Rac1 and connective tissue growth factor. The missing link between atrial remodeling and the pathogenesis of atrial fibrillation?
Rac1 and connective tissue growth factor. The missing link between atrial remodeling and the pathogenesis of atrial fibrillation?
复制标题
Rac1 和结缔组织生长因子。
DOI:
10.1016/j.jacc.2009.07.071
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发表时间:
2010
影响因子:
24
通讯作者:
Liao,JamesK
中科院分区:
文献类型:
--
作者:
Liao,JamesK
Atrial fibrillation (AF) is the most common type of cardiac arrhythmia and a major cause of morbidity and mortality (1). AF typically occurs after cardiac surgery or in patients with hypertension or ischemic, valvular, structural, or metabolic heart disease (2). In some cases, AF has no clear etiology, which is often referred to as lone or idiopathic AF. Nevertheless, most patients with AF have increased left atrial size (3), and AF patients with left atrial enlargement have poorer cardiovascular prognosis compared with patients who have normal left atrial dimensions (4). However, left atrium enlargement could also be a consequence of AF (5). Histological biopsy studies in patients with lone AF revealed increased atrial inflammation and fibrosis (6). Indeed, fibrosis and extracellular matrix remodeling are important components of left atrial enlargement (7, 8), and increased left atrial volume is a strong predictor of postoperative AF (9). These findings suggest that left atrial fibrosis could contribute to the pathogenesis of AF. However, the precise signaling pathways that mediate these changes in the left atrium are not known.