February 18, 2003Circulation
Widening of the Excitable Gap and Enlargement of the Core of Reentry During Atrial Fibrillation With a Pure Sodium Channel Blocker in Canine Atria
Why the study?
Does pilsicainide alter electrophysiological action and wavefront dynamics during atrial fibrillation in canine atria?
Population
Isolated, perfused, and superfused canine atria with atrial fibrillation induced by 1 to 5 micromol/L…
Comparison
Pilsicainide infusion vs Baseline (before pilsicainide infusion)
Design
Preclinical
Authors
Discussion
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Implication
Hypothesis-generating for pilsicainide in AF; human trials required before clinical consideration.
Structured PICO
Does pilsicainide alter electrophysiological action and wavefront dynamics during atrial fibrillation in canine atria?
P
Population
Isolated, perfused, and superfused canine atria (n=12) with atrial fibrillation induced by 1 to 5 micromol/L acetylcholine
I
Intervention
Pilsicainide infusion (2.5 microg/mL and increasing dosage)
C
Comparator
Baseline (before pilsicainide infusion)
O
Outcome
Electrophysiological action and wavefront dynamics during atrial fibrillation (AF cycle length, refractory period, conduction velocity, excitable gap, and the core of the mother rotor)surrogate
In a canine model, pilsicainide terminates atrial fibrillation by widening the excitable gap and facilitating excitation of the core of the mother rotor.
Cite This Study
Kawase et al. (2003) studied this question.