Key result
Cardiovascular simulations demonstrated that left ventricular chamber size and hypertrophy in left-sided valvular disease are primarily determined by preservation of wall shear and myocardial fiber stress.
Why the study?
The authors hypothesized that biomechanical factors alone can explain changes in myocardial volume and chamber size in valve disease, despite the involvement of numerous biomolecular pathways.
Can biomechanical factors (preservation of wall shear stress and myocardial fiber stress) alone explain changes in myocardial volume and chamber size in left-sided valvular disease?
Can biomechanical factors (preservation of wall shear stress and myocardial fiber stress) alone explain changes in myocardial volume and chamber size in left-sided valvular disease?
Computational simulations demonstrate that mechanical stress preservation alone can quantitatively and qualitatively predict cardiac remodeling patterns in left-sided valvular disease.
Answers are grounded in this paper and cite their sources.
May refine LV remodeling assessment in valvular disease; leaves open prospective validation and therapeutic trials.
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. 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. 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 in both stenotic and regurgitant valvular disease. 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. NEW & NOTEWORTHY Cardiovascular simulations with adaptive feedback that normalizes wall shear stress and fiber stress in the cardiac chambers could predict, in a quantitative and qualitative manner, remodeling patterns seen in patients with left-sided valvular disease. This highlights how mechanical stress remains a fundamental aspect of cardiac remodeling. This in silico study validated with clinical data paves the way for future patient-specific predictions of remodeling in valvular disease.
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Maksuti et al. (2019) studied Aortic and mitral valve disease. Simulation of left-sided valvular disease (aortic stenosis, mitral regurgitation, aortic regurgitation) was evaluated on Cardiac remodeling (changes in myocardial volume and chamber size). Cardiovascular simulations demonstrated that left ventricular chamber size and hypertrophy in left-sided valvular disease are primarily determined by preservation of wall shear and myocardial fiber stress.
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