Why the study?
Does pilsicainide or MS-551 improve atrial fibrillation termination and electrophysiological parameters in a canine model of vagal nerve stimulation-induced atrial fibrillation?
Does pilsicainide or MS-551 improve atrial fibrillation termination and electrophysiological parameters in a canine model of vagal nerve stimulation-induced atrial fibrillation?
Sodium channel blockers like pilsicainide effectively terminate atrial fibrillation by increasing postrepolarization refractoriness during rapid excitation, unlike potassium channel blockers which show reverse use-dependent block.
Pilsicainide may outperform MS-551 for AF termination in this model; leaves open translation to human AF and requires clinical trials.
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Kanki et al. (1998) studied this question.
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