Atrial fibrillation (AF), the most prevalent rhythm disorder in clinical practice, is currently significantly contributing
to morbidity and mortality of the ageing population. In the past decades, a tremendous amount of research resulted in
valuable insights into AF pathophysiology, with a primary focus on atrial remodeling. Defined as a persistent change
in atrial function and structure, remodeling has the intrinsic properties to enhance the probability of focal (ectopic)
and/or re-entrant pursuits, thus supporting AF persistence. The hallmark of structural remodeling is represented by
atrial fibrosis, a multifactorial process involving an interaction between neurohormonal and cellular mediators. This
paper provides a brief summary of the recent knowledge with respect to electrical and structural remodeling and
novel insights into the pathogenesis of atrial fibrosis. Since current drug options for AF treatment are far from being
optimal we also discuss the therapeutic principles and current alternatives for counteracting atrial fibrosis, and thus
preventing arrhythmia recurrence
