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Query: UMLS:C0012833 (dizziness)
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The efficacy of flecainide acetate in suppressing ventricular premature contractions in 14 patients was evaluated in a double-blind, cross-over, placebo controlled, randomized and balanced study. Each treatment period was 2 weeks followed by a 3-4 d placebo washout period and the study lasted 5 weeks. Flecainide was given in a dose of 200 mg twice daily. A significant reduction in the total number of QRS complexes in a 24 h period was observed during the active compared with placebo treatment (P less than 0.05). In comparison with placebo, flecainide reduced the number of aberrant and premature aberrant QRS complexes (P less than 0.01). The mean suppression rate of aberrant QRS complexes during flecainide treatment was 85.4% and that of premature aberrant complexes was 93.2%. Maximum heart rate measured by 24 h ECG decreased significantly during flecainide therapy (P less than 0.01), although no change occurred with resting heart rate measured clinically or by ECG. Severe dizziness associated with flecainide therapy necessitated withdrawal of 2 patients from the study. A proarrhythmic effect of flecainide, ventricular tachycardia, was observed in one patient.
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PMID:Evaluation of the efficacy of flecainide acetate in the treatment of ventricular premature contractions. 240 43

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.
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PMID:Intravenous flecainide acetate for the clinical management of paroxysmal tachycardias. 310 95

The electrophysiologic effects and antiarrhythmic efficacy of flecainide were evaluated by electrophysiologic study (EPS) in 20 patients with ventricular tachycardia (VT) refractory to an average 2.9 drugs. In 19 patients EPSs were performed with patients not receiving antiarrhythmic medications and receiving oral flecainide therapy at steady state (mean dose, 235 +/- 67 mg/day). Flecainide significantly increased the QRS complex duration (27%, P less than .001), PR interval (17%, P less than .001), and right ventricular effective refractory periods 8.5% and 21.1% (P less than .01) for the first and second extrastimuli, respectively. During baseline EPS, 17 patients were induced into VT and two were noninducible. Flecainide prevented EPS-induced VT in five patients and the induced VT became slow and hemodynamically stable in three. Two patients who failed flecainide monotherapy were induced into slow hemodynamically stable VT with flecainide in combination with amiodarone. The two noninducible patients, during baseline EPS, had suppression of spontaneous VT with flecainide. Overall, 13 of 20 patients received flecainide either alone or in combination with amiodarone for chronic therapy. Side effects encountered during the study consisted of blurred vision, dizziness, weakness, lethargy, nausea, worsened heart failure and bradyarrhythmias. After a mean 9-month follow-up (3 to 16 months) nine patients remain on flecainide therapy. There were three recurrences of slow, hemodynamically stable VT and no episodes of sudden death. Low-dose flecainide, either alone or in combination with other agents, is effective therapy for certain patients with refractory VT but heart failure remains a significant concern in patients with depressed left ventricular function.
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PMID:Clinical and electrophysiologic effects of flecainide in patients with refractory ventricular tachycardia. 312 56

The efficacy of flecainide acetate for conversion of atrial fibrillation into sinus rhythm was assessed in 69 patients (mean age of 63 +/- 14 years). Mean duration of the arrhythmia was 49 +/- 45 days. Mean cardiothoracic index was 0.49 +/- 0.03. Flecainide treatment was started intravenously with a bolus of 2 mg/kg over 10 minutes, followed by oral treatment (200 to 300 mg/day) according to body weight. Conversion to sinus rhythm was obtained in 49 patients (71%). The mean delay between initiation of treatment and restoration of sinus rhythm was 301 minutes (range 5 to 1,600). The left atrial diameter was smaller (40 +/- 1 mm) in patients who had successful cardioversion than in those who did not (46 +/- 1 mm) (p less than 0.05). Patients with atrial fibrillation lasting for less than 10 days had a higher conversion rate (79%) than patients with long-standing atrial fibrillation, in whom the conversion rate was only 38% (p less than 0.05). Conversion to sinus rhythm occurred in 33 patients during the first 5 minutes after injection. Adverse effects necessitated discontinuation of treatment in 4 patients (5.8%). Gastrointestinal disorders and dizziness occurred in 5 other patients but did not necessitate discontinuing treatment. In conclusion, flecainide is an effective drug for converting atrial fibrillation into sinus rhythm. Unlike quinidine, flecainide can be administered intravenously. The conversion rate with flecainide is higher in patients with a shorter duration of atrial fibrillation and smaller atria.
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PMID:Restoration of sinus rhythm with flecainide in patients with atrial fibrillation. 313 34

