What question did this study set out to answer?

To determine how rate-dependent electrophysiological properties and refractoriness prolongation affect the ability of class Ia, Ic, and III antiarrhythmic drugs to terminate sustained atrial fibrillation.

September 1, 1993CirculationOpen Access

Comparative mechanisms of antiarrhythmic drug action in experimental atrial fibrillation. Importance of use-dependent effects on refractoriness.

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Why the study?

Do antiarrhythmic drugs (procainamide, propafenone, sotalol) terminate experimental atrial fibrillation by altering refractoriness and wavelength for reentry in anesthetized dogs?

Population

Anesthetized, open-chest dogs with sustained cholinergic atrial fibrillation

Comparison

Class Ia, Ic, and III antiarrhythmic drugs… vs Drug-free conditions

Design

Preclinical

Authors

JWJ WangCapital Medical University GBGerald W. BourneKaiser Permanente ZWZhiguo WangON Semiconductor (United States)

Discussion

Member takes

Implication

No immediate change to clinical AAD use; extends reentry wavelength mechanism in canine AF but leaves open human translation.

Key Points

To determine how rate-dependent electrophysiological properties and refractoriness prolongation affect the ability of class Ia, Ic, and III antiarrhythmic drugs to terminate sustained atrial fibrillation.
Administered representative class Ia (procainamide), Ic (propafenone), and III (sotalol) antiarrhythmic drugs via loading and maintenance infusions to achieve stable plasma concentrations in anesthetized, open-chest dogs with sustained cholinergic atrial fibrillation.
Utilized high-resolution 112-electrode computer-based epicardial mapping to record atrial conduction, refractory periods, and activation patterns during rapid pacing and atrial fibrillation.
Clinical doses terminated atrial fibrillation in 100% (13/13) of dogs with procainamide and 70% (7/10) with propafenone, compared with only 25% (2/8) with sotalol 2 mg/kg (P = .0005 vs procainamide, P = .08 vs propafenone).
Induction of atrial fibrillation was prevented in 100% (13/13) with procainamide and 70% (7/10) with propafenone, compared with 0% (0/8) with sotalol 2 mg/kg (P < .0001 vs procainamide, P = .004 vs propafenone), though high-dose sotalol (8 mg/kg) achieved 100% efficacy.
Propafenone produced use-dependent refractory period lengthening that expanded the reentry wavelength at rapid rates, whereas sotalol exhibited reverse use dependence that diminished refractory prolongation and wavelength expansion during tachycardia.

Structured PICO

Do antiarrhythmic drugs (procainamide, propafenone, sotalol) terminate experimental atrial fibrillation by altering refractoriness and wavelength for reentry in anesthetized dogs?

Population

Anesthetized, open-chest dogs with sustained cholinergic atrial fibrillation

Intervention

Class Ia (procainamide), Ic (propafenone), and III (sotalol) antiarrhythmic drugs administered via loading and maintenance doses to produce stable plasma concentrations

Comparator

Drug-free conditions

Outcome

Termination of atrial fibrillation and prevention of atrial fibrillation inductionsurrogate

Antiarrhythmic drugs terminate experimental atrial fibrillation by increasing the wavelength for reentry at rapid rates, with use-dependent effects on refractoriness determining their efficacy.

Cite This Study

Wang et al. (1993) studied this question.

synapsesocial.com/papers/6a0d28fdd7cdc72b86656665 https://doi.org/10.1161/01.cir.88.3.1030

Topics

Atrial fibrillation Persistent AF management Anticoagulation in AF AF ablation outcomes

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Comparative mechanisms of antiarrhythmic drug action in experimental atrial fibrillation. Importance of use-dependent effects on refractoriness.

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Topics

Comparative mechanisms of antiarrhythmic drug action in experimental atrial fibrillation. Importance of use-dependent effects on refractoriness.

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

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Topics

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