Experimental measurement of dynamic fluid shear stress on the aortic surface of the aortic valve leaflet

Abstract

Aortic valve (AV) calcification is a highly prevalent disease with serious impact on mortality and morbidity. Although exact causes and mechanisms of AV calcification are unclear, previous studies suggest that mechanical forces play a role. Since calcium deposits occur almost exclusively on the aortic surfaces of AV leaflets, it has been hypothesized that adverse patterns of fluid shear stress on the aortic surface of AV leaflets promote calcification. The current study characterizes AV leaflet aortic surface fluid shear stresses using Laser Doppler velocimetry and an in vitro pulsatile flow loop. The valve model used was a native porcine valve mounted on a suturing ring and preserved using 0.15% glutaraldehyde solution. This valve model was inserted in a mounting chamber with sinus geometries, which is made of clear acrylic to provide optical access for measurements. To understand the effects of hemodynamics on fluid shear stress, shear stress was measured across a range of conditions: varying stroke volumes at the same heart rate and varying heart rates at the same stroke volume. Systolic shear stress magnitude was found to be much higher than diastolic shear stress magnitude due to the stronger flow in the sinuses during systole, reaching up to 20 dyn/cm2 at mid-systole. Upon increasing stroke volume, fluid shear stresses increased due to stronger sinus fluid motion. Upon increasing heart rate, fluid shear stresses decreased due to reduced systolic duration that restricted the formation of strong sinus flow. Significant changes in the shear stress waveform were observed at 90 beats/ min, most likely due to altered leaflet dynamics at this higher heart rate. Overall, this study represents the most well-resolved shear stress measurements to date across a range of conditions on the aortic side of the AV. The data presented can be used for further investigation to understand AV biological response to shear stresses.

In Vitro Characterization of Bicuspid Aortic Valve Hemodynamics Using Particle Image Velocimetry

“…3), to simulate pulsatile