Vessel structural stress mediates aortic media degeneration in bicuspid aortopathy: New insights based on patient-specific fluid-structure interaction analysis.

Ascending aorta Bicuspid aortic valve Elastin Vessel structural stress Wall shear stress

Journal

Journal of biomechanics
ISSN: 1873-2380
Titre abrégé: J Biomech
Pays: United States
ID NLM: 0157375

Informations de publication

Date de publication:
02 12 2021
Historique:
received: 16 03 2021
revised: 06 10 2021
accepted: 06 10 2021
pubmed: 23 10 2021
medline: 1 1 2022
entrez: 22 10 2021
Statut: ppublish

Résumé

This study aimed to assess the relationship between local mechanical stimuli and regional aortic tissue degeneration using fluid-structure interaction (FSI) analysis in patients with bicuspid aortic valve (BAV) disease. Nine patients underwent ascending aortic replacement were recruited. Tissues were collected to evaluate the pathology features in four regions, greater curvature (GC-region), posterior (P-region), anterior (A-region), and lesser curvature (LC-region). FSI analysis was performed to quantify vessel structural stress (VSS) and flow-induced parameters, including wall shear stress (WSS), oscillatory shear index (OSI), and particle relative residence time (RRT). The correlation between these biomechanical metrics and tissue degeneration was analyzed. Elastin in the medial layer and media thickness were thinnest and the gap between fibers was biggest in the GC-region, followed by the P-region and A-region, while the elastin and media thickness were thickest and the gap smallest in the LC-region. The collagen deposition followed a pattern with the biggest in the GC-region and least in the LC-region. There is a strong negative correlation between mean or peak VSS and elastin thickness in the arterial wall in the GC-region (r = -0.917; p = 0.001 and r = -0.899; p = 0.001), A-region (r = -0.748; p = 0.020 and r = -0.700; p = 0.036) and P-region (r = -0.773; p = 0.014 and r = -0.769; p = 0.015), and between mean VSS and fiber distance in the A-region (r = -0.702, p = 0.035). Moreover, strong negative correlation between mean or peak VSS and media thickness was also observed. No correlation was found between WSS, OSI, and RRT and aortic tissue degeneration in these four regions. These findings indicate that increased VSS correlated with local elastin degradation and aortic media degeneration, implying that it could be a potential biomechanical parameter for a refined risk stratification for patients with BAV.

Identifiants

pubmed: 34678623
pii: S0021-9290(21)00567-4
doi: 10.1016/j.jbiomech.2021.110805
pii:
doi:

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

110805

Subventions

Organisme : Department of Health
ID : BRC-1215-20014
Pays : United Kingdom

Informations de copyright

Copyright © 2021 Elsevier Ltd. All rights reserved.

Auteurs

Fei Li (F)

Department of Structural Heart Disease, Fuwai Hospital, Beijing, China; National Clinical Research Center of Cardiovascular Diseases, State Key Laboratory of Cardiovascular Disease, National Center for Cardiovascular Diseases, Beijing, China; Department of Magnetic Resonance Imaging, Fuwai Hospital, Beijing, China.

Shuo Wang (S)

Data Science Institute, Imperial College London, UK.

Qi Gao (Q)

Division of Fluid Engineering, School of Aeronautics and Astronautics, Zhejiang University, Hangzhou, China.

Xiuyu Chen (X)

Department of Magnetic Resonance Imaging, Fuwai Hospital, Beijing, China.

Gang Yin (G)

Department of Magnetic Resonance Imaging, Fuwai Hospital, Beijing, China.

Cuntao Yu (C)

Department of Vascular Surgery, Fuwai Hospital, Beijing, China.

Yuetang Wang (Y)

Department of Structural Heart Disease, Fuwai Hospital, Beijing, China; National Clinical Research Center of Cardiovascular Diseases, State Key Laboratory of Cardiovascular Disease, National Center for Cardiovascular Diseases, Beijing, China.

Xu Wang (X)

Department of Structural Heart Disease, Fuwai Hospital, Beijing, China; National Clinical Research Center of Cardiovascular Diseases, State Key Laboratory of Cardiovascular Disease, National Center for Cardiovascular Diseases, Beijing, China.

En Qiao (E)

Department of Structural Heart Disease, Fuwai Hospital, Beijing, China; National Clinical Research Center of Cardiovascular Diseases, State Key Laboratory of Cardiovascular Disease, National Center for Cardiovascular Diseases, Beijing, China.

Zakaria Meddings (Z)

Department of Radiology, University of Cambridge, UK.

Wei Wang (W)

Department of Structural Heart Disease, Fuwai Hospital, Beijing, China; National Clinical Research Center of Cardiovascular Diseases, State Key Laboratory of Cardiovascular Disease, National Center for Cardiovascular Diseases, Beijing, China. Electronic address: weiwangfuwai@163.com.

Shihua Zhao (S)

National Clinical Research Center of Cardiovascular Diseases, State Key Laboratory of Cardiovascular Disease, National Center for Cardiovascular Diseases, Beijing, China; Department of Magnetic Resonance Imaging, Fuwai Hospital, Beijing, China. Electronic address: zhaoshihua0202@126.com.

Zhongzhao Teng (Z)

Department of Radiology, University of Cambridge, UK. Electronic address: zt215@cam.ac.uk.

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