Effects of disopyramide on electrophysiological properties of specialized conduction system in man and on accessory atrioventricular pathway in Wolff-Parkinson-White syndrome.

Spurrell, R. A. J.; Thorburn, Charles W.; Camm, John; Sowton, Edgar; Deuchar, D C

doi:10.1136/hrt.37.8.861

Cited by 101 publications

(21 citation statements)

References 11 publications

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“…This distinction is of some importance because the effect of intravenous disopyramide may be very different in each of these arrhythmias for reasons discussed above. The results obtained in patients with paroxysmal atrioventricular tachycardia in the WPW syndrome are similar to those demonstrated in previous reports (Spurrell et al, 1975;Camm & Spurrell, 1977). In one case, however, there was marked acceleration of the tachycardia prior to termination.…”

Section: Discussionsupporting

confidence: 80%

“…Disopyramide also increases action potential duration (Sekiya & Vaughan-Williams, 1963) and tissue refractoriness (Gough, Driefus, De Azevedo & Katz, 1974;Danilo & Rosen, 1976) in in vitro preparations. In man, the drug has been shown to increase the refractory period of the atrial and venricular myocardium (Befeler, Castellanos, Wells, Vaguiero, Yen & Myerburg, 1975;Josephson, Caracta, Lau, Gallagher & Damato, 1973) and direct A-V anomalous bundles (Spurrell, Thorburn, Camm, Sowton & Deuchar, 1975;Camm & Spurrell, 1977). The effect on the A-V node is variable and depends on the balance between the direct and anti-cholinergic effects of the drug (Birkhead & Vaughan-Williams, 1977).…”

Section: Discussionmentioning

confidence: 99%

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The effect of intravenous disopyramide phosphate on recurrent paroxysmal tachycardias.

Camm¹,

Ward²,

Spurrell³

1979

Brit J Clinical Pharma

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1 Recurrent paroxysmal atrial, atrioventricular and ventricular tachycardias in 50 patients without acute coronary insufficiency, heart failure or metabolic abnormality were treated with disopyramide phosphate in a dose of 2 mg/kg body weight infused over 5 min. 2 Conversion to sinus rhythm within 10 min of the completed infusion occurred in 10 of 14 (7 1%) patients with paroxysmal 'lone' atrial fibrillation, 3 of 7 (43%) patients with paroxysmal atrial flutter, 6 of 9 (67%) patients with paroxysmal atrial tachycardia, 5 of 9 (56%) patients with paroxysmal atrioventricular tachycardia associated with the Wolff-Parkinson-White syndrome and 8 of 11 (73%) patients with paroxysmal ventricular tachycardia. 3 Side effects: significant systemic hypotension in 3, high grade AV block in 1, an increased ventricular response producing symptoms in 4, post conversion asystole in 1 and sinus bradycardia in 2. 4 The anti-arrhythmic effect and arrhythmogenic side effects may be related to both the direct membrane stabilizing effect and the anticholinergic effect of disopyramide.

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Section: Discussionsupporting

confidence: 80%

Section: Discussionmentioning

confidence: 99%

The effect of intravenous disopyramide phosphate on recurrent paroxysmal tachycardias.

Camm¹,

Ward²,

Spurrell³

1979

Brit J Clinical Pharma

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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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“…In addition, it has been used successfully in the treatment of a variety of arrhythmias (Hirtel, Louhija & Konttinen, 1974;Mizgala & Huvelle, 1976;Niarchos, 1976). It acts principally by slowing conduction in the His-Purkinje system and by increasing the effective refractory period of the atria and ventricles (Spurrell, Thorburn, Camm, Sowton & Deuchar, 1975). Recent work has indicated a dual effect on atrial and atrioventricular conduction and refractory periods (Birkhead & Vaughan Williams, 1977).…”

Section: Disopyramidementioning

confidence: 99%

Disopyramide serum and pharmacologic effect kinetics applied to the assessment of bioavailability.

Bryson¹,

Whiting²,

Lawrence³

1978

Brit J Clinical Pharma

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I Serum, urine and pharmacologic effect (prolongation of the QT interval) kinetics of the antiarrhythmic disopyramide have been investigated in eight volunteers after intravenous administration (2 mg/kg) and oral administration (300 mg) of the two commercially available preparations, Rythmodan (Roussel Laboratories) and Norpace (Searle Laboratories). 2 An open one compartment body model adequately described the kinetics of disopyramide in serum and urine. 3 After intravenous administration, the following average pharmacokinetic parameters were found: biological half-life, 7.8 h; total clearance, 95 ml/min; renal clearance, 54 ml/min; apparent volume of distribution, 60 litres. 4 After oral Rythmodan and Norpace, serum concentration profiles and urinary excretion data revealed significant differences in rates of absorption, times required to achieve peak serum concentrations and biological half-lives. These differences were largely due to the relatively slow absorption characteristics of Norpace. SThe absence of hysteresis in plots of QT prolongation against disopyramide serum concentration after oral administration indicated that serum and pharmacologic effect kinetics were indistinguishable within a kinetically equivalent compartment. 6 Analysis of both serum and urine data showed that while Norpace had a significantly higher degree of bioavailability (P< 0.005), the 5-15% difference between the two formulations should not normally be of any clinical significance.

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Effects of disopyramide on electrophysiological properties of specialized conduction system in man and on accessory atrioventricular pathway in Wolff-Parkinson-White syndrome.

Cited by 101 publications

References 11 publications

The effect of intravenous disopyramide phosphate on recurrent paroxysmal tachycardias.

The effect of intravenous disopyramide phosphate on recurrent paroxysmal tachycardias.

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

Disopyramide serum and pharmacologic effect kinetics applied to the assessment of bioavailability.

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