The perception of atrial fibrillation development has changed drastically over the last decade. The pulmonary veins have been targeted as the source of arrhythmogenic activity involved in the initiation of atrial fibrillation. This activity appears to be localized in the myocardial sleeves of the vessels. Extensive study of cells within this tissue has helped create a new model for atrial fibrillation. This review attempts to show how the development, architecture and electrophysiologic properties of the pulmonary veins influence the initiation and perpetuation of atrial fibrillation. It also examines the potential long-term effects of pulmonary vein activity on arrhythmia development.