دورية أكاديمية
Chamber-specific wall thickness features in human atrial fibrillation.
| العنوان: | Chamber-specific wall thickness features in human atrial fibrillation. |
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| المؤلفون: | Zhao J; Auckland Bioengineering Institute, University of Auckland, Auckland, New Zealand., Kennelly J; Auckland Bioengineering Institute, University of Auckland, Auckland, New Zealand., Nalar A; Auckland Bioengineering Institute, University of Auckland, Auckland, New Zealand., Kulathilaka A; Auckland Bioengineering Institute, University of Auckland, Auckland, New Zealand., Sharma R; Auckland Bioengineering Institute, University of Auckland, Auckland, New Zealand., Bai J; Auckland Bioengineering Institute, University of Auckland, Auckland, New Zealand., Li N; 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., Fedorov VV; 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. |
| المصدر: | Interface focus [Interface Focus] 2023 Dec 15; Vol. 13 (6), pp. 20230044. Date of Electronic Publication: 2023 Dec 15 (Print Publication: 2023). |
| نوع المنشور: | Journal Article |
| اللغة: | English |
| بيانات الدورية: | Publisher: Royal Society Country of Publication: England NLM ID: 101531990 Publication Model: eCollection Cited Medium: Print ISSN: 2042-8898 (Print) Linking ISSN: 20428898 NLM ISO Abbreviation: Interface Focus Subsets: PubMed not MEDLINE |
| أسماء مطبوعة: | Original Publication: London : Royal Society, 2011- |
| مستخلص: | 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 ex vivo . Coronary-perfused intact human atria ( n = 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 3 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 ( n = 4) with AF drivers were thicker with greater AWT variation than RA ( n = 3) without drivers (5.4 ± 2.6 mm versus 5.0 ± 2.4 mm, T -test p < 0.05; F -test p < 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, T -test p < 0.05; F -test p < 0.05). On the other hand, LA ( n = 3) with drivers was thinner than the LA ( n = 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, T -test p < 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. Competing Interests: The authors declare no conflicts of interest. (© 2023 The Authors.) |
| References: | Circ Arrhythm Electrophysiol. 2012 Apr;5(2):361-70. (PMID: 22423141) J Am Coll Cardiol. 2017 Mar 14;69(10):1247-1256. (PMID: 28279291) Anat Rec A Discov Mol Cell Evol Biol. 2004 Oct;280(2):1053-61. (PMID: 15372488) JAMA. 2022 Jun 21;327(23):2296-2305. (PMID: 35727277) IEEE Trans Med Imaging. 2017 Aug;36(8):1607-1614. (PMID: 28422654) Europace. 2016 Mar;18(3):376-83. (PMID: 25842272) Heart Rhythm. 2010 Jun;7(6):835-46. (PMID: 20206320) Circ Res. 1998 Aug 24;83(4):448-62. (PMID: 9721702) Med Image Anal. 2018 Dec;50:36-53. (PMID: 30208355) J Arrhythm. 2022 Jan 13;38(2):221-231. (PMID: 35387140) Interface Focus. 2023 Dec 15;13(6):20230044. (PMID: 38106912) J Am Coll Cardiol. 2017 Mar 14;69(10):1257-1269. (PMID: 28279292) J Am Heart Assoc. 2017 Aug 22;6(8):. (PMID: 28862969) Phys Rev Lett. 2015 Feb 13;114(6):068302. (PMID: 25723248) Comput Biol Med. 2019 Nov;114:103444. (PMID: 31542646) Eur Heart J. 2015 Sep 14;36(35):2390-401. (PMID: 26059724) Front Physiol. 2018 Oct 04;9:1352. (PMID: 30349483) JACC Clin Electrophysiol. 2018 Dec;4(12):1501-1515. (PMID: 30573112) |
| معلومات مُعتمدة: | R01 HL115580 United States HL NHLBI NIH HHS; R01 HL135109 United States HL NHLBI NIH HHS |
| فهرسة مساهمة: | Keywords: atrial fibrillation; atrial wall thickness; cardiac arrhythmogenesis; human atria |
| تواريخ الأحداث: | Date Created: 20231218 Latest Revision: 20240123 |
| رمز التحديث: | 20240123 |
| مُعرف محوري في PubMed: | PMC10722209 |
| DOI: | 10.1098/rsfs.2023.0044 |
| PMID: | 38106912 |
| قاعدة البيانات: | MEDLINE |
| تدمد: | 2042-8898 |
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| DOI: | 10.1098/rsfs.2023.0044 |