Recent advances in the molecular pathophysiology of atrial fibrillation

被引:467
作者
Wakili, Reza [1 ,2 ,3 ]
Voigt, Niels [4 ]
Kaeaeb, Stefan [3 ]
Dobrev, Dobromir [4 ]
Nattell, Stanley [1 ,2 ]
机构
[1] Montreal Heart Inst, Dept Med, Res Ctr, Montreal, PQ H1T 1C8, Canada
[2] Univ Montreal, Montreal, PQ, Canada
[3] Univ Munich, Klinikum Grosshadern, Dept Med 1, D-8000 Munich, Germany
[4] Heidelberg Univ, Med Fac Mannheim, Div Expt Cardiol, D-6800 Mannheim, Germany
基金
加拿大健康研究院;
关键词
OF-FUNCTION MUTATION; TISSUE GROWTH-FACTOR; VALVULAR HEART-DISEASE; LONG-QT SYNDROME; RYANODINE RECEPTOR; DOWN-REGULATION; POTASSIUM CURRENT; POTENTIAL ROLE; CONTRACTILE DYSFUNCTION; DEPENDENT REGULATION;
D O I
10.1172/JCI46315
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Atrial fibrillation (AF) is an extremely common cardiac rhythm disorder that causes substantial morbidity and contributes to mortality. The mechanisms underlying AF are complex, involving both increased spontaneous ectopic firing of atrial cells and impulse reentry through atrial tissue. Over the past ten years, there has been enormous progress in understanding the underlying molecular pathobiology. This article reviews the basic mechanisms and molecular processes causing AF. We discuss the ways in which cardiac disease states, extracardiac factors, and abnormal genetic control lead to the arrhythmia. We conclude with a discussion of the potential therapeutic implications that might arise from an improved mechanistic understanding.
引用
收藏
页码:2955 / 2968
页数:14
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