Flecainide acetate is a new class 1 c antiarrhythmic drug. It slows conduction in the working myocardium and the specialized conduction system and may depress sinus node activity in patients with pre-existing sinus node disease. Its hemodynamic effects are minimal. The drug is completely absorbed and shows a half-life of 7-22 hours. Elimination is mainly through the kidneys. Flecainide is highly effective in the treatment of ventricular arrhythmias, pre-excitation syndromes and AV reentry tachycardias. Side effects are mild and consist mostly of dizziness, visual disturbances, and nervousness. They rarely require discontinuation of therapy. Proarrhythmic effects have been reported. Caution is required in patients with congestive heart failure, AV block, and/or bundle-branch block or sinus node dysfunction.
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PMID:Flecainide: a new antiarrhythmic drug. 351 Jul 88

Flecainide is a Class I antiarrhythmic drug of the local anaesthetic type. It can be given either intravenously or orally and its pharmacokinetic properties allow relatively long (12 hours) dosing intervals with oral administration. In several open and a few controlled therapeutic trials, orally administered flecainide has brought about a greater than 90% suppression of ventricular ectopic beats in about 80% of patients. A similar percentage of patients (83%) experienced at least an 80% suppression of their ventricular tachycardia in these trials. A slightly greater response rate was reported with intravenous infusion of flecainide. Initial results in arrhythmias complicating the Wolff-Parkinson-White syndrome have been favourable. Comparative trials are few in number but flecainide has proved to be more effective than quinidine, and possibly more effective than disopyramide, mexiletine, tocainide and propafenone, in suppressing ventricular ectopic activity. The most commonly reported extracardiac adverse effects have been dizziness and visual disturbances. Proarrhythmic effects have been reported in 7 to 8% of patients, with a higher incidence in patients with serious ventricular tachycardia and reduced myocardial function. The moderate negative inotropic effects of flecainide can become clinically significant in patients with impaired ventricular function. Thus flecainide, with its convenient dose schedule and apparently low incidence of serious side effects, would appear to be a useful addition to the antiarrhythmic agents available. Further studies are needed though, to confirm its long term tolerability when used prophylactically.
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PMID:Flecainide. A preliminary review of its pharmacodynamic properties and therapeutic efficacy. 388 90

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

The effectiveness and safety of intravenous flecainide was evaluated in 33 patients with chronic high frequency premature ventricular complexes (mean value of PVCs 23.7 min-1). Flecainide was injected intravenously at a rate of 20 mg per 2 min until complete disappearance of ventricular arrhythmias or up to a total dose not exceeding 200 mg. Total suppression of PVCs occurred in 31 out of 33 patients at the end of the injection (mean dose 132 mg). The overall reduction of PVCs was 94 per cent (P less than 0.001) at the end of infusion and 74 per cent (P less than 0.001) 1 h later. The mean plasma drug level attained 1 h after administration was 287 ng ml-1 (range 82-984). Heart rate and blood pressure did not change, but a significant increase (P less than 0.001) in PR (+12%), QRS (+13%) and QTc (+4%) duration occurred after drug administration. Flecainide was well tolerated. An idioventricular tachycardia was induced in one patient and two patients experienced side effects of the central nervous type: dizziness, blurring of vision and a sensation of warmth. In view of its activity flecainide appears to be a valuable addition to the antiarrhythmic armamentarium.
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PMID:Efficacy and tolerance of intravenous flecainide in patients with chronic high frequency ventricular arrhythmias. 639 56


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