Atrial fibrillation (AF) is the most commonly encountered arrhythmia in clinical practice. Despite advances in our understanding of the pathophysiology of this complex arrhythmia, current therapeutic options remain suboptimal. This review aimed to delineate the atrial structural and functional remodeling leading to the perpetuation of AF. We explored the complex changes seen in the atria in various substrates for AF and the therapeutic options available to prevent these changes or for reverse remodeling. Here we also highlighted the emerging role of aggressive risk factor management aimed at the arrhythmogenic atrial substrate to prevent or retard AF progression.