Atrial Fibrillation: Epidemiology, Pathophysiology, and Clinical Outcomes.
Atrial Fibrillation: Epidemiology, Pathophysiology, and Clinical Outcomes.
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DOI：
10.1161/circresaha.117.309732
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发表时间：
2017-04-28
影响因子：
20.1
通讯作者：
Helm RH
中科院分区：
文献类型：
--
作者：
Staerk L;Sherer JA;Ko D;Benjamin EJ;Helm RH
过去三十年来，房颤（AF）的临床治疗知识和进展呈指数增长。目前已知AF的发生需要脆弱的心房基质，并且该基质的形成和组成可能取决于共病条件、遗传学、性别和其他因素而变化。基于人群的研究已经确定了许多改变心房基质和增加AF易感性的因素。迄今为止，遗传学研究已经在14个基因组区域报告了17个独立的AF信号。研究表明，高龄、男性和欧洲血统是主要的房颤风险因素。其他可改变的风险因素，包括久坐不动的生活方式、吸烟、肥胖、糖尿病、阻塞性睡眠呼吸暂停和血压升高易患AF，并且每种因素均已被证明可诱导心房的结构和电重构。心力衰竭和心肌梗死都会增加房颤的风险，反之亦然，形成前馈循环，增加死亡率。AF引起的其他心血管结局（包括卒中和血栓栓塞）已得到充分证实，流行病学研究支持减轻这些不良结局的治疗方法。然而，抗凝治疗在预防房颤所致痴呆中的作用尚不明确。我们的综述是对与房颤不可改变和可改变的危险因素相关的流行病学数据以及支持每个危险因素与房颤发生之间的机制联系的病理生理学证据的全面检查。我们的综述还严格审查了关于AF临床结局的流行病学数据，并总结了将每种结局与AF联系起来的现有证据。
The last three decades have been characterized by an exponential growth in knowledge and advances in the clinical treatment of atrial fibrillation (AF). It is now known that AF genesis requires a vulnerable atrial substrate and that the formation and composition of this substrate may vary depending on comorbid conditions, genetics, sex, and other factors. Population-based studies have identified numerous factors that modify the atrial substrate and increase AF susceptibility. To date, genetic studies have reported seventeen independent signals for AF at fourteen genomic regions. Studies have established that advanced age, male sex, and European ancestry are prominent AF risk factors. Other modifiable risk factors, including sedentary lifestyle, smoking, obesity, diabetes mellitus, obstructive sleep apnea, and elevated blood pressure predispose to AF and each factor has been shown to induce structural and electrical remodeling of the atria. Both heart failure and myocardial infarction increase risk of AF and vice versa creating a feed forward loop that increases mortality. Other cardiovascular outcomes attributed to AF, including stroke and thromboembolism, are well established and epidemiology studies have championed therapeutics that mitigate these adverse outcomes. However, the role of anticoagulation for preventing dementia attributed to AF is less established. Our review is a comprehensive examination of the epidemiological data associating unmodifiable and modifiable risk factors for AF and of the pathophysiological evidence supporting the mechanistic link between each risk factor and AF genesis. Our review also critically examines the epidemiological data on clinical outcomes attributed to AF and summarizes current evidence linking each outcome with AF.