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 56,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Flecainide acetate is a new orally active antidysrhythmic agent classified in the Ic category. Flecainide is effective in suppressing 88 to 100 percent of abnormal cardiac rhythms in the form of complex ventricular dysrhythmias, including couplets, ventricular tachycardia, reentrant junctional tachycardia, and Wolff-Parkinson-White syndrome. Flecainide appears to have a greater effect on conduction than on repolarization and only minimal effects on hemodynamic parameters. Flecainide is rapidly and completely absorbed after oral administration and has a 13-hour elimination half-life, allowing for twice-daily dosing regimens. Flecainide is generally well tolerated, with dizziness, blurred vision, nausea, and headache the most common side effects. Flecainide has been shown to be superior to quinidine and disopyramide in suppressing ventricular ectopic activity and may be considered a first-line oral agent for this indication. It is believe that flecainide has enough therapeutic advantages to be added to drug formularies.
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PMID:Flecainide: a new class Ic antidysrhythmic. 390 29

The efficacy of the new class Ic anti-arrhythmic (aa) drug, Flecainide, has been evaluated in patients (pts) affected by frequent and/or severe chronic ventricular arrhythmias (VA), as assessed by 24 hours Holter monitoring and maximal exercise stress testing. The protocol consisted in a preliminary screening with multiple aa drugs (average 6.0 per pt) using the acute oral drug testing. The most effective drug was then given for 72 hours and 24 hours Holter monitoring and exercise stress testing repeated; if the efficacy was confirmed, chronic treatment was initiated and control visits were repeated after 3, 6 and 12 months. The study population consisted of 27 pts; 22 (81%) were in Lown class 4A (18%) or 4B (63%). Eight pts (30%) had a previous (greater than 1 year) myocardial infarction, while in 14 (52%) no evidence of cardiac disease was found. During acute oral drug testing a positive response (reduction of PVC's greater than 90% and abolition of grades 4A and 4B) was obtained with Flecainide, 200 mg, in 20 pts (74%). In 6 pts (22%) no effect was observed, while a possible proarrhythmic effect was observed in 1 pt (4%). Eighteen pts entered the second phase of the study with an average dose of Flecainide of 175 mg b.i.d. In 83% of the pts there was a positive concordance between the acute oral testing and the 72 hours treatment, as in 15 out of 18 pts grades 4A and 4B were totally abolished and the mean frequency of PVC's was reduced by 99%. In 3 pts (17%) no response was observed. Flecainide increased significantly PR (37 msec), QRS (20 msec) and QTc (28 msec). The plasma levels attained with chronic therapy (846 ng/ml) were higher than those achieved with the acute oral testing (372 ng/ml). Mild side effects (dizziness, tremor and headache) were observed in 33% of the pts and were all eliminated by a 100 mg reduction in Flecainide dose. Fifteen pts entered the third phase (long term treatment): in this group there was a 93.3% correlation with phase two, as in 14 out of 15 pts there was a complete abolition of grade 4B arrhythmias, a 98.8% reduction of couplets and a reduction in the number of PVC's greater than 85%. This study shows that Flecainide is a quite powerful aa drug with modest side effects. Its efficacy against chronic VA is high, also when compared to the most effective and available aa drugs.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Evaluation of flecainide in the therapy of chronic ventricular arrhythmia using the acute oral load method]. 401 65

The antiarrhythmic efficacy and safety of oral flecainide acetate and quinidine sulfate were compared in a double-blind, 16-center parallel trial involving 280 patients with chronic premature ventricular complexes (PVCs). Eighty-five percent of the flecainide patients had at least 80% suppression of PVCs, vs 57% of the quinidine patients (p less than 0.0001). Sixty-eight percent of the flecainide patients met the above criterion and also had complete suppression of couplets and beats of ventricular tachycardia, vs 33% of the quinidine patients (p less than 0.0001). PR and QRS intervals were prolonged by flecainide without clinical consequence, but they were not substantially affected by quinidine (p less than 0.0001). Quinidine prolonged JT (QT minus QRS) intervals significantly more than flecainide (p less than 0.05). Nineteen of 141 flecainide patients and 21 of 139 quinidine patients discontinued therapy because of side effects (p greater than 0.50). Flecainide side effects included dizziness, blurred vision, headache and nausea. Quinidine side effects included diarrhea, nausea, headache and dizziness. Flecainide was more effective than quinidine in suppressing chronic ventricular arrhythmias (especially complex forms), and thus is an important new antiarrhythmic agent.
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PMID:Flecainide versus quinidine for treatment of chronic ventricular arrhythmias. A multicenter clinical trial. 633 10

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.
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PMID: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. 860 95

Flecainide is a sodium channel blocker used mainly in the treatment of supraventricular arrhythmias. Central nervous system side effects such as dizziness, visual disturbances, headache and nausea are commonly associated with flecainide, but severe central nervous system toxicity is rare. We report the first case of flecainide toxicity in a patient with end-stage renal failure. Cessation of flecainide therapy resulted in a fall in serum flecainide levels, with associated resolution of adverse central nervous system effects. We also review the pharmacokinetics of flecainide in patients with chronic kidney disease.
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PMID:Paranoid psychosis and myoclonus: flecainide toxicity in renal failure. 1837 17

Flecainide is a class 1c antiarrhythmic that acts by blocking sodium channels to reduce intracardiac conduction and is used mainly in the treatment of supraventricular arrhythmias. Dizziness, visual disturbances, headache, and nausea are commonly associated with flecainide, but severe central nervous system toxicity is rare. Here, we report the case of a 71-year-old woman with a history of renal transplantation who developed severe myoclonus 24 hours after being started on flecainide, 100 mg 2 times a day, because of atrial fibrillation. This symptom completely disappeared once the drug was removed. Only 2 patients presenting with flecainide-induced myoclonus have been previously reported. Although the exact pathophysiologic explanation of this phenomenon remains unclear, it is well known that the susceptibility to severe flecainide toxicity is increased in patients with chronic kidney disease.
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PMID:Flecainide-induced myoclonus. 2461 65