Key result
In a computational simulation, severe aortic stenosis significantly increased global left ventricular myofiber peak systolic stress to 16.18 kPa compared to 9.31 kPa at baseline (p<0.001).
Why the study?
Traditional hemodynamic parameters have limitations in effectively grading aortic stenosis severity in the presence of LV dysfunction.
Does simulated aortic stenosis increase LV myofiber stress in a finite element model of the human heart?
Population
Finite element model of the human heart with a coupled lumped-parameter circulatory system
Comparison
Moderate AS and severe AS vs baseline
Design
Finite element analysis simulation study
Authors
Loading...
Computational simulations demonstrate that increasing severity of aortic stenosis progressively elevates LV myofiber peak systolic stress, providing a biomechanical basis for LV dysfunction in AS.
Does simulated aortic stenosis increase LV myofiber stress in a finite element model of the human heart?
Absolute Event Rate: 16.18% vs 9.31%
p-value: p=<0.001
Computational simulations demonstrate that increasing severity of aortic stenosis progressively elevates LV myofiber peak systolic stress, providing a biomechanical basis for LV dysfunction in AS.
Wisneski et al. (2020) studied Aortic Stenosis. Simulated Aortic Stenosis vs. Baseline (normal aortic valve) was evaluated on Global LV myofiber peak systolic stress (kPa) (p=<0.001). In a computational simulation, severe aortic stenosis significantly increased global left ventricular myofiber peak systolic stress to 16.18 kPa compared to 9.31 kPa at baseline (p<0.001).
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: