The Journal of Tehran University Heart Center have been reported with its long-term use.30 It is the most frequently used antiarrhythmic drug for AF treatment in that it prolongs the repolarization in the atria and ventricles.31 the elimination half-life of amiodarone is 30-55 days.32 It may give rise to thyroid dysfunction, pulmonary fibrosis, dermatological changes, and ophthalmic involvement.31 Roy et al. posited that low-dose amiodarone (< 600 mg daily) was more effective than sotalol or propanofenone for the prevention of AF. In their study, the recurrence rate of AF in a 16-month follow-up period was 35% in the amiodarone group versus 63% in the other group.33 Some other studies have also shown similar success rates (50-70%) in achieving and maintaining sinus rhythm for amiodarone.34, 35 Cardioversion rate for class IC and III drugs is approximately 60-80% in AF episodes lasting less than 48 hours.13 Dronedarone is a benzofuran-derivate of amiodarone with the same electropharmacological profile36 but without side effects on the pulmonary system.37 It has a shorter half-life than amiodarone (1 - 2 days).32 By blocking multiple channels and having some antiadrenergic properties, it prolongs action potential duration and, therefore, reduces the heart rate. Additionally, it has low risk of Torsade de pointes.6 The EURIDIS and ADONIS trials showed that 400mg dronedarone orally, twice daily, was more effective than placebo in slowing the ventricular response and maintaining sinus rhythm in AF patients.38 The ANDROMEDA study was terminated prematurely because of increased mortality due to the worsening of heart failure in the dronedarone group.39 Therefore, dronedarone is contraindicated in patients with moderate to severe heart failure.6 The ATHENA trial supported the idea that dronedarone could reduce both primary and secondary end-points. The median time to the recurrence of AF was prolonged with this drug.40 Dronedarone can reduce the rate of death or hospitalization in AF patients.40 Data from the DIONYSOS trial suggested higher tolerability for dronedarone than that for amiodarone but less efficacy.6 Budiodarone (ATI-2042) is another analogue of amiodarone. Its half-life is 7 hours and is administrated orally up to 1200 mg daily. Even in low doses, it can be effective in the reduction of AF episodes and the duration of the mean episode.41 This drug is undergoing phase II trials.42 Celivarone is another analogue of amiodarone and is still under investigation. It can be consumed both by oral and intravenous (IV) routes and can act similarly to all categories of antiarrhythmic agents. It is effective in the management of hypokalemic and vagotonic AF. In experimental animal models, it was at least as potent as amiodarone and dronedarone.43 174 Gholamreza Davoodi et al. Ibutilide is a class III antiarrhythmic agent that can convert AF to sinus rhythm more rapidly than can procainamide or sotalol. Its dosage is 0.008 mg/kg over 10 minutes. It has been shown that ibutilide has no significant advantage compared with amiodarone for the conversion of AF but severe hypotension was not seen with ibutilide.44 For acute AF, conversion to sinus rhythm with ibutilide is about 59%, but there is 1.7% risk of polymorphic ventricular tachycardia with this drug. As a result, it is advised to keep the patients receiving ibutilide under monitoring for at least 24 hours after the infusion of this drug.45 Dofetilide is another class III antiarrhythmic drug that can be used for maintaining sinus rhythm in congestive heart failure patients with AF. The DIAMOND CHF trial showed that it could reduce hospitalization due to heart failure. Heart failure worsening was reduced by 25%.46 Dofetilide is known to be more effective in patients with persistent AF compared with those with paroxysmal AF, and significant proarrhythmic adverse effects can occur even with close monitoring.47 Ranolazine is an antianginal agent that can block several ion channels and consequently increase the QT interval modestly (2 - 6 millisecond). This agent has higher affinity for sodium channels in the atria than in the ventricles. Phase III human trial is planned for this agent.48 Azimilide is also a class III antiarrhythmic drug with the dosage of 100 - 125 mg daily orally and a half-life of 4 days. A trial demonstrated that azimilide was a safe and effective drug for the management of AF in patients with left ventricular dysfunction after myocardial infarction.49 Tedisamil is another drug from class III family. It can prolong action potential in the atria more than ventricles and its half-life is 8 - 13 hours. It has a rapid onset of action and can convert AF to sinus rhythm in the majority of patients by 30 - 40 minutes fallowing an IV injection (0.4 - 0.6 mg/ kg).50 Impaired conduction between myocytes is associated with increased risk of AF, and this effect is more prominent in patients with heart failure and mitral insufficiency. Rotigoptide can improve cell-to-cell conduction by the augmentation of the gap junction conductance. In an animal model, rotigoptide was effective in the management of AF associated with mitral regurgitation or ischemia but was not effective in the presence of heart failure or atrial enlargement.51 Introduction of drugs with selective affinity for channels that specifically contribute in atrial repolarization is an interesting aspect in the AF management. These drugs are called atrial repolarization delaying agents.42 By the application of these agents, the proarrhythmic effect of traditional drugs can be minimized.42 Inhibition of ultra rapid delayed rectifier potassium current (Ikur) is an example for atrium-selective approach because this channel is located exclusively in the atria.52