Efficacy and safety of flecainide acetate for atrial tachycardia or fibrillation

Berns, Ellison; Rinkenberger, Robert L.; Jeang, Ming K.; Dougherty, Anne H.; Jenkins, Mary Ann; Naccarelli, Gerald V.

doi:10.1016/0002-9149(87)90915-5

Cited by 86 publications

(10 citation statements)

References 19 publications

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“…Twenty-eight patients in each group were evaluated, and at 6 months, 81% of the patients receiving flecainide were still in sinus rhythm compared with 44% in the group of patients receiving disopyramide (p<0.01). 16 The fact that these patients were not previously DC converted or prophylactically treated may explain the high success rate for flecainide, whereas the somewhat low disopyramide efficacy is more difficult to explain except by the few patients comprising each group, which increases the risk of results not reproducible in larger series of patients.…”

Section: Discussionmentioning

confidence: 99%

Sotalol versus quinidine for the maintenance of sinus rhythm after direct current conversion of atrial fibrillation.

1990

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This open, parallel-group study compares quinidine and sotalol treatment for maintenance of sinus rhythm after direct current conversion of patients with chronic atrial fibrillation. The patients from 15 centers in Sweden were randomized to sotalol (98 patients) or quinidine (85 patients) after 2 hours of sinus rhythm after direct current conversion. According to primary efficacy assessment, 52% of the patients in the sotalol group and 48% of the patients in the quinidine group remained in sinus rhythm during the following 6-month treatment period (NS). Furthermore, 34% of the patients treated with sotalol and 22% of the patients treated with quinidine relapsed into atrial fibrillation (NS). Heart rate after relapsing into atrial fibrillation was higher in the patients treated with quinidine (109 beats/min) than in the patients treated with sotalol (78 beats/min, p

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Section: Discussionmentioning

confidence: 99%

Sotalol versus quinidine for the maintenance of sinus rhythm after direct current conversion of atrial fibrillation.

1990

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“…We chose flecainide as the prototype class IC drug for study because it has been the IC agent most extensively evaluated in the treatment of atrial fibrillation. [10][11][12][13][14][15][16][17][18][19] Quinidine was chosen as a reference class IA compound because of its widespread and longstanding use in the treatment of atrial fibrillation. 31 We compared the effects of flecainide with those of quinidine on atrial action potentials as a function of activation rate, using tissue from patients undergoing coronary artery bypass surgery, as well as from three animal species (guinea pigs, rabbits, and dogs).…”

Section: Wanzg Et Al Effects Of Flecainide and Quinidine On Atrial Acmentioning

confidence: 99%

Effects of flecainide and quinidine on human atrial action potentials. Role of rate-dependence and comparison with guinea pig, rabbit, and dog tissues.

et al. 1990

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Flecainide and other class IC antiarrhythmic drugs are effective in the prevention and termination of atrial fibrillation, but the mechanism of this action is unknown. To gain insights into potential cellular mechanisms, we evaluated the response of human atrial action potentials to equimolar therapeutic concentrations of flecainide and quinidine and compared this response to that of guinea pig, rabbit, and dog atria. Both compounds reduced Vm, more as activation rate increased, but flecainide was more potent than quinidine and had slower kinetics. The rate-dependence of Viax reduction was similar for all species, but human tissue was more sensitive to the drugs tested. In contrast to changes in Vmax, drug-induced alterations in action potential duration showed opposite rate-dependence for the two drugs. Quinidine increased action potential duration to 95% repolarization (APD95) in human atria by 33±7% (mean+SD) at a cycle length of 1,000 msec, but this effect was reduced as cycle length decreased, to 12+±4% (p

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“…It appears that the stability of sinus rhythm may be dependent on a certain length of the voltage-dependent refractoriness in atrial muscle [8]. Furthermore, drugs such as flecainide that markedly depress conduction velocity may aggravate or perpetuate atrial flutter [30]. Studies of the effects of antiarrhythmic drugs in an anatomic obstacle model of atrial flutter in the dog also support this contention [9][10]12].…”

Section: Possible Mechansisms Of the Antiarrhythmic Action Of N-acetymentioning

confidence: 98%

Oral N-acetylprocainamide compared to quinidine plus digoxin in the chronic suppression of atrial flutter in humans

Feld

Nademanee

Нолль

et al. 1989

Cardiovasc Drug Ther

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Antiarrhythmic therapy for the suppression of atrial flutter has conventionally entailed the use of a class Ia agent such as quinidine or procainamide. However, atrial flutter often recurs despite the use of these conventional antiarrhythmic regimens. Experimental and clinical evidence suggests that the pharmacologic suppression of atrial flutter may depend on the prolongation of the atrial action potential duration and consequently the voltage-dependent refractoriness. Therefore, the efficacy and tolerance of the class III antiarrhythmic agent N-acetylprocainamide was compared to that of the conventional regimen of the class Ia agent quinidine combined with digoxin (to control ventricular response) in patients with a history of symptomatic sustained atrial flutter. The study was randomized but nonblinded, with a crossover to the alternate regimen if the first failed. Eighteen patients entered the study and were followed for up to 18 months. Of the 12 receiving N-acetylprocainamide (eight randomized and four crossovers), one (8%) failed therapy due to side effects, but none had atrial flutter. Of the 11 receiving quinidine and digoxin (10 randomized and one crossover), three (28%) had a recurrence of atrial flutter, two of whom also had intolerable side effects, and two more (18%) had side effects alone requiring withdrawal of therapy (total 46% failed). The probability of therapeutic success over time was greater (p less than 0.04) for N-acetylprocainamide than for quinidine and digoxin. The data suggest that N-acetylprocainamide may be more effective and better tolerated than the conventional regimen of quinidine plus digoxin. Therefore, large-scale blinded studies of the efficacy of N-acetylprocainamide in the suppression of atrial flutter may be warranted.

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Efficacy and safety of flecainide acetate for atrial tachycardia or fibrillation

Cited by 86 publications

References 19 publications

Sotalol versus quinidine for the maintenance of sinus rhythm after direct current conversion of atrial fibrillation.

Sotalol versus quinidine for the maintenance of sinus rhythm after direct current conversion of atrial fibrillation.

Effects of flecainide and quinidine on human atrial action potentials. Role of rate-dependence and comparison with guinea pig, rabbit, and dog tissues.

Oral N-acetylprocainamide compared to quinidine plus digoxin in the chronic suppression of atrial flutter in humans

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