Antiarrhythmic drugs have been largely used to convert atrial fibrillation to sinus rhythm. Classes Ia, Ic and III antiarrhythmic agents are all known to be effective. Nevertheless, the electrophysiological properties of such agents even of the same class are very different. The mechanisms of the pharmacological termination of atrial fibrillation is an interesting issue that has not been so extensively studied yet. In this review we try to summarize the principal concepts about the electrophysiological substrate of atrial fibrillation and to give a unified and modern overview of the issue of the mechanisms of the pharmacological termination of the arrhythmia.