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Simulation of plaque formation in a realistic geometry of a human aorta: effects of endothelial layer properties,
Amirabbas Benvidi1, Bahar Firoozabadi2
1School of Mechanical Engineering, Sharif University of Technology, Tehran, Iran.
This study numerically investigates foam cell accumulation in the aorta, a key indicator of atherosclerosis. Hypertension significantly increases foam cell buildup, highlighting its critical role in cardiovascular disease progression.
Area of Science:
- Biomedical Engineering
- Computational Fluid Dynamics
- Cardiovascular Science
Background:
- Cardiovascular diseases are the leading global cause of death.
- Atherosclerosis, characterized by arterial narrowing, begins with endothelial inflammation and LDL infiltration.
- Foam cells are critical indicators of atherosclerosis development.
Purpose of the Study:
- To numerically investigate foam cell accumulation in a patient-specific human thoracic aorta model.
- To analyze the impact of endothelial layer modeling, heart rate (HR), and hypertension on foam cell distribution.
- To understand the relationship between hemodynamic factors and atherosclerosis progression.
Main Methods:
- Utilized Navier-Stokes, Darcy, and mass transfer equations for numerical simulations.
- Modeled patient-specific human thoracic aorta geometry.
- Investigated effects of time-averaged wall shear stress and oscillatory shear rate on endothelial properties.
Main Results:
- Foam cell accumulation location varied based on endothelial cell property determinants (outer curvature vs. inner curvature).
- Increased heart rate (HR) led to a slight decrease in average foam cell concentration.
- Hypertension significantly increased foam cell concentration, indicating a heightened risk of circulatory problems.
Conclusions:
- Endothelial cell properties, influenced by shear stress, dictate foam cell distribution patterns.
- While HR has a minor effect, hypertension poses a substantial risk for atherosclerosis development.
- Findings underscore the critical impact of blood pressure on cardiovascular health and potential for irreversible circulatory damage.
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