Montreal Heart Institute, Université de Montréal, Montreal, Québec, Canada; AP-HP, Groupe Hospitalier Pitié-Salpêtrière, Institut de Cardiologie, Paris, France.
Montreal Heart Institute, Université de Montréal, Montreal, Québec, Canada.
Can J Cardiol. 2018 Nov;34(11):1396-1406. doi: 10.1016/j.cjca.2018.08.007. Epub 2018 Aug 8.
The incidence of atrial fibrillation (AF), the most common sustained arrhythmia and a major public health burden, increases exponentially with age. However, mechanisms underlying this long-recognized association remain incompletely understood. Experimental and human studies have demonstrated the involvement of aging in several arrhythmogenic processes, including atrial electrical and structural remodelling, disturbed calcium homeostasis, and enhanced atrial ectopic activity/increased vulnerability to re-entry induction. Given this wide range of putative mechanisms, the task of delineating the specific effects of aging responsible for AF promotion is not simple, as aging is itself associated with increasing prevalence of a host of AF-predisposing conditions, including heart failure, coronary artery disease, and hypertension. Although we usually think of old age promoting AF, there is also evidence that young age may actually have a protective effect against AF occurrence. For example, the low AF incidence among populations of young patients with significant structural congenital heart disease and substantial atrial enlargement/remodelling suggests that younger age might protect against fibrillation in the diseased atrium; efforts at understating how younger age may prevent AF might be helpful in elucidating missing mechanistic links between AF and age. The goal of this paper is to review the epidemiologic and pathophysiologic evidence regarding mechanisms underlying age-related AF. Although the therapeutic options for AF have recently improved, major gaps still remain and a better understanding of the special relationship between age and AF may be important for the identification of new targets for therapeutic innovation.
心房颤动（房颤）的发病率随着年龄的增长呈指数级增长，是最常见的持续性心律失常，也是一个主要的公共健康负担。然而，这种长期以来被认识到的关联的机制仍不完全清楚。实验和人体研究表明，衰老参与了几种心律失常的发生机制，包括心房电重构和结构重构、钙稳态紊乱以及心房异位活动增加/折返诱导易感性增加。鉴于这种广泛的潜在机制，明确导致房颤发生的衰老的具体影响并不简单，因为衰老是导致多种房颤易患条件（包括心力衰竭、冠状动脉疾病和高血压）患病率增加的一个因素。虽然我们通常认为衰老会促进房颤，但也有证据表明，年轻实际上可能对房颤的发生具有保护作用。例如，在患有明显结构性先天性心脏病和大量心房扩大/重构的年轻患者人群中，房颤的发病率较低，这表明年轻可能对病变心房的颤动有保护作用；努力了解年轻如何可能预防房颤可能有助于阐明房颤和年龄之间缺失的机制联系。本文的目的是回顾与年龄相关房颤的流行病学和病理生理学证据。尽管房颤的治疗选择最近有所改善，但仍存在重大差距，更好地了解年龄与房颤之间的特殊关系可能对确定治疗创新的新靶点很重要。
