furthermore, the predictive value of programmed electrical stimulation, Holter monitoring, and exercise testing on outcome of long-term treatment was studied. Etiology of the tachyarrhythmia was coronary artery disease in 37 patients and other etiologies in 13 patients. The success rate of flecainide after 1 year, based on intention to treat, was 54%. The success rate during the in-hospital phase was 84% (in six patients flecainide was discontinued because of tachyarrhythmia and in two because of side effects). Calculated after 4 weeks hospitalization, the success rate was 78% for patients with tachyarrhythmias based on coronary artery disease and 55% for patients with tachyarrhythmias based on other etiologies (11 patients showed recurrences and two patients severe side effects). Patients with tachyarrhythmias based on coronary artery disease showed a lower ejection fraction and earlier recurrence than patients with arrhythmias based on other etiologies. Proarrhythmic effects developed in six patients (12%). Electrophysiological evaluation was performed in 28 patients at baseline and after intravenous flecainide. Negative predictive value of the electrophysiological evaluation after intravenous flecainide for patients with inducible tachyarrhythmias at baseline (n = 21) was 40%. For Holter monitoring (n = 24) this value was 86%. Non-ischemia-related induction of tachycardia by exercise was present in two of 30 patients on flecainide; both patients showed recurrence of the tachycardia.(ABSTRACT TRUNCATED AT 250 WORDS)

Efficacy of flecainide acetate for atrial arrhythmias following coronary artery bypass grafting

The antiarrhythmic efficacy of intravenous flecainide and intravenous digoxin was assessed in 29 patients (26 men), aged 43 to 73 (63 ± 7) years who developed atrial arrhythmias in the first 96 hours after coronary artery bypass grafting. Twenty-seven had atrial fibrillation and 2 had atrial flutter. Patients were entered into the study if the arrhythmia persisted for at least 15 minutes with a ventricular rate >120 beats/min. Fifteen patients were randomized to flecainide (group 1) and 14 to digoxin (group 2). Flecainide was given as a bolus of 1 mg/kg over 10 minutes followed by an infusion of 1.5 mg/kg/hr for 1 hour and then 0.25 mg/kg/hr for the rest of the study period (24 hours). Digoxin was given as 3 bolus doses (0.5 mg followed after 6 and 12 hours by 0.25 mg). In both groups, 10 mg of verapamil was given intravenously after 45 minutes if the arrhythmia persisted with a mean ventricular rate >100 beats/min. The antiarrhythmic efficacy was assessed by 24-hour Holter monitoring and frequent 15-second rhythm strips. Within 45 minutes control of arrhythmia, which was maintained for the rest of the study period, was achieved in 10 of 15 patients in group 1 and 2 of 14 in group 2 (p < 0.01). Nine of 15 reverted to sinus rhythm in group 1 compared to 0 of 14 in group 2 and 1 of 15 remained in arrhythmia with a controlled ventricular rate in group 1 compared to 2 of 14 in group 2. Within 1 hour arrhythmia was controlled in 12 of 15 in group 1 compared to 3 of 14 in group 2 (p < 0.01). Ten of 15 reverted to sinus rhythm in group 1 compared to 0 of 14 in group 2 and 2 of 15 remained in arrhythmia with a controlled ventricular rate in group 1 compared to 3 of 14 in group 2. There were no serious adverse effects. Intravenous flecainide is safe and more effective than intravenous digoxin for recent onset atrial tachyarrhythmias after bypass grafting.

Intravenous flecainide versus verapamil for acute conversion of paroxysmal atrial fibrillation or flutter to sinus rhythm

