Does K(2P)3.1 channel inhibition reverse action potential duration shortening in patients with chronic atrial fibrillation?
K(2P)3.1 channel inhibition reverses action potential duration shortening in chronic AF, highlighting its potential as a novel mechanism-based therapeutic target.
Enhancement of atrium-selective K(2P)3.1 currents contributes to APD shortening in patients with chronic AF, and K(2P)3.1 channel inhibition reverses AF-related APD shortening. These results highlight the potential of K(2P)3.1 as a novel drug target for mechanism-based AF therapy.
Schmidt et al. (Fri,) studied this question.
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