Suppression of atrial fibrillation with drugs has always been a difficult issue. Most agents which suppress atrial fibrillation have certain problems like pro-arrhythmia or extra cardiac side effects. A novel strategy which has been proposed is the development of agents which act preferentially on the atria rather than on the ventricles. The ultrarapid delayed rectifier potassium current (IKur) is expressed in the atria, but not in the ventricles. Inhibition of IKur has been considered as an atrial selective antiarrhythmic treatment. Atrial selective sodium channel blockade ( Ann N Y Acad Sci. 2008 Mar;1123:105-12.) with drugs like ranolazine is another approach which has been evaluated.
Kv 1.5 channels are responsible for the IKur and Kv 1.5 channels are encoded by the gene KCNA5. Some concern has been raised because IKur block may abbreviate atrial repolarization and loss of function mutations in KCNA5 has been associated with familial atrial fibrillation Heart Rhythm. 2008;5:1304-9.