New insights into mechanisms of atrial fibrillation

Physiol Res. 2010;59(1):1-12. doi: 10.33549/physiolres.931651. Epub 2009 Feb 27.


Although atrial fibrillation (AF) is the most common cardiac arrhythmia in clinical practice, precise mechanisms that lead to the onset and persistence of AF have not completely been elucidated. Over the last decade, outstanding progress has been made in understanding the complex pathophysiology of AF. The key role of ectopic foci in pulmonary veins as a trigger of AF has been recognized. Furthermore, structural remodeling was identified as the main mechanism for AF persistence, confirming predominant role of atrial fibrosis. Systemic inflammatory state, oxidative stress injury, autonomic balance and neurohormonal activation were discerned as important modifiers that affect AF susceptibility. This new understanding of AF pathophysiology has led to the emergence of novel therapies. Ablative interventions, renin-angiotensin system blockade, modulation of oxidative stress and targeting tissue fibrosis represent new approaches in tackling AF. This review aims to provide a brief summary of novel insights into AF mechanisms and consequent therapeutic strategies.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Atrial Fibrillation / etiology
  • Atrial Fibrillation / pathology
  • Atrial Fibrillation / physiopathology*
  • Atrial Fibrillation / therapy
  • Atrial Function*
  • Autonomic Nervous System / physiopathology
  • Fibrosis
  • Heart Atria / pathology
  • Heart Atria / physiopathology
  • Heart Conduction System / physiopathology*
  • Humans
  • Inflammation / physiopathology
  • Oxidative Stress
  • Pulmonary Veins / physiopathology
  • Renin-Angiotensin System
  • Risk Factors