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Atrial fibrillation (AF) is the most frequently encountered cardiac arrhythmia in the clinical practice with prevalence of over 2,200,000 and 1,300,000 in the United States and Japan, respectively. The prevalence of AF is strongly age dependent; less than 1% of individuals aged <60 years, but approximately 5% of those older than 65 years and about 8% of those older than 80 years are affected by AF (Furberg et al., 1994; Kannel et al., 1998). AF is not lethal arrhythmia but associated with an increased long-term risk of stroke, heart failure, and all-cause mortality (Stewart et al., 2002). One of the most debilitating consequences of AF is the accompanying risk of stroke, which occurs in an estimated 60,000 patients with AF per year in the United States (Go et al., 2001). Antiarrhythmic drug therapy remains a cornerstone to restore and maintain sinus rhythm for patient both with paroxysmal and persistent AF. However, conventional drugs such as sodium channel blockers (class I antiarrhythmic drugs) and potassium channel blockers (class III antiarrhythmic drugs) have limited efficacy, especially in persistent AF patients. Clinical studies have shown that the potassium channel blockers can terminate AF in only 30% of cases (Ellenbogen et al., 1996; Falk et al., 1997). Sodium channel blockers are more effective than potassium channel blockers, but a potent sodium channel blocker, pilsicainide demonstrated a modest efficacy in converting AF to sinus rhythm, with a conversion rate of 45% within 90 min in patients with recent-onset AF compared with 8.6% on placebo and was ineffective in chronic AF (Okishige at al., 2006). In addition, these conventional drugs have severe problematic risks of ventricular proarrhythmia, such as torsade de pointes (TdP) through excessive delay of ventricular replarization (Waldo et al., 1996; Trop-Pederson et al., 1999) and left ventricular contractile dysfunction. Thus, the development of new antiarrhythmic agents which have more effective and safer profile is highly desirable. These days, the pharmaceutical industry has focused on “atrial-specific antiarrhythmic drug” in the search for safer drugs to terminate or prevent AF (Wirth et al., 2003; Vos 2004; Goldstein & Stambler 2005). The acetylcholine-activated potassium channel (IKACh channel) is one of the most promising targets for atrial-specific antiarrhythmic agent, because the channel is more abundantly expressed in the atrial than ventricle myocytes (Krapivinsky et al., 1995). In this article, the pathophysiolosical roles of IKACh channel in AF are summarized. In

Acetylcholine-Activated Potassium Channel as a Novel Target for AF Treatment