In a single-blind randomized study, the efficacy of intravenous flecainide (2 mg/kg/10 minutes) versus verapamil (10 mg/1 minute) was assessed in 40 patients with paroxysmal atrial fibrillation (AF) or atrial flutter (AFI). The treatment was considered successful if sinus rhythm occurred within 1 hour. Of 20 patients receiving flecainide, 14 of 17 (82%) with AF converted to sinus rhythm, but in 3 patients with AFI flecainide failed. All patients treated with verapamil (17 AF, 3 AFI) showed lower ventricular rates after 1 hour; however, only 1 (6%) with AF converted to sinus rhythm and 1 (6%) converted to AFI. Patients who did not convert to sinus rhythm after treatment with verapamil were treated with flecainide and observed for another hour. After the change to flecainide, 9 of 15 patients (60%) with AF still converted. Thus, 23 of 32 patients (72%) with AF and none of 7 with AFI converted to sinus rhythm after treatment with flecainide. Conversion to sinus rhythm was achieved in 19 of 22 patients (86%) when AF lasted <24 hours and in 4 of 10 (40%) when the arrhythmia lasted >24 hours. Transient adverse effects were noted in 10 patients (26%) after flecainide. In summary, flecainide is an effective and safe drug for conversion of paroxysmal AF to sinus rhythm, but ineffective for AFI. Verapamil appears to be of no use for conversion of AF or AFI to sinus rhythm.

Encainide versus flecainide for chronic atrial and junctional ectopic tachycardia

For treatment of chronic atrial and Junctional ectopic tachycardia, standard antiarrhythmic therapy has been shown to be ineffective in most patients. Both the intravenous efficacy and the oral efficacy of 2 class IC, were studied in 16 patients with atrial ectopic tachycardia and in 3 patients with junctional ectopic tachycardia, using exercise testing, 24-hour long-term electrocardiography and programmed electrical stimulation. All patients had been previously treated unsuccessfully with several antiarrhythmic drugs. In 5 patients, tachycardia was persistent; in the remaining patients, it occurred intermittently for more than 12 hours/day. Intravenous encainide, in doses ranging from 0.3 to 2.0 mg/kg body weight, was given to 5 patients with atrial ectopic tachycardia, and it terminated atrial ectopic tachycardia in all patients. Intravenous flecainide was given to 9 patients, and it terminated atrial tachycardia in 4 and slowed the tachycardia rate in 2. It terminated Junctional tachycardia in 2 patients and slowed tachycardia rate in 1. During a follow-up period of 10 ± 5 months, oral encainide, in dosages between 150 and 225 mg/day, completely suppressed atrial ectopic activity in 4 patients. In the remaining patient, encainide reduced the number of tachycardia episodes markedly but had to be withdrawn because of intolerable side effects. During a 12 ± 11-month (median 6) follow-up, oral flecainide at dosages between 200 and 300 mg/day, completely suppressed ectopic activity in 7 patients and improved symptoms in 5. Only 1 patient failed to respond to oral flecainide. The results of this study indicate that both encainide and flecainide are effective in the treatment of chronic ectopic atrial and junctional tachycardia.

Experience with flecainide for the treatment of cardiac arrhythmias in children.

We treated 22 children, aged 3 days to 16 years 6 months (median 11 years 1 month), with flecainide for a variety of arrhythmias where a Class I agent was indicated. In 16, conventional antiarrhythmic treatment had failed. Structural heart disease was present in nine. The arrhythmia was paroxysmal re-entry atrioventricular tachycardia in nine; paroxysmal atrial tachycardia, flutter or fibrillation in five; paroxysmal ventricular tachycardia in five and frequent ventricular extrasystoles (with couplets) in three. Sinus rhythm was achieved in all four children who received flecainide during tachycardia (three received intravenous flecainide, one oral). During follow-up of 3-24 months (median 12 months), arrhythmia control was obtained in 13 children (59%). Combination therapy was used in seven of these; with digoxin in four and a beta blocker in three. Flecainide doses used in this study ranged from 1-11 mg kg-1 day-1 (median 4 mg kg-1 day-1), 25-297 mg m-2 day-1 (median 113 mg m-2 day-1). The median, pre-dose flecainide concentration in those responding to therapy was 225 micrograms l-1 and in those failing to respond was 417 micrograms l-1. An arrhythmogenic effect occurred in one child.

