Disopyramide in the prevention of recurrence of atrial fibrillation after electroconversion

Härtel, Gottfried; Louhija, Antti; Konttinen, Aarne

doi:10.1002/cpt1974156551

Cited by 95 publications

(11 citation statements)

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“…[1][2][3][4][5][6] This variability may be attributed to the relative efficacy of disopyramide's opposing dual effects and to the underlying cholinergic tone. The results of the present study suggest that disopyramide has dual actions on isolated normal sinus node of the rabbit at therapeutic concentrations, and the response to these dual actions mostly depend on the underlying cholinergic tone of the tissue and on the concentration of the drug.…”

Section: Discussionmentioning

confidence: 99%

The cellular electrophysiologic mechanism of the dual actions of disopyramide on rabbit sinus node function.

Katoh¹,

Karagueuzian²,

Jordan³

et al. 1982

Circulation

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To determine the contribution of disopyramide's suggested opposing direct depressant and indirect acceleratory actions on sinus node function, we studied the effects of disopyramide, 1 x 10(-7) to 1 x 10(-4) M, on isolated rabbit sinus node preparations using standard microelectrode techniques. Transmembrane potentials were recorded simultaneously from the sinus node and adjoining crista terminalis area. Disopyramide, as much as 1 x 10(-5) M, had no effects on the sinus cycle length. At a concentration of 1 x 10(-4) M, sinus cycle length was significantly prolonged due to prolongation of the sinus nodal action potential duration. During cholinergic blockade with atropine, 1 x 10(-6) M, disopyramide, 1 x 10(-7) to 1 x 10(-4) M, significantly prolonged sinus cycle length as a result of a prolongation of the sinus nodal action potential duration and a decrease of the slope of phase 4 depolarization. During cholinergic stimulation with carbamyl choline, 1 x 10(-9) M, disopyramide, 1 x 10(-7) to 1 x 10(-6) M, tended to reverse carbamyl choline-induced prolongation of the sinus cycle length (NS). This acceleratory action of disopyramide was caused by a significant increase of the slope of phase 4 depolarization. Disopyramide, 1 x 10(-7) to 1 x 10(-4) M, had no significant effects on corrected sinus node recovery time or on sinoatrial conduction time under any conditions studied. We conclude that disopyramide has a direct depressant action on normal sinus node cells at the upper therapeutic and toxic levels, which is enhanced during cholinergic blockade, and that disopyramide's acceleratory action appears only at much lower concentrations and only during cholinergic stimulation.

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Section: Discussionmentioning

confidence: 99%

The cellular electrophysiologic mechanism of the dual actions of disopyramide on rabbit sinus node function.

Katoh¹,

Karagueuzian²,

Jordan³

et al. 1982

Circulation

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“…The electrophysiologic effects of disopyramide phosphate have been studied in sinus node, atrioventricular node and atrial and ventricular muscle.6"18 The effects of the drug reflect a balance between the direct prolongation of refractoriness and the anticholinergic effect of the drug.25 27 In clinical studies, disopyramide has been shown to be effective in reducing both premature ventricular or atrial complexes and atrial arrhythmias.6' 25,26,[28][29][30][31][32][33][34][35][36][37][38] Spurrell et al8 examined the effects of i.v. disopyramide, 2 mg/kg, in three patients with WPW.…”

Section: Discussionmentioning

confidence: 99%

Electrophysiologic effects of disopyramide phosphate in patients with Wolff-Parkinson-White syndrome.

Kerr¹,

Prystowsky²,

Smith³

et al. 1982

Circulation

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“…This opinion arises from a double-blind controlled study of Haertel et al [142], in which disopyramide was more effective than a placebo and as effective as quinidine in preventing AF relapses; however, another study [143] comparing the relative efficacy of quinidine, disopyramide, and a placebo at 6 months after AF cardioversion did not show significant difference among the three groups in the number of patients maintaining sinus rhythm.…”

Section: Drug Prophylaxis Of Atrial Fibrillationmentioning

confidence: 96%

The pharmacologic treatment of atrial fibrillation

Bolognesi

1991

Cardiovasc Drug Ther

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The pharmacologic treatment of atrial fibrillation (AF) is aimed at controlling the ventricular response, restoring sinus rhythm, and preventing or delaying relapses. In the control of ventricular response, digitalis maintains a primary role when the arrhythmia is accompanied by heart failure. In ischemic, hypertensive, and degenerative (whose number is increasing at present) cardiopathies without evident ventricular dilatation, treatments with calcium antagonists (such as verapamil, gallopamil, or diltiazem) or beta-blocking agents must be preferred. In order to control the ventricular response in patients with chronic AF during physical activity, the association of digitalis with beta-blocking agents or calcium antagonists seems to provide satisfactory results. The drugs of the IC class, especially flecainide, represent a certain therapeutical progress in the restoration of sinus rhythm in the treatment of paroxysmal atrial fibrillation affecting subjects without evident alterations of ventricular function, particularly in subjects with Wolff-Parkinson-White syndrome, with forms of vagal origin, or with atrial fibrillation alone. A therapeutic combination of digitalis and quinidine may produce resolution of the arrhythmia in the presence of altered ventricular function or when AF is of an uncertain onset. In patients with hypertensive, ischemic, and/or degenerative cardiopathy without evident ventricular or advanced heart failure, the verapamil-quinidine association may also be effective and even quicker. The combination of drugs of the I and III class for restoration of the sinus rhythm in particularly resistant forms of AF without evident structural heart alterations is promising but must be verified in a greater number of patients. In the prevention of relapses amiodarone appears to have the widest spectrum of advantages from an electrophysiologic point of view; however, because of its many side effects, amiodarone represents a late therapeutical choice. The promising results obtained with flecainide are disputed by the results of the CAST, which limit the possibilities of using this drug to a low number of cases (W.P.W. syndrome, AF of vagal origin, atrial fibrillation alone). In the past, quinidine and disopyramide have been the drugs most widely used in the prophylaxis of AF. These drugs have a similar efficacy, and both of them provided some positive results. However, because of untoward side effects (especially for quinidine) during chronic treatment, the use of these drugs has been questioned. Perhaps in the majority of patients, the less dangerous therapeutic choice after the termination of the fibrillation is a combination of drugs slowly down AV node activity (digitalis or calcium antagonists and beta blockers) with class IA antiarrhythmics.

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Disopyramide in the prevention of recurrence of atrial fibrillation after electroconversion

Cited by 95 publications

References 0 publications

The cellular electrophysiologic mechanism of the dual actions of disopyramide on rabbit sinus node function.

The cellular electrophysiologic mechanism of the dual actions of disopyramide on rabbit sinus node function.

Electrophysiologic effects of disopyramide phosphate in patients with Wolff-Parkinson-White syndrome.

The pharmacologic treatment of atrial fibrillation

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