Effects of Persistent Atrial Fibrillation-Induced Electrical Remodeling on Atrial Electro-Mechanics - Insights from a 3D Model of the Human Atria.
Effects of Persistent Atrial Fibrillation-Induced Electrical Remodeling on Atrial Electro-Mechanics - Insights from a 3D Model of the Human Atria.
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DOI：
10.1371/journal.pone.0142397
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发表时间：
2015
期刊：
影响因子：
3.7
通讯作者：
Zhang H
中科院分区：
文献类型：
--
作者：
Adeniran I;MacIver DH;Garratt CJ;Ye J;Hancox JC;Zhang H
成功心脏复律后可能会发生心房顿抑，即心房机械收缩丧失。据推测，持续性心房颤动引起的心房电生理学电重塑（AFER）可能是造成心房力学受损的原因。本模拟研究旨在研究 AFER 对心房机电的影响。开发了人类心房的 3D 机电模型来研究 AFER 对心房机电的影响。在3种条件下进行4种状态的模拟：（i）对照条件，代表正常组织（状态1）和心脏复律后2-3个月的组织（状态2），此时心房组织在完成反向电生理重塑后恢复其电生理特性； (ii) 具有正常窦性心律 (SR) 的 AF 重塑组织的 AFER-SR 条件（状态 3）； (iii) 具有重入激励波的 AF 重塑组织的 AFER-AF 条件（状态 4）。我们的结果表明，在细胞水平上，与对照条件（状态 1 和 2）相比，AFER（状态 3 和 4）缩短了动作电位并降低了肌浆网中的 Ca2+ 含量，导致细胞内 Ca2+ 瞬变幅度降低，从而导致细胞活性力降低和细胞缩短。因此，在整个器官水平上，AFER-SR 条件（状态 3）下的心房收缩显着减少。在 AFER-AF 状态（状态 4）中，心房收缩几乎消失。这项研究为理解心房机电学提供了新的见解，说明 AFER 由于细胞内 Ca2+ 瞬变减少而损害心房收缩。
Atrial stunning, a loss of atrial mechanical contraction, can occur following a successful cardioversion. It is hypothesized that persistent atrial fibrillation-induced electrical remodeling (AFER) on atrial electrophysiology may be responsible for such impaired atrial mechanics. This simulation study aimed to investigate the effects of AFER on atrial electro-mechanics. A 3D electromechanical model of the human atria was developed to investigate the effects of AFER on atrial electro-mechanics. Simulations were carried out in 3 conditions for 4 states: (i) the control condition, representing the normal tissue (state 1) and the tissue 2–3 months after cardioversion (state 2) when the atrial tissue recovers its electrophysiological properties after completion of reverse electrophysiological remodelling; (ii) AFER-SR condition for AF-remodeled tissue with normal sinus rhythm (SR) (state 3); and (iii) AFER-AF condition for AF-remodeled tissue with re-entrant excitation waves (state 4). Our results indicate that at the cellular level, AFER (states 3 & 4) abbreviated action potentials and reduced the Ca2+ content in the sarcoplasmic reticulum, resulting in a reduced amplitude of the intracellular Ca2+ transient leading to decreased cell active force and cell shortening as compared to the control condition (states 1 & 2). Consequently at the whole organ level, atrial contraction in AFER-SR condition (state 3) was dramatically reduced. In the AFER-AF condition (state 4) atrial contraction was almost abolished. This study provides novel insights into understanding atrial electro-mechanics illustrating that AFER impairs atrial contraction due to reduced intracellular Ca2+ transients.