Distribution of normal human left ventricular myofiber stress at end diastole and end systole: a target for in silico design of heart failure treatments

Ventricular wall stress is believed to be responsible for many physical mechanisms taking place in the human heart, including ventricular remodeling, which is frequently associated with heart failure. Therefore, normalization of ventricular wall stress is the cornerstone of many existing and new tre...

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Published inJournal of applied physiology (1985) Vol. 117; no. 2; pp. 142 - 152
Main Authors Genet, Martin, Lee, Lik Chuan, Nguyen, Rebecca, Haraldsson, Henrik, Acevedo-Bolton, Gabriel, Zhang, Zhihong, Ge, Liang, Ordovas, Karen, Kozerke, Sebastian, Guccione, Julius M.
Format Journal Article
LanguageEnglish
Published United States American Physiological Society 15.07.2014
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Summary:Ventricular wall stress is believed to be responsible for many physical mechanisms taking place in the human heart, including ventricular remodeling, which is frequently associated with heart failure. Therefore, normalization of ventricular wall stress is the cornerstone of many existing and new treatments for heart failure. In this paper, we sought to construct reference maps of normal ventricular wall stress in humans that could be used as a target for in silico optimization studies of existing and potential new treatments for heart failure. To do so, we constructed personalized computational models of the left ventricles of five normal human subjects using magnetic resonance images and the finite-element method. These models were calibrated using left ventricular volume data extracted from magnetic resonance imaging (MRI) and validated through comparison with strain measurements from tagged MRI (950 ± 170 strain comparisons/subject). The calibrated passive material parameter values were C 0 = 0.115 ± 0.008 kPa and B 0 = 14.4 ± 3.18; the active material parameter value was T max = 143 ± 11.1 kPa. These values could serve as a reference for future construction of normal human left ventricular computational models. The differences between the predicted and the measured circumferential and longitudinal strains in each subject were 3.4 ± 6.3 and 0.5 ± 5.9%, respectively. The predicted end-diastolic and end-systolic myofiber stress fields for the five subjects were 2.21 ± 0.58 and 16.54 ± 4.73 kPa, respectively. Thus these stresses could serve as targets for in silico design of heart failure treatments.
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PMCID: PMC4101610
ISSN:8750-7587
1522-1601
1522-1601
DOI:10.1152/japplphysiol.00255.2014