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Left Atrial Remodeling Mechanisms Associated with Atrial Fibrillation
Cardiovascular Engineering and Technology ( IF 1.8 ) Pub Date : 2021-03-01 , DOI: 10.1007/s13239-021-00527-w
Defu Qiu 1 , Liqing Peng 2 , Dhanjoo N Ghista 3, 4 , Kelvin K L Wong 1, 3
Affiliation  

Heart disease has always been one of the important diseases that endanger health and cause death. Therefore, it is particularly important to understand left atrium reconstruction and atrial fibrillation before heart image processing. The purpose of this paper is to provide an important review of the mechanisms of left atrial remodeling (LAR) associated with atrial fibrillation (AF). LAR refers to the spectrum of pathophysiological changes in (i) atrial structure and physiological function, and (ii) electric, ionic, and molecular milieu of the LA, in response to stresses imposed by conditions such as hypertension, myocardial ischemia, autonomic denervation and congestive heart failure. The main mechanisms of LAR include electrical remodeling, structural remodeling, metabolic remodeling, autonomic remodeling, neurohormones and inflammation, and other influencing factors. LAR is not only the basic mechanism of AF and heart failure, but also the pathophysiological basis of its progression. In clinical practice, AF is the most common persistent arrhythmia, and is believed to be the result of a combination of mechanisms that have triggers and maintenance mechanisms, including spontaneous ectopic pacing and multiple wavelet reentry. While LA electrophysiological, structural, and ultra-structural changes trigger AF, in turn, AF alters the LA electrical and structural properties that promote its maintenance and recurrence. Chronic AF leads to extensive changes in atrial cellular substructures, including loss of myofibrils, accumulation of glycogen, changes in mitochondrial shape and size, fragmentation of sarcoplasmic reticulum, and dispersion of nuclear chromatin. Electrical remodeling and structural remodeling of the atria during AF, involving structural changes and functional impairment of the left atrium, can lead to serious decline in left ventricular function and severe heart failure. Therefore, LAR and AF are inter-activating phenomena, and the resulting complications can cause serious disabling and fatal events. In this paper, we present (i) the mechanisms of LAR, in the form of structural, electrical, metabolic, and neurohormonal changes, and (ii) their interactive roles in initiating and maintaining AF. These in-depth understanding of the atrial remodeling mechanisms can in turn provide useful insights into the treatment of AF and heart failure.



中文翻译:

与心房颤动相关的左心房重构机制

心脏病历来是危害健康和导致死亡的重要疾病之一。因此,在心脏图像处理之前了解左心房重建和心房颤动就显得尤为重要。本文的目的是对与心房颤动 (AF) 相关的左心房重构 (LAR) 机制进行重要回顾。LAR 是指 (i) 心房结构和生理功能,以及 (ii) LA 的电、离子和分子环境的病理生理变化谱,以响应由高血压、心肌缺血、自主神经去神经支配和充血性心力衰竭。LAR 的主要机制包括电重构、结构重构、代谢重构、自主神经重构、神经激素和炎症,以及其他影响因素。LAR不仅是AF和心力衰竭发生的基本机制,也是其进展的病理生理基础。在临床实践中,AF 是最常见的持续性心律失常,并且被认为是具有触发和维持机制的机制组合的结果,包括自发性异位起搏和多次小波折返。虽然 LA 电生理、结构和超微结构的变化会触发 AF,但反过来,AF 会改变 LA 的电和结构特性,促进其维持和复发。慢性房颤会导致心房细胞亚结构的广泛变化,包括肌原纤维的丢失、糖原的积累、线粒体形状和大小的变化、肌浆网的碎裂和核染色质的分散。房颤期间心房的电重构和结构重构,涉及左心房的结构变化和功能障碍,可导致左心室功能严重下降和严重心力衰竭。因此,LAR 和 AF 是相互激活的现象,由此产生的并发症会导致严重的致残和致命事件。在本文中,我们介绍了 (i) LAR 的机制,以结构、电、代谢和神经激素变化的形式,以及 (ii) 它们在启动和维持 AF 中的交互作用。这些对心房重塑机制的深入了解反过来可以为 AF 和心力衰竭的治疗提供有用的见解。可导致左心室功能严重下降和严重心力衰竭。因此,LAR 和 AF 是相互激活的现象,由此产生的并发症会导致严重的致残和致命事件。在本文中,我们介绍了 (i) LAR 的机制,以结构、电、代谢和神经激素变化的形式,以及 (ii) 它们在启动和维持 AF 中的交互作用。这些对心房重塑机制的深入了解反过来可以为 AF 和心力衰竭的治疗提供有用的见解。可导致左心室功能严重下降和严重心力衰竭。因此,LAR 和 AF 是相互激活的现象,由此产生的并发症会导致严重的致残和致命事件。在本文中,我们介绍了 (i) LAR 的机制,以结构、电、代谢和神经激素变化的形式,以及 (ii) 它们在启动和维持 AF 中的交互作用。这些对心房重塑机制的深入了解反过来可以为 AF 和心力衰竭的治疗提供有用的见解。和神经激素变化,以及(ii)它们在启动和维持 AF 中的相互作用。这些对心房重塑机制的深入了解反过来可以为 AF 和心力衰竭的治疗提供有用的见解。和神经激素变化,以及(ii)它们在启动和维持 AF 中的相互作用。这些对心房重塑机制的深入了解反过来可以为 AF 和心力衰竭的治疗提供有用的见解。

更新日期:2021-03-02
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