Current concepts in the pathogenesis of atrial fibrillation
Current concepts in the pathogenesis of atrial fibrillation
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DOI：
10.1016/j.ahj.2008.10.009
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发表时间：
2009-02-01
影响因子：
4.8
通讯作者：
Camm, John
中科院分区：
文献类型：
--
作者：
Kourliouros, Antonios;Savelieva, Irina;Camm, John
目前的证据表明，心房颤动（AF）的发病机制是多因素的。AF一旦出现，就会改变心房肌的电生理特性，导致心律失常的自我延续，这一观察结果提高了电重构在其发病机制中的重要性。虽然这些变化可能是可逆的，但即使在电重构发生后，AF的维持仍在继续。临床和实验研究已经强调了一个敏感的心房解剖基板的作用，在启动和维持AF的肌细胞变性和间质纤维化的功能。最后，增加炎症负荷与AF的存在和未来的发展的关联有牵连的炎症的发病机制的心律失常。本综述的目的是提供当前关于房颤发病机制的主要理论的证据，即电重构、结构重构和炎症;描述所使用的各种实验模型和方法;并确定存在的因果关系。此外，负责AF的不同机制之间的相互关系将被证明，提供进一步深入了解复杂的pothophysiology。(Am Heart J 2009; 157：243-52.）
Current evidence suggests that the pathogenesis of atrial fibrillation (AF) is multifactorial. The observation that AF, once present, alters the electrophysiologic properties of the atrial myocardium causing self-perpetuation of the arrhythmia raised the importance of electrical remodeling in its pathogenesis. Although these changes are potentially reversible, maintenance of AF continues even after electrical remodeling has occurred. Clinical and experimental studies have highlighted the role of a susceptible atrial anatomical substrate with features of myocyte degeneration and interstitial fibrosis in the initiation and maintenance of AF. Finally, the association of increased inflammatory burden with the presence and future development of AF has implicated inflammation in the pathogenesis of the arrhythmia. The purpose of this review is to provide current evidence on the dominant theories on AF pathogenesis, namely, electrical remodeling, structural remodeling, and inflammation; describe the various experimental models and methods used; and identify a cause-effect association, when present. In addition, the interrelation between different mechanisms responsible for AF will be demonstrated, providing further insight into the complex pothophysiology. (Am Heart J 2009; 157:243-52.)