• Title of article

    Atrial Fibrosis: Mechanisms and Clinical Relevance in Atrial Fibrillation Review Article

  • Author/Authors

    Brett Burstein، نويسنده , , Stanley Nattel، نويسنده ,

  • Issue Information
    روزنامه با شماره پیاپی سال 2008
  • Pages
    8
  • From page
    802
  • To page
    809
  • Abstract
    Atrial fibrillation (AF) is the most common arrhythmia in the clinical setting, and traditional pharmacological approaches have proved to have important weaknesses. Structural remodeling has been observed in both clinical and experimental AF paradigms, and is an important feature of the AF substrate, producing fibrosis that alters atrial tissue composition and function. The precise mechanisms underlying atrial fibrosis are not fully elucidated, but recent experimental studies and clinical investigations have provided valuable insights. A variety of signaling systems, particularly involving angiotensin II and related mediators, seem to be centrally involved in the promotion of fibrosis. This paper reviews the current understanding of how atrial fibrosis creates a substrate for AF, summarizes what is known about the mechanisms underlying fibrosis and its progression, and highlights emerging therapeutic approaches aimed at attenuating structural remodeling to prevent AF.
  • Keywords
    ACE , extracellular matrix , Atrial fibrillation , angiotensin II , angiotensin-converting enzyme , PDGF , ECM , Congestive heart failure , AF , CHF , TGF , transforming growth factor , AT1 , angiotensin II type 1 , platelet-derived growth factor , AngII , VTP , ventricular tachypacing
  • Journal title
    JACC (Journal of the American College of Cardiology)
  • Serial Year
    2008
  • Journal title
    JACC (Journal of the American College of Cardiology)
  • Record number

    473130