The electrophysiological mechanism of atrial fibrillation (AF) has been the subject of interest for almost a hundred years. The mechanism that leads to the induction of atrial fibrillation can be a single automatic focus firing impulses with high rate (e.g. pulmonary vein) as well as macro- or more frequently micro-re-entrant circuits. The focal mechanism has been recently shown to be responsible for at least a particular group of AF cases. Cellular and electrophysiological abnormalities such as partly depolarised cells, fibrosis, conduction abnormalities, shortening of the refractoriness and the increase in dispersion of refractoriness in the atrium can be the underlying factors for the genesis of atrial fibrillation. Factors such as the autonomic nervous system, aging, enlargement of the atria can modulate these electrophysiological features. AF can be maintained in the existence of particular conditions and AF itself leads to some changes in the atrium that are thought to be the base of perpetuation of fibrillation in the atria. These changes in the atrial electrophysiology and anatomy are called AF-induced atrial remodeling. Whatever it is the triggering mechanism for AF, “multiple wavelet re-entry” has been widely accepted to be the maintaining mechanism of AF. Finally, it can be considered that we are facing the different types of AF that can be induced with different mechanisms, that need special conditions to perpetuate and maintain, but present with similar findings in the electrocardiogram.