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人类心房颤动中特定腔室的壁厚度特征

Chamber-specific wall thickness features in human atrial fibrillation.

作者信息

Zhao Jichao, Kennelly James, Nalar Aaqel, Kulathilaka Anuradha, Sharma Roshan, Bai Jieyun, Li Ning, Fedorov Vadim V

机构信息

Auckland Bioengineering Institute, University of Auckland, Auckland, New Zealand.

Department of Physiology and Cell Biology, Bob and Corrine Frick Center for Heart Failure and Arrhythmia, The Ohio State University Wexner Medical Center, Columbus, OH, USA.

出版信息

Interface Focus. 2023 Dec 15;13(6):20230044. doi: 10.1098/rsfs.2023.0044. eCollection 2023 Dec 6.

DOI:10.1098/rsfs.2023.0044
PMID:38106912
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10722209/
Abstract

Persistent atrial fibrillation (AF) is not effectively treated due to a lack of adequate tools for identifying patient-specific AF substrates. Recent studies revealed that in 30-50% of patients, persistent AF is maintained by localized drivers not only in the left atrium (LA) but also in the right atrium (RA). The chamber-specific atrial wall thickness (AWT) features underlying AF remain elusive, though the important role of AWT in AF is widely acknowledged. We aimed to provide direct evidence of the existence of distinguished RA and LA AWT features underlying AF drivers by analysing functionally and structurally mapped human hearts . Coronary-perfused intact human atria ( = 7, 47 ± 14 y.o.; two female) were mapped using panoramic near-infrared optical mapping during pacing-induced AF. Then the hearts were imaged at approximately 170 µm resolution by 9.4 T gadolinium-enhanced MRI. The heart was segmented, and 3D AWT throughout atrial chambers was estimated and analysed. Optical mapping identified six localized RA re-entrant drivers in four hearts and four LA drivers in three hearts. All RA AF drivers were anchored to the pectinate muscle junctions with the crista terminalis or atrial walls. The four LA AF drivers were in the posterior LA. RA ( = 4) with AF drivers were thicker with greater AWT variation than RA ( = 3) without drivers (5.4 ± 2.6 mm versus 5.0 ± 2.4 mm, -test < 0.05; -test < 0.05). Furthermore, AWT in RA driver regions was thicker and varied more than in RA non-driver regions (5.1 ± 2.5 mm versus 4.4 ± 2.2 mm, -test < 0.05; -test < 0.05). On the other hand, LA ( = 3) with drivers was thinner than the LA ( = 4) without drivers. In particular, LA driver regions were thinner than the rest of LA regions (3.4 ± 1.0 mm versus 4.2 ± 1.0 mm, -test < 0.05). This study demonstrates chamber-specific AWT features of AF drivers. In RA, driver regions are thicker and have more variable AWT than non-driver regions. By contrast, LA drivers are thinner than non-drivers. Robust evaluation of patient-specific AWT features should be considered for chamber-specific targeted ablation.

摘要

由于缺乏用于识别患者特异性房颤基质的适当工具,持续性房颤(AF)无法得到有效治疗。最近的研究表明,在30%-50%的患者中,持续性房颤不仅由左心房(LA)中的局部驱动因素维持,右心房(RA)中也存在此类因素。尽管心房壁厚度(AWT)在房颤中的重要作用已得到广泛认可,但房颤背后特定腔室的心房壁厚度特征仍不明确。我们旨在通过分析功能和结构映射的人类心脏,为房颤驱动因素背后存在独特的右心房和左心房AWT特征提供直接证据。在起搏诱发房颤期间,使用全景近红外光学映射对冠状动脉灌注的完整人类心房(n = 7,47±14岁;两名女性)进行映射。然后,通过9.4T钆增强MRI以约170µm的分辨率对心脏进行成像。对心脏进行分割,并估计和分析整个心房腔室的三维AWT。光学映射在四个心脏中识别出六个局部右心房折返驱动因素,在三个心脏中识别出四个左心房驱动因素。所有右心房房颤驱动因素均锚定在梳状肌与界嵴或心房壁的交界处。四个左心房房颤驱动因素位于左心房后部。有房颤驱动因素的右心房(n = 4)比无驱动因素的右心房(n = 3)更厚,AWT变化更大(5.4±2.6mm对5.0±2.4mm,t检验P<0.05;F检验P<0.05)。此外,右心房驱动因素区域的AWT比非驱动因素区域更厚且变化更大(5.1±2.5mm对4.4±2.2mm,t检验P<0.05;F检验P<0.05)。另一方面,有驱动因素的左心房(n = 3)比无驱动因素的左心房(n = 4)更薄。特别是,左心房驱动因素区域比左心房其他区域更薄(3.4±1.0mm对4.2±1.0mm,t检验P<0.05)。本研究证明了房颤驱动因素的特定腔室AWT特征。在右心房中,驱动因素区域比非驱动因素区域更厚,AWT变化更大。相比之下,左心房驱动因素比非驱动因素更薄。对于特定腔室的靶向消融,应考虑对患者特异性AWT特征进行稳健评估。

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本文引用的文献

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JAMA. 2022 Jun 21;327(23):2296-2305. doi: 10.1001/jama.2022.8831.
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The impact of the atrial wall thickness in normal/mild late-gadolinium enhancement areas on atrial fibrillation rotors in persistent atrial fibrillation patients.正常/轻度延迟钆增强区域的心房壁厚度对持续性心房颤动患者心房颤动转子的影响。
J Arrhythm. 2022 Jan 13;38(2):221-231. doi: 10.1002/joa3.12676. eCollection 2022 Apr.
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A robust computational framework for estimating 3D Bi-Atrial chamber wall thickness.
一种用于估计 3D 双心房室壁厚度的强大计算框架。
Comput Biol Med. 2019 Nov;114:103444. doi: 10.1016/j.compbiomed.2019.103444. Epub 2019 Sep 12.
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JACC Clin Electrophysiol. 2018 Dec;4(12):1501-1515. doi: 10.1016/j.jacep.2018.08.024. Epub 2018 Nov 1.
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