Inherent Atrial Fibrillation Vulnerability in the Appendages Exacerbated in Heart Failure

Shaleka Agrawal, Joseph Ashby, Jeiyun Bai, Fan Feng, Xue J. Cai, Joseph Yanni, Caroline B. Jones, Sunil J.R.J. Logantha, Akbar Vohra, Robert C. Hutcheon, Antonio F. Corno, Halina Dobrzynski, Robert S. Stephenson, Mark Boyett, George Hart, Jonathan Jarvis, Bruce Smaill, Jichao Zhao

Research output: Chapter in Book/Report/Conference proceedingConference contributionpeer-review

Abstract

Atrial fibrillation (AF) frequently accompanies heart failure (HF), however, the causal mechanism underlying their atrial electrophysiological substrates remains unclear. In the present study, we evaluated the effects of abnormal anatomical characteristics on the electrophysiology of rabbit atria with HF. Micro-CT images from adult New Zealand white rabbit hearts (n = 4 HF and n = 4 control) were acquired. Novel imaging methods were used to reconstruct atrial myofiber architecture at a high resolution of 21 µm3/voxel for quantitative analysis of the structural remodelling. Effects of this structural remodelling on the vulnerability to atrial re-entrant waves was analysed using computer simulation. Reconstructed data showed increased chamber lumen and an uneven reduction in wall thickness across the appendages in HF. Anatomically, myofibers in epicardial walls of the appendages were identified to be circumferential, perpendicular to the pectinate muscles (PMs). The relative ratio of average PM thickness to the atrial wall was larger in HF vs. control (right atrial appendages: 3.5 versus 2.7 and left atrial appendages: 4.4 versus 3.7, p < 0.001). Furthermore, the uncoupled myofiber orientation between the PMs and atrial wall was verified using confocal microscopy at a spatial resolution of 0.2 µm3. Computer simulations suggested (1) uncoupled myofiber orientation of the PMs and the atrial wall may increase the vulnerability to AF; and (2) decreased atrial thickness and dilated chambers may amplify the unstable substrates leading to re-entry formation in HF. Our ex-vivo to in-silico results demonstrate that uncoupled myofiber orientation in the atria is an important component of the structural remodelling, facilitating the development and maintenance of AF in HF.

Original languageEnglish
Title of host publicationStatistical Atlases and Computational Models of the Heart. Regular and CMRxRecon Challenge Papers - 14th International Workshop, STACOM 2023, Held in Conjunction with MICCAI 2023, Revised Selected Papers
EditorsOscar Camara, Esther Puyol-Antón, Avan Suinesiaputra, Alistair Young, Maxime Sermesant, Qian Tao, Chengyan Wang
PublisherSpringer Nature
Pages220-229
Number of pages10
ISBN (Print)9783031524479
DOIs
Publication statusPublished - 2024
Event14th International Workshop on Statistical Atlases and Computational Models of the Heart, STACOM 2023 held in Conjunction with MICCAI 2023 - Vancouver, Canada
Duration: 12 Oct 202312 Oct 2023

Publication series

NameLecture Notes in Computer Science (including subseries Lecture Notes in Artificial Intelligence and Lecture Notes in Bioinformatics)
Volume14507 LNCS
ISSN (Print)0302-9743
ISSN (Electronic)1611-3349

Conference

Conference14th International Workshop on Statistical Atlases and Computational Models of the Heart, STACOM 2023 held in Conjunction with MICCAI 2023
Country/TerritoryCanada
CityVancouver
Period12/10/2312/10/23

Keywords

  • atrial appendage
  • Atrial fibrillation
  • computer modelling
  • heart failure
  • myofiber architecture

Fingerprint

Dive into the research topics of 'Inherent Atrial Fibrillation Vulnerability in the Appendages Exacerbated in Heart Failure'. Together they form a unique fingerprint.

Cite this