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Updated: May 11, 2026
Design of a Cyclic Pressure Bioreactor for the Ex Vivo Study of Aortic Heart Valves
Published on: August 23, 2011
In-Silico assessment of aortic valve function and mechanics under hypertension
Jason A Shar1, Philippe Sucosky2
1Rand Simulation, Charlottesville, VA, United States.
Insights
Hypertension significantly alters aortic valve leaflet mechanics, increasing stress and potentially driving calcific aortic valve disease (CAVD) development. This study reveals pressure-dependent changes in fluid wall shear stress and leaflet stretching under hypertensive conditions.
Area of Science:
- Cardiovascular Mechanics
- Biomedical Engineering
- Pathophysiology of Valve Disease
Background:
- Calcific aortic valve disease (CAVD) is the most prevalent heart valve disorder.
- Hypertension is a significant risk factor for CAVD, but underlying mechanisms remain unclear.
- Aortic valve (AV) tissue is sensitive to mechanical forces, suggesting a role for hypertension-induced stress.
Purpose of the Study:
- To investigate the impact of normotensive, pre-hypertensive, and hypertensive conditions on AV function and mechanics.
- To test the hypothesis that hypertension induces mechanical stress states conducive to CAVD.
- To utilize fluid-structure interaction modeling to compare AV behavior across different blood pressure levels.
Main Methods:
- Fluid-structure interaction modeling was employed in an idealized aortic root geometry.
- Arbitrary Lagrangian-Eulerian approach computed AV flow and leaflet dynamics.
- Analysis focused on fluid wall shear stress (fWSS) and leaflet mechanics (coaptation angle, tensile stretch) under varying pressure conditions.
Main Results:
- Hypertensive conditions increased flow vorticity and reduced leaflet coaptation angle in a pressure-dependent manner.
- Elevated pressures led to increased fluid wall shear stress (fWSS) on leaflets, with varied regional alterations.
- Hypertension increased leaflet tensile stretch, particularly on the left- and non-coronary leaflets.
Conclusions:
- Hypertension induces complex fluid and structural stress alterations in AV leaflets.
- Findings support a mechanical etiology for CAVD in hypertensive individuals.
- This mechano-etiology may explain the high prevalence of CAVD in patients with hypertension.
Introduction:
Calcific aortic valve disease (CAVD) is the most common heart valve disorder. While hypertension is a major risk factor, the mechanisms by which elevated blood pressure contributes to calcification are largely unknown. Given the established sensitivity of aortic valve (AV) tissue to mechanical cues, hypertension may subject AV leaflets to a stress state conducive to CAVD. To address this hypothesis, the objective of this study was to compare AV function and mechanics under normotensive (NTN, 120/80 mmHg), pre-hypertensive (preHTN, 125/80 mmHg) and hypertensive (HTN, 130/90 mmHg) conditions using fluid-structure interaction modeling.
Methods:
AV flow and leaflet dynamics were computed in an idealized aortic root geometry using the arbitrary Lagrangian-Eulerian approach. Boundary conditions achieving physiologic cardiac output and coronary perfusion, proper leaflet coaptation, and reflecting preHTN and HTN aortic pressure elevations were determined and applied. The fluid wall shear stress (fWSS) on the leaflet fibrosa was analyzed in terms of regional temporal shear magnitude (TSM) and oscillatory shear index (OSI). Leaflet mechanics was characterized in terms of leaflet profile, coaptation angle, and regional tensile stretch (tS) ratios.
Results:
Hypertensive conditions increased early diastolic flow vorticity and decreased the leaflet coaptation angle in a pressure-dependent manner. PreHTN and HTN subjected all leaflets to fWSS overloads (up to 45% increase in radial TSM vs. NTN). While preHTN and HTN resulted in contrasted radial TSM alterations in the leaflet base (up to 0.6- and 1.3-fold change, respectively, vs. NTN), both conditions caused an increase in radial TSM in the belly and tip regions (up to 1.5-fold increase vs. NTN). Radial fWSS bidirectionality increased in a pressure-dependent manner in the base of the left- and non-coronary leaflets (up to 0.23-point increase in OSI vs. NTN) but was attenuated in the belly region (up to 0.19-point decrease). Hypertension caused a pressure-dependent increase in tS ratio (up to 5% increase vs. NTN) on the left- and non-coronary leaflets.
Discussion:
Hypertension subjects AV leaflets to complex fluid and structural stress alterations. The results support the existence of a mechano-etiology for CAVD in hypertensive patients and could explain the prevalence of this disease in this patient population.
