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
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