Electrophysiologic and clinical effects of flecainide for recurrent paroxysmal supraventricular tachycardia

The antiarrhythmic effects of flecainide acetate were evaluated in 9 patients with paroxysmal atrioventricular (AV) nodal tachycardia and 17 patients with AV tachycardia. An electrophysiologic study was performed before and after intravenous flecainide acetate, 2 mg/kg body weight, was infused over 15 minutes and was followed by a maintenance infusion of 1.6 mg/kg given over 1 hour to 26 patients and during oral treatment to 15. Treatment with oral flecainide acetate was continued for 14 ± 5 months. Intravenous flecainide acetate terminated AV nodal tachycardia by blocking the retrograde fast pathway conduction in 7 of 7 patients and AV tachycardia by blocking retrograde conduction in the extranodal pathway in 10 of 10 patients. AV nodal tachycardia and AV tachycardia were noninducible in 8 of 9 patients (90%, p < 0.001) and 11 of 17 patients (65%, p < 0.001), respectively. Long-term treatment with oral flecainide acetate suppressed AV nodal tachycardia and AV tachycardia in 8 of 9 patients (90%, p < 0.001) and 11 of 17 patients (65%, p < 0.001), respectively. A favorable outcome was associated with block in the accessory pathway after intravenous flecainide acetate and noninducibility during oral treatment. Recurrences preferentially occurred in the younger patients. Flecainide acetate is effective in the acute and long-term management of paroxysmal supraventricular reentry tachycardia by suppressing conduction through the retrograde fast limb of the tachycardia circuit. The clinical effect can be predicted by electrophysiologic testing.

Summary of efficacy and safety of flecainide for supraventricular arrhythmias

This report provides an overview of the safety and efficacy of flecainide for supraventricular tachyarrhythmias (SVT) based on a review of the world literature. This review provided 107 entries, but 5 were review articles and 22 were articles not tranlated into English. The remaining 80 articles or published abstracts form the basis for this report. A total of 1,371 courses of therapy with intravenous or oral flecainide, or both, were represented. Efficacy was defined by each investigator. Intravenous flecainide was successful in terminating ongoing tachycardias in 81% of reported cases of atrioventricular (AV) nodal reentrant tachycardias, 88% of AV reentrant tachycardias and 100% of atrial tachycardias. Atrial fibrillation or flutter was terminated by intravenous flecainide in 62% of cases and arrhythmias associated with Wolff-Parkinson-White syndrome in 73%. Oral flecainide was successful in longer-term management of arrhythmia in 74 and 81% of patients with AV nodal and AV reentrant tachycardia, respectively, and in 83% with atrial tachycardia. Atrial flutter or fibrillation responded to oral drug in 61% of cases and arrhythmias related to Wolff-Parkinson-White syndrome in 61%. Adverse experiences were reported in studies totaling 695 patients (designated “at-risk patients”). They were not commented on in studies with the remaining 594 patients. Overall, a total of 6.9% of at-risk patients (3.7% of total patients) reported cardiac adverse experiences; 19% of at-risk patients (10% of total patients) reported at least 1 noncardiac adverse effect. Cardiac adverse events included worsened arrhythmias in 28, conduction disturbances in 15 and congestive heart failure in 5. The most frequent noncardiac adverse experiences were paresthesia and visual disturbance. In conclusion, flecainide provides effective therapy for SVT in two-thirds to three-fourths of patients, most of whom had no success with standard therapies, and is generally well tolerated. Patients with AV and AV nodal reciprocating tachycardias and atrial tachycardias are particularly responsive (>80%). Two-thirds of patients with Wolff-Parkinson-White syndrome-related SVT and recent-onset atrial fibrillation had successful results. Insufficient data with chronic atrial fibrillation are available to assess the use of flecainide. This experience suggests that flecainide represents an important addition to the treatment of symptomatic SVT.

Electrophysiologic effects and clinical efficacy of flecainide in children with recurrent paroxysmal supraventricular tachycardia

