Calcium in the Pathophysiology of Atrial Fibrillation and Heart Failure.

Calcium in the Pathophysiology of Atrial Fibrillation and Heart Failure.
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心房颤动和心力衰竭病理生理学中的钙。

DOI:
10.3389/fphys.2018.01380
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发表时间:
2018
影响因子:
4
通讯作者:
Dibb KM
Dibb KM
中科院分区:
医学2区
文献类型:
--
作者:
Denham NC;Pearman CM;Caldwell JL;Madders GWP;Eisner DA;Trafford AW;Dibb KM

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心房颤动(AF)通常与心力衰竭相关。AF加重心力衰竭,导致心力衰竭症状、住院和心血管死亡显著增加,而心力衰竭导致的心房病理性重塑增加了AF的风险。如果我们要打破这种恶性循环,全面了解AF的病理生理学是必不可少的。在这篇综述中,最新的证据将显示钙在房颤的诱导和维持中的重要作用。概述心房电生理和钙处理后,钙依赖性后除极和心房复极交替在触发房颤中的作用将被考虑。将讨论心房对快速刺激的反应,包括钙信号沉默形式的钙超载的短期保护,以及最终进展为舒张期钙泄漏引起后去极化和电基质的发展,使AF永久化。然后将讨论钙在心力衰竭和AF之间的双向关系中的作用。心力衰竭对促进AF的心房钙处理的影响将进行审查,包括对心房肌细胞和肺静脉的影响,然后再讨论加重心力衰竭的AF方面。最后,将探讨人类和动物研究的局限性,允许将有时不一致的结果纳入背景。
Atrial fibrillation (AF) is commonly associated with heart failure. A bidirectional relationship exists between the two—AF exacerbates heart failure causing a significant increase in heart failure symptoms, admissions to hospital and cardiovascular death, while pathological remodeling of the atria as a result of heart failure increases the risk of AF. A comprehensive understanding of the pathophysiology of AF is essential if we are to break this vicious circle. In this review, the latest evidence will be presented showing a fundamental role for calcium in both the induction and maintenance of AF. After outlining atrial electrophysiology and calcium handling, the role of calcium-dependent afterdepolarizations and atrial repolarization alternans in triggering AF will be considered. The atrial response to rapid stimulation will be discussed, including the short-term protection from calcium overload in the form of calcium signaling silencing and the eventual progression to diastolic calcium leak causing afterdepolarizations and the development of an electrical substrate that perpetuates AF. The role of calcium in the bidirectional relationship between heart failure and AF will then be covered. The effects of heart failure on atrial calcium handling that promote AF will be reviewed, including effects on both atrial myocytes and the pulmonary veins, before the aspects of AF which exacerbate heart failure are discussed. Finally, the limitations of human and animal studies will be explored allowing contextualization of what are sometimes discordant results.
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