Burstein Brett, Nattel Stanley
Research Center and Department of Medicine, Montreal Heart Institute and Université de Montréal, and Department of Pharmacology and Therapeutics, McGill University, Montreal, Quebec, Canada.
J Am Coll Cardiol. 2008 Feb 26;51(8):802-9. doi: 10.1016/j.jacc.2007.09.064.
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.
心房颤动（AF）是临床环境中最常见的心律失常，传统的药理学方法已被证明存在重要缺陷。在临床和实验性房颤模型中均观察到结构重塑，这是房颤基质的一个重要特征，会产生纤维化，从而改变心房组织的组成和功能。心房纤维化的确切机制尚未完全阐明，但最近的实验研究和临床调查提供了有价值的见解。多种信号系统，特别是涉及血管紧张素II和相关介质的信号系统，似乎在促进纤维化过程中起核心作用。本文综述了目前对心房纤维化如何为房颤创造基质的理解，总结了关于纤维化及其进展的潜在机制的已知情况，并强调了旨在减轻结构重塑以预防房颤的新兴治疗方法。