The electrophysiologic effects of intravenous flecainide were evaluated in 16 patients aged 9 ± 4 years: 15 with recurrent paroxysmal supraventricular tachycardia (SVT) and 1 with overt accessory pathway and history of syncope. Eleven patients had an accessory pathway; it was concealed in 2, overt in 9 and in 10 of these patients an orthodromic atrioventricular reentrant tachycardia was induced. Five patients without accessory pathway had an atrioventricular nodal reentrant tachycardia. After intravenous flecainide (1.5 mg/kg) the effective refractory period of the atrium and ventricle increased significantly; the anterograde and retrograde effective refractory periods of the atrioventricular node did not. Flecainide blocked retrograde conduction in the accessory pathway in 4 patients (effective refractory period 245 ± 41 ms) and anterograde conduction in 8 of 9 patients (effective refractory period 284 ± 57 ms). The mean cycle length of orthodromic reciprocating tachycardia and atrioventricular nodal reentrant tachycardia increased significantly. After flecainide tachycardia was noninducible in 6 patients with orthodromic reciprocating tachycardia and in 1 with atrioventricular nodal reentrant tachycardia. It was inducible but nonsustained (<30 seconds) in 1 patient with orthodromic reciprocating tachycardia and in 3 with atrioventricular nodal reentrant tachycardia. Fifteen patients continued oral flecainide treatment for 19 ± 11 months. Tachycardia recurred in 3 of 4 patients whose arrhythmia was still inducible and sustained after intravenous flecainide, and in 1 of 11 patients in whom tachycardia was noninducible (7 patients) or inducible but nonsustained (4 patients). During long-term administration in 11 patients, flecainide plasma levels, 2 to 3 hours after morning dose, ranged from 254 to 584 μg/liter (370 ± 130). These data suggest that flecainide is a promising drug for short- and long-term therapy of SVT in children.

Intravenous flecainide acetate for supraventricular tachycardias

Flecainide acetate, 2 mg/kg body weight, given intravenously at 10 mg/min was administered to 128 (74 male and 54 female) patients whose ages ranged from 11 to 86 years (mean 44). All patients had supraventricular tachycardias (SVT) that developed spontaneously or were induced during electrophysiologic study. There were 26 patients with atrial flutter, 34 with atrial fibrillation, 7 with ectopic atrial tachycardia, 41 with atrioventricular (AV) reentrant tachycardia and 40 with AV nodal reentrant tachycardia. Twenty patients had more than 1 variety of SVT. Flecainide was administered during SVT to 9 patients with atrial flutter, 11 with atrial fibrillation, 7 with atrial tachycardia, 38 with AV reentrant tachycardia and 34 with AV nodal reentrant tachycardia. In the remaining 31 patients with inducible SVT at electrophysiologic study, flecainide was administered during sinus rhythm. Reinitiation of SVT was attempted in these patients after completion of flecainide administration. Flecainide successfully terminated atrial flutter in 2 patients (22%), atrial fibrillation in 9 (82%), atrial tachycardia in 5 (71%), AV reentrant tachycardia in 32 (84%) and AV nodal reentrant tachycardia in 30 (88%). Reinitiation of SVT was possible in 10 of 26 patients with atrial flutter (38%), 5 of 34 with atrial fibrillation (15%), 3 of 7 with atrial tachycardia (43%), 14 of 41 with AV reentrant tachycardia (34%) and 11 of 40 with AV nodal reentrant tachycardia (27%). In patients with AV reentrant tachycardia and AV nodal reentrant tachycardia, reinitiation occurred when retrograde anomalous pathway refractoriness was not significantly prolonged by intravenous flecainide. Intravenous flecainide is successful in the acute termination of atrial fibrillation, atrial tachycardia, AV reentrant tachycardia and AV nodal reentrant tachycardia but appears to be of limited value for atrial flutter. Reinitiation of SVT may occur despite successful termination.

Treatment of atrial tachyarrhythmias and preexcitation syndrome with flecainide acetate

Sixteen consecutive patients who had ventricular preexcitation complicated by atrial fibrillation or flutter were treated with intravenous flecainide acetate after treatment with as many as 5 unsuccessful trial regimens with other drugs. In 15 patients who had atrial fibrillation, the shortest RR interval during spontaneous episodes was 210 ± 39 ms (mean ± standard deviation), and the average ventricular rate was 208 ± 37 beats/min. Intravenous flecainide prevented induction of atrial fibrillation in 4 of 9 patients and eliminated anterograde accessory pathway conduction in 9 of the 16 patients. In 5 patients whose atrial fibrillation remained inducible and who continued to have preexcitation, the shortest preexcited RR interval increased from 185 ± 29 to 281 ± 46 ms (p < 0.01). Fourteen patients who had favorable responses to intravenous flecainide were given an oral regimen of the drug. Oral treatment was discontinued early because of proarrhythmic effects in 2 patients, and after 2 1 2 months because of headaches in 1 patient. Eleven patients, 5 receiving concomitant β-blockade therapy, have continued to receive a regimen of flecainide for a mean of 21 months (range 3 to 48). Seven patients have had no clinical recurrence of arrhythmias. Recurrences in 4 patients have been rare and brief with no changes in therapy required.

