The European Society of Cardiology (ESC) and the European Heart Rhythm Association (EHRA) have developed the 2010 Clinical Practice Guidelines covering atrial fibrillation (AF), the most common cardiac arrhythmia occurring in 1-2% of the general population. Advance has been made regarding the dynamic development of AF from a preclinical state to an irreversible cardiac arrhythmia and a novel classification of AF has been adopted based on the presentation and duration of the arrhythmia: first diagnosed, paroxysmal, persistent, long-standing persistent and permanent AF are the 5 types of AF in use for clinical management of patients with AF.Structural and electrical remodelling are hallmarks of the pathophysiological changes facilitating the initiation and perpetuation of AF. While atrial fibrosis was the main cause of nonhomogeneity of conduction according to earlier ESC guidelines, nowadays any kind of structural abnormality (inflammatory changes, amyloid deposit, apoptosis, necrosis, hypertrophy, microvascular changes, etc.) is believed to trigger the electrical dissociation between muscle bundles and permit small re-entrant circuits to stabilize the arrhythmia. The adage ‘atrial fibrillation begets atrial fibrillation’ describes electrical remodelling due to shortening of atrial refractory period, which is attributed to down-regulation of the L-type Ca2+ inward current and up-regulation of inward rectifier K+ currents. Although the exact role of the genome in the pathogenesis of AF is not known, numerous inherited cardiac syndromes and mutations have lately been associated with AF and should be elucidated. Mutations in the gene coding for atrial natriuretic peptide, loss of function mutations in the cardiac sodium channel gene SCN5A or gain of function mutations in the cardiac potassium channel are related to familial AF and genetic loci close to the PITX2 and ZFHX3 genes are currently associated with enhanced risk for cardioembolic stroke... (excerpt