The basic underlying mechanisms behind atrial fibrillation (AF), the most abundant therapy demanding cardiac dysrhythmia, have until recently being largely unknown. Once established, AF is not only self-perpetuating but also self-destructive, prompting rapid treatment against possible initiating mechanisms. Recent observations reveal that the ectopic beats, initiating AF, often originate in the walls of the pulmonary veins and that the deterioration of the ectopic impulse to AF may be linked to an impaired inferoposterior interatrial conduction. The underlying mechanisms behind these functional defects are still obscure. The observations has however, permitted evaluation of new types of treatment, directly interfering with the newly verified findings.