Flecainide acetate for treatment of bypass tract mediated reentrant tachycardia

Flecainide acetate was administered to 19 patients who had inducible sustained orthodromic atrioventricular reentrant tachycardia. Eleven of 18 patients had no inducible tachycardia and 7 patients continued to have inducible tachycardia while receiving flecainide. The effects of flecainide could not be evaluated because of hypotension during intravenous infusion in 1 patient. The main effect of the drug was a selective depression of retrograde conduction over the bypass tract, resulting in abolition of reentry or prolongation of tachycardia cycle length. The electrophysiologic effects of intravenous flecainide were concordant with those of oral flecainide in 5 patients who were studied during both regimens. Fifteen patients were discharged from the hospital on a regimen of flecainide. One patient received concomitant β-blocking therapy. During an average follow-up of 18.5 months (range 2 to 48), 9 patients remained symptom free. Recurrences were observed in 5 patients, 3 of whom still had inducible tachycardia during electrophysiologic testing. Treatment had to be discontinued in 1 patient because of drug intolerance. Thus, flecainide is likely to be effective and well tolerated in the long-term treatment of at least 50% of patients who present with bypass tract mediated orthodromic reentrant tachycardia.

The development and testing of intravenous dosing regimens: application to flecainide for the suppression of ventricular arrhythmias.

A two-part pharmacokinetic approach was used to prospectively develop and test intravenous flecainide infusion regimens for the acute therapy for ventricular arrhythmias. Initially, each of nine known responders to oral flecainide was given a rapid flecainide infusion to characterize pharmacokinetic parameters and determine the minimum effective concentration for each patient. These data were used to calculate individually appropriate three-stage flecainide infusions of predetermined durations in eight patients. The three-stage infusions (0.15 +/- 0.02 mg flecainide acetate/kg/min for 5 minutes, 0.046 +/- 0.004 mg/kg/min for 60 minutes, and 0.31 +/- 0.05 mg/kg/hr for 5 to 47 hours; mean +/- SE) resulted in 95% +/- 0.1% suppression of ventricular ectopic depolarizations. Based on these results, six additional patients received a uniform infusion regimen (0.1 mg/kg/min for 5 minutes, 0.025 mg/kg/min for 2 hours, and 0.25 mg/kg/hr for 46 hours). Supplemental doses of 0.25 mg/kg were given (four doses per patient). With this protocol, ventricular ectopic depolarizations were 82.6% +/- 8.5% suppressed. Measured plasma flecainide concentrations were not significantly different from those predicted by pharmacokinetic models. A prompt and sustained antiarrhythmic effect was obtained with an intravenous regimen of flecainide determined by a prospective pharmacokinetic approach. However, the dosages developed in this study may have to be modified for patients with impaired cardiac or renal function.

Flecainide acetate in the treatment of tachycardias associated with Mahaim fibres.

