Abstract
Background: Atrial fibrillation (AF) is the most common cardiac arrhythmia. The contribution of genetic factors to AF susceptibility has been emphasized by the discovery of mutations that enhance outward potassium current, predicted to shorten atrial action potential duration and predispose to re-entrant arrhythmia mechanisms. Understanding the genetic basis for familial AF can inspire new ideas regarding treatment of this common arrhythmia. We hypothesized that potassium channel mutations predisposing to AF may have distinct pharmacological properties from wild-type channels.
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