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Cardiac Remodeling in Aortic and Mitral Valve Disease - a Simulation Study with Clinical Validation

Maksuti, Elira ; Westerhof, Berend E ; Ugander, Martin LU ; Donker, Dirk W ; Carlsson, Marcus LU and Broome, Michael (2019) In Journal of Applied Physiology 126(5). p.1377-1389
Abstract

BACKGROUND: Remodeling is an important long-term determinant of cardiac function throughout the progression of heart disease. Numerous biomolecular pathways for mechanosensing and transduction are involved. However, we hypothesize that biomechanical factors alone can explain changes in myocardial volume and chamber size in valve disease.

METHODS: A validated model of the human vasculature and the four cardiac chambers was used to simulate aortic stenosis, mitral regurgitation and aortic regurgitation. Remodeling was simulated with adaptive feedback preserving myocardial fiber stress and wall shear stress in all four cardiac chambers. Briefly, the model used myocardial fiber stress to determine wall thickness and cardiac chamber... (More)

BACKGROUND: Remodeling is an important long-term determinant of cardiac function throughout the progression of heart disease. Numerous biomolecular pathways for mechanosensing and transduction are involved. However, we hypothesize that biomechanical factors alone can explain changes in myocardial volume and chamber size in valve disease.

METHODS: A validated model of the human vasculature and the four cardiac chambers was used to simulate aortic stenosis, mitral regurgitation and aortic regurgitation. Remodeling was simulated with adaptive feedback preserving myocardial fiber stress and wall shear stress in all four cardiac chambers. Briefly, the model used myocardial fiber stress to determine wall thickness and cardiac chamber wall shear stress to determine chamber volume.

RESULTS: Aortic stenosis resulted in the development of concentric left ventricular hypertrophy. Aortic and mitral regurgitation resulted in eccentric remodeling and eccentric hypertrophy, with more pronounced hypertrophy for aortic regurgitation. Comparisons with published clinical data showed the same direction and similar magnitudes of changes in end-diastolic volume index and left ventricular diameters. Changes in myocardial wall volume and wall thickness were within a realistic range both in stenotic and regurgitant valvular disease.

CONCLUSIONS: Simulations of remodeling in left-sided valvular disease support, in both a qualitative and quantitative manner, that left ventricular chamber size and hypertrophy are primarily determined by preservation of wall shear stress and myocardial fiber stress.

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organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Journal of Applied Physiology
volume
126
issue
5
pages
1377 - 1389
publisher
American Physiological Society
external identifiers
  • scopus:85065863859
  • pmid:30730809
ISSN
1522-1601
DOI
10.1152/japplphysiol.00791.2018
language
English
LU publication?
yes
id
faaa9095-be38-4254-9419-a5b3622fb011
date added to LUP
2019-05-14 14:11:19
date last changed
2024-06-11 11:04:15
@article{faaa9095-be38-4254-9419-a5b3622fb011,
  abstract     = {{<p>BACKGROUND: Remodeling is an important long-term determinant of cardiac function throughout the progression of heart disease. Numerous biomolecular pathways for mechanosensing and transduction are involved. However, we hypothesize that biomechanical factors alone can explain changes in myocardial volume and chamber size in valve disease.</p><p>METHODS: A validated model of the human vasculature and the four cardiac chambers was used to simulate aortic stenosis, mitral regurgitation and aortic regurgitation. Remodeling was simulated with adaptive feedback preserving myocardial fiber stress and wall shear stress in all four cardiac chambers. Briefly, the model used myocardial fiber stress to determine wall thickness and cardiac chamber wall shear stress to determine chamber volume.</p><p>RESULTS: Aortic stenosis resulted in the development of concentric left ventricular hypertrophy. Aortic and mitral regurgitation resulted in eccentric remodeling and eccentric hypertrophy, with more pronounced hypertrophy for aortic regurgitation. Comparisons with published clinical data showed the same direction and similar magnitudes of changes in end-diastolic volume index and left ventricular diameters. Changes in myocardial wall volume and wall thickness were within a realistic range both in stenotic and regurgitant valvular disease.</p><p>CONCLUSIONS: Simulations of remodeling in left-sided valvular disease support, in both a qualitative and quantitative manner, that left ventricular chamber size and hypertrophy are primarily determined by preservation of wall shear stress and myocardial fiber stress.</p>}},
  author       = {{Maksuti, Elira and Westerhof, Berend E and Ugander, Martin and Donker, Dirk W and Carlsson, Marcus and Broome, Michael}},
  issn         = {{1522-1601}},
  language     = {{eng}},
  month        = {{02}},
  number       = {{5}},
  pages        = {{1377--1389}},
  publisher    = {{American Physiological Society}},
  series       = {{Journal of Applied Physiology}},
  title        = {{Cardiac Remodeling in Aortic and Mitral Valve Disease - a Simulation Study with Clinical Validation}},
  url          = {{http://dx.doi.org/10.1152/japplphysiol.00791.2018}},
  doi          = {{10.1152/japplphysiol.00791.2018}},
  volume       = {{126}},
  year         = {{2019}},
}