Patients with Mahaim fibres are susceptible to tachycardias which can be refractory to conventional drug therapy, leading to treatment with surgery and catheter ablation. The effects of flecainide acetate were studied in 3 patients (61, 21 and 35 years of age) with Mahaim fibres presenting with tachycardias refractory to beta-blockers, quinidine and verapamil. One also had ophthalmic side-effects from amiodarone. Three types of tachycardias were induced: a reentrant tachycardia with left bundle branch block morphology (LBBBM) in all 3 patients, atrial flutter in one and atrial fibrillation in another. Intravenous flecainide acetate (2 mg kg-1) terminated reentrant tachycardia and abolished duality of atrioventricular conduction in patient 1. In patient 2, it abolished preexcitation during atrial flutter prior to termination. Atrial fibrillation could not be induced in patient 3 after flecainide acetate. In all patients, retrograde conduction was blocked, preexcitation was not present with atrial pacing and no tachycardia was induced after flecainide. All have remained asymptomatic on oral flecainide acetate (100 mg bd) for a mean follow-up period of 9 months. We conclude that (1) flecainide acetate is effective for the treatment of various tachycardias associated with Mahaim fibres; (2) since different mechanisms responsible for the tachycardia with LBBBM may be present in the same patient and difficult to determine in some, treatment with flecainide acetate which affects both the atrioventricular node and Mahaim fibre conduction may be appropriate for the condition and; (3) its use should be considered before more aggressive therapies.

Chronic flecainide therapy selected by electrophysiology testing of intravenous flecainide

The utility of flecainide acetate was evaluated in 93 patients by means of electrophyslologic studies before and affer 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 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 μg/ml for procainamide. Both fleccainide 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 electrophyslologic testing, and 24 on amiodarone (when all other agents falled). 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. While receiving the acute intravenous administration of flecainide, seven patients developed spontaneous sustained VT (serum level 357 ± 72 ng/ml). Two episodes eventually terminated spontaneously, one required defibrillation, while four patients falled defibrillation but responded to lidocaine. Evaluation with electrophysiologic testing of flecainide administered intravenously appears to predict successful chronic therapy. Flecainide appears well tolerated both intravenously and orally, but does possess a significant incidence of arrhythmogenicity.

Flecainide acetate for conversion of acute supraventricular tachycardia to sinus rhythm

The efficacy of intravenous flecainide acetate (maximum 2 mg/kg or 150 mg given at a rate of 15 mg/min) was assessed in patients with acute supraventricular, tachycardia (SVT) (within 24 hours). Fifty patients were studied, 46 with spontaneous SVT and 4 with induced SVT at. electrophysiologic assessment. Conversion to sinus rhythm was achieved within 45 minutes in 76 %: in 25 patients with atria[ fibrillation (76% conversion), 15 with atrioventricular (AV) nodal or AV reentrant tachycardia (100% conversion) and 10 with atrial flutter or atrial reentrant tachycardia (40% conversion). Adverse effects were noted in 21 patients (42%): paresthesia in 9, drowsiness in 8, nausea in 2, accelerated ventricular rate in 5, ventricular tachycardia in 1, sinus bradycardia in 1 and hypotension in 5. Adverse effects were associated with larger dosage and atrial flutter or atrial reentrant tachycardia. Thus, flecainide acetate is effective in converting to sinus rhythm acute atrial fibrillation and AV nodal and AV reentrant tachycardias, but not atrial flutter or atrial reentrant tachycardia.

Intravenous flecainide acetate for the clinical management of paroxysmal tachycardias.

Intravenous flecainide acetate (2 mg/kg) was administered to 40 patients undergoing routine electrophysiological evaluation for the investigation of recurrent paroxysmal tachycardias. Ten patients had recurrent atrial flutter, 11 patients had recurrent atrial fibrillation, one of whom also had paroxysmal left atrial tachycardia, and 19 patients had recurrent ventricular tachyarrhythmias (17 with recurrent ventricular tachycardia and 2 with recurrent fascicular tachycardia). Flecainide was administered during tachycardia (over 5 to 10 minutes) to all patients with atrial flutter, to 10 patients with atrial fibrillation, and to 17 patients with ventricular tachyarrhythmias. In the remaining 3 patients with ill-sustained arrhythmias flecainide was administered during sinus rhythm and reinitiation of tachycardia was then attempted. Flecainide restored sinus rhythm in only 2 patients with atrial flutter (20%), in 9 patients with atrial fibrillation (90%), in 12 patients with ventricular tachycardia (80%), and in one of the 2 patients with fasicular tachycardia. Flecainide also successfully terminated the left atrial tachycardia. Two patients experienced proarrhythmic side effects during flecainide administration, one of whom required intervention by cardioversion. Minor dose effects included oral paresthesia, transient drowsiness or dizziness, and occasional visual blurring. Flecainide acetate is an effective antiarrhythmic agent for the acute termination of recent onset paroxysmal atrial and ventricular tachyarrhythmias.

The response of paediatric arrhythmias to intravenous and oral flecainide.

Flecainide acetate was administered intravenously and orally to 12 consecutive children, aged 1-15 years, presenting with arrhythmias that were life threatening or resistant to conventional medical treatment. Three children had arrhythmias related to Wolff-Parkinson-White syndrome, four had concealed accessory pathways, two had His bundle tachycardia, and three had ventricular tachycardia. Of seven patients who were given flecainide intravenously, four returned to sinus rhythm and in a fifth successful rate control of His bundle tachycardia was achieved. All 12 patients were given the drug orally: in nine it was successful in preventing recurrence of arrhythmia, in one satisfactory rate control was achieved, and in two it was withdrawn because it produced more frequent attacks of tachycardia. No other adverse effects occurred. The efficacy and low toxicity of treatment in this study suggests that flecainide acetate may have an important role in the management of selected paediatric arrhythmias.

Effect of flecainide on regional left ventricular wall motion after acute intravenous, acute oral and chronic oral administration late after coronary artery bypass grafting

Epicardial marker motion was measured in 14 patients before flecainide administration, immediately after an intravenous dose of 2 mg/kg over 15 minutes (maximum 150 mg) and 15 minutes thereafter. Platinum epicardial markers had been implanted more than 4 years earlier at the time of coronary artery bypass grafting. Maximal and minimal marker separation (Lmax and Lmin) during the cardiac cycle were measured and regional shortening fraction (Lmax — Lmin)/Lmax) was determined as a percentage. After intravenous flecainide, a significant increase in end-diastolic (immediately after 2.8%; after 15 minutes 2.1%) and end-systolic (3.6% and 3.2%) regional dimensions was observed, together with a decrease in regional myocardial shortening (9.3% and 9.0%). One week later, after a single oral dose of 200 mg of flecainide, Lmax and Lmin had increased 2.4% and 2.7%, while regional myocardial shortening did not differ significantly from baseline values. In 10 patients measurements were repeated after 6 weeks of chronic oral treatment with 300 mg/day. Despite plasma flecainide levels similar to those after intravenous administration, no significant changes in end-diastolic and end-systolic dimensions or regional shortening fraction were observed. Thus, acute intravenous or oral flecainide administration increases regional end-diastolic and end-systolic dimensions, but only intravenous administration decreases regional shortening fraction. Values during chronic administration indicate that regional myocardial function is more affected at the time of rising or acutely changing flecainide plasma levels than when stable plasma levels are achieved.

Treatment of paroxysmal reentrant supraventricular tachycardia with flecainide acetate

The electrophysiologic effects and therapeutic efficacy of intravenous and oral flecainide were studied in 15 patients with spontaneous and inducible sustained paroxysmal supraventricular tachycardia (SVT). Twelve patients had atrioventricular (AV) reentrance using an accessory pathway for retrograde conduction and 3 had AV nodal reentrance. Fourteen patients received intravenous flecainide (2 mg/ kg body weight over 15 minutes) during an initial electrophysiologic study. Nine patients were restudied during oral flecainide administration (200 to 400 mg/day). After intravenous or oral flecainide therapy, reentrant SVT was noninducible in 6 patients with AV reentrance and in the 3 with AV nodal reentrance. In these 9 patients, intravenous flecainide prevented induction of reentrant SVT by depressing conduction over the retrograde limb of the reentry circuits. In the 6 patients with inducible sustained AV reentrant SVT before and after flecainide therapy, the cycle length of tachycardia increased significantly, mainly as the result of an increase in ventriculoatrial conduction time. There was concordance between the intravenous and the oral effects of flecainide on the mechanism of the SVT. Twelve patients continued oral flecainide treatment for a mean of 16 months (range 5 to 28). Tachycardia recurred in 3 of 4 patients whose arrhythmia remained inducible after flecainide therapy and in 1 of 8 patients whose SVT was suppressed. It is concluded that flecainide is an effective and convenient antiarrhythmic agent to treat patients who have AV nodal or AV reentrant SVT.