In the last few years many studies have been performed with the aim of gaining a better understanding of the pathophysiological nature of atrial fibrillation. These recent observations provide new insights into the initiation and perpetuation of atrial fibrillation, underlying the importance of the pulmonary veins as major sources of atrial triggers and introducing new concepts such as the atrial electrical remodeling and the spatial heterogeneity of the electrophysiological characteristics of this arrhythmia. The increasing knowledge about the cardiac ion channel structure and function and about the electrophysiological actions of the antiarrhythmic drugs may contribute to a better comprehension of the mechanisms of the pharmacological termination of the arrhythmia. In part I of the review we try to give a unified vision of the old models and new concepts about the molecular and ionic fundamentals of antiarrhythmic drug actions.