Abstract
Atrial fibrillation is the most common cardiac arrhythmia associated with heart failure, stroke and mortality. Existing treatment of atrial fibrillation with class I or class III antiarrhythmic agents produces negative feedback on the ventricular repolarisations, which is widely considered as a critical risk factor of Torsades de pointes. The serious side effects hinder the appropriate usage and fair evaluation of these antiarrhythmic agents in clinical trials. Specifically existing in the ventricular, the ultra-rapid delayed rectifier potassium current (IKur), encoded by the Kv1.5 gene, is a crucial determinant of Phase I repolarisation during action potential duration. All evidence suggests that the Kv1.5 gene would be a potent target for the treatment of atrial fibrillation. This review describes the progress of Kv1.5 inhibitors in up-to-date literatures and awarded patents, and the latest information in clinical and preclinical trials.
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