Reverse Use Dependence of Antiarrhythmic Class la, Ib, and Ic: Effects of Drugs on the Action Potential Duration?

Langenfeld, Heiner; Köhler, Christiane; Weirich, J.; Kirstein, Michael; Kochsiek, K

doi:10.1111/j.1540-8159.1992.tb03028.x

Cited by 3 publications

(1 citation statement)

References 12 publications

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“…Flecainide has a high affinity for sodium channels in the open state and the effect is therefore strongly use dependent . Flecainide also has some blocking effects on potassium channels, but this effect is decreased at higher HRs (reverse use dependency) . Consequently, increased HR will result in a greater decrease in ventricular conduction velocity by flecainide and could lead to increased risk of re‐entry arrhythmias .…”

Section: Discussionmentioning

confidence: 99%

Time‐dependent antiarrhythmic effects of flecainide on induced atrial fibrillation in horses

Carstensen

Hesselkilde

Fenner

et al. 2018

Veterinary Internal Medicne

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BackgroundPharmacological treatment of atrial fibrillation (AF) in horses can be challenging because of low efficacy and adverse effects. Flecainide has been tested with variable efficacy.ObjectiveTo test whether the efficacy of flecainide is dependent on AF duration.AnimalsNine Standardbred mares.MethodsFactorial study design. All horses were instrumented with a pacemaker and assigned to a control or an AF group. On day 0, all horses were in sinus rhythm and received 2 mg/kg flecainide IV. Atrial fibrillation subsequently was induced in the AF group by pacemaker stimulation. On days 3, 9, 27, and 55, flecainide was administered to all horses, regardless of heart rhythm.ResultsAll horses in AF cardioverted to sinus rhythm on days 3 and 9. On day 27, 5/6 horses cardioverted, whereas only 2/6 cardioverted on day 55. The time from the start of flecainide infusion to cardioversion (range, 3–185 min, log transformed) showed linear correlation with the cumulative duration of AF (r 2 = .80, P < .0001). Flecainide induced abnormal QRS complexes in 4/6 AF horses and 1/3 controls. A positive correlation was found between heart rate before flecainide infusion and number of abnormal QRS complexes (0.14, P < .05). One horse suffered from cardiac arrest and died after flecainide infusion.Conclusions and Clinical ImportanceFlecainide is effective for cardioversion of short‐term induced AF, but the effect decreases with AF duration. Controlling heart rate may minimize adverse effects caused by flecainide, but the drug should be used with great caution.

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Section: Discussionmentioning

confidence: 99%

Time‐dependent antiarrhythmic effects of flecainide on induced atrial fibrillation in horses

Carstensen

Hesselkilde

Fenner

et al. 2018

Veterinary Internal Medicne

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Postrepolarization Refractoriness Versus Conduction Slowing Caused by Class I Antiarrhythmic Drugs

1998

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Background-Conduction block may be both antiarrhythmic and proarrhythmic. Drug-induced postrepolarization refractoriness (PRR) may prevent premature excitation and tachyarrhythmia induction. The effects of propafenone and procainamide on these parameters, and their antiarrhythmic or proarrhythmic consequences, were investigated. Methods and Results-In 11 isolated Langendorff-perfused rabbit hearts, monophasic action potentials (MAPs) were recorded simultaneously from six to seven different right and left ventricular sites, along with a volume-conducted ECG. All recordings were used to discern ventricular tachycardia (VT) or ventricular fibrillation (VF) induced by repetitive extrastimulation (S2-S5) or 10-second burst stimulation at 25 to 200 Hz at baseline and after addition of procainamide (20 mol/L) or propafenone (1 mol/L) to the perfusate. MAPs were analyzed for action potential duration at 90% repolarization (APD 90 ), conduction times (CT) between the pacing site and the other MAPs, and PRR (effective refractory periodϪAPD 90 ϭPRR) and related to the induction of VT or VF. During steady-state pacing, procainamide and propafenone prolonged APD 90 by 12% and 14%, respectively. Procainamide slowed mean CT by 40% during S2-S5 pacing, whereas propafenone slowed mean CT by up to 400% (PϽ0.001 versus baseline and procainamide). Wavelength was not changed significantly by procainamide but was shortened fourfold by propafenone at S5. Both drugs produced PRR, which was associated with a 70% decrease in VF inducibility with procainamide and elimination of VF with propafenone. Despite this protection from VF, monomorphic VT was induced with propafenone in 57% of burst stimulations. Conclusions-Drug-induced PRR protects against VF induction. Propafenone promotes slow monomorphic VT, probably by use-dependent conduction slowing and wavelength shortening. (Circulation. 1998;97:2567-2574.)

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Review : Electrophysiologic and Antiarrhythmic Effects of Propafenone: Focus on Atrial Fibrillation

Valderrábano

Singh

1999

J Cardiovasc Pharmacol Ther

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Reverse Use Dependence of Antiarrhythmic Class la, Ib, and Ic: Effects of Drugs on the Action Potential Duration?

Cited by 3 publications

References 12 publications

Time‐dependent antiarrhythmic effects of flecainide on induced atrial fibrillation in horses

Time‐dependent antiarrhythmic effects of flecainide on induced atrial fibrillation in horses

Postrepolarization Refractoriness Versus Conduction Slowing Caused by Class I Antiarrhythmic Drugs

Review : Electrophysiologic and Antiarrhythmic Effects of Propafenone: Focus on Atrial Fibrillation

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