TY - JOUR
T1 - Structural remodeling in atrial fibrillation
AU - Corradi, Domenico
AU - Callegari, Sergio
AU - Maestri, Roberta
AU - Benussi, Stefano
AU - Alfieri, Ottavio
PY - 2008
Y1 - 2008
N2 - Atrial fibrillation occurs and maintains itself in the context of a morphologically and functionally altered atrial substrate that can be induced by stressors such as underlying diseases (cardiac or noncardiac) or aging. The resultant structural remodeling is a slow process that progressively affects myocytes and the myocardial interstitium, and takes place from as early as the first days of atrial tachyarrhythmia. The left atrium, and particularly its posterior wall, is the location where remodeling is concentrated to the greatest extent. The mechanisms that underlie the remodeling process in atrial fibrillation have not yet been completely elucidated, although experimental and clinical investigations have indicated a number of signaling systems, inflammation, oxidative stress, atrial stretching and ischemia as factors involved in the cascade of events that leads to atrial fibrillation. The aim of this Review is to provide a comprehensive overview of the morphological changes that characterize the fibrillating atrial myocardium at histological and ultrastructural levels, and the established and hypothetical pathogenetic mechanisms involved in structural remodeling. This article also highlights the emerging therapies being developed to prevent progression of atrial fibrillation.
AB - Atrial fibrillation occurs and maintains itself in the context of a morphologically and functionally altered atrial substrate that can be induced by stressors such as underlying diseases (cardiac or noncardiac) or aging. The resultant structural remodeling is a slow process that progressively affects myocytes and the myocardial interstitium, and takes place from as early as the first days of atrial tachyarrhythmia. The left atrium, and particularly its posterior wall, is the location where remodeling is concentrated to the greatest extent. The mechanisms that underlie the remodeling process in atrial fibrillation have not yet been completely elucidated, although experimental and clinical investigations have indicated a number of signaling systems, inflammation, oxidative stress, atrial stretching and ischemia as factors involved in the cascade of events that leads to atrial fibrillation. The aim of this Review is to provide a comprehensive overview of the morphological changes that characterize the fibrillating atrial myocardium at histological and ultrastructural levels, and the established and hypothetical pathogenetic mechanisms involved in structural remodeling. This article also highlights the emerging therapies being developed to prevent progression of atrial fibrillation.
UR - http://www.scopus.com/inward/record.url?scp=57049106771&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=57049106771&partnerID=8YFLogxK
U2 - 10.1038/ncpcardio1370
DO - 10.1038/ncpcardio1370
M3 - Article
C2 - 18852714
AN - SCOPUS:57049106771
VL - 5
SP - 782
EP - 796
JO - Nature Clinical Practice Cardiovascular Medicine
JF - Nature Clinical Practice Cardiovascular Medicine
SN - 1743-4297
IS - 12
ER -