In-Silico assessment of aortic valve function and mechanics under 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.