Linking statistical shape models and simulated function in the healthy adult human heart

Author:

Rodero CristobalORCID,Strocchi MarinaORCID,Marciniak MaciejORCID,Longobardi StefanoORCID,Whitaker JohnORCID,O’Neill Mark D.ORCID,Gillette KarliORCID,Augustin ChristophORCID,Plank GernotORCID,Vigmond Edward J.ORCID,Lamata PabloORCID,Niederer Steven A.ORCID

Abstract

Cardiac anatomy plays a crucial role in determining cardiac function. However, there is a poor understanding of how specific and localised anatomical changes affect different cardiac functional outputs. In this work, we test the hypothesis that in a statistical shape model (SSM), the modes that are most relevant for describing anatomy are also most important for determining the output of cardiac electromechanics simulations. We made patient-specific four-chamber heart meshes (n = 20) from cardiac CT images in asymptomatic subjects and created a SSM from 19 cases. Nine modes captured 90% of the anatomical variation in the SSM. Functional simulation outputs correlated best with modes 2, 3 and 9 on average (R = 0.49 ± 0.17, 0.37 ± 0.23 and 0.34 ± 0.17 respectively). We performed a global sensitivity analysis to identify the different modes responsible for different simulated electrical and mechanical measures of cardiac function. Modes 2 and 9 were the most important for determining simulated left ventricular mechanics and pressure-derived phenotypes. Mode 2 explained 28.56 ± 16.48% and 25.5 ± 20.85, and mode 9 explained 12.1 ± 8.74% and 13.54 ± 16.91% of the variances of mechanics and pressure-derived phenotypes, respectively. Electrophysiological biomarkers were explained by the interaction of 3 ± 1 modes. In the healthy adult human heart, shape modes that explain large portions of anatomical variance do not explain equivalent levels of electromechanical functional variation. As a result, in cardiac models, representing patient anatomy using a limited number of modes of anatomical variation can cause a loss in accuracy of simulated electromechanical function.

Publisher

Public Library of Science (PLoS)

Subject

Computational Theory and Mathematics,Cellular and Molecular Neuroscience,Genetics,Molecular Biology,Ecology,Modelling and Simulation,Ecology, Evolution, Behavior and Systematics

Reference92 articles.

1. Mineralocorticoid receptor antagonism prevents the electrical remodeling that precedes cellular hypertrophy after myocardial infarction;E Perrier;Circulation,2004

2. Progressive ventricular remodeling in rat with myocardial infarction;JM Pfeffer;American Journal of Physiology-Heart and Circulatory Physiology,1991

3. Survival, haemodynamics and cardiac remodelling follow up in mice after myocardial infarction;S Pons;Clinical and experimental pharmacology and physiology,2003

4. The ‘Digital Twin’to enable the vision of precision cardiology;J Corral-Acero;European Heart Journal,2020

5. Virtual Electrophysiological Study of Atrial Fibrillation in Fibrotic Remodeling;KS McDowell;PLOS ONE,2015

Cited by 41 articles. 订阅此论文施引文献 订阅此论文施引文献,注册后可以免费订阅5篇论文的施引文献,订阅后可以查看论文全部施引文献

同舟云学术

1.学者识别学者识别

2.学术分析学术分析

3.人才评估人才评估

"同舟云学术"是以全球学者为主线,采集、加工和组织学术论文而形成的新型学术文献查询和分析系统,可以对全球学者进行文献检索和人才价值评估。用户可以通过关注某些学科领域的顶尖人物而持续追踪该领域的学科进展和研究前沿。经过近期的数据扩容,当前同舟云学术共收录了国内外主流学术期刊6万余种,收集的期刊论文及会议论文总量共计约1.5亿篇,并以每天添加12000余篇中外论文的速度递增。我们也可以为用户提供个性化、定制化的学者数据。欢迎来电咨询!咨询电话:010-8811{复制后删除}0370

www.globalauthorid.com

TOP

Copyright © 2019-2024 北京同舟云网络信息技术有限公司
京公网安备11010802033243号  京ICP备18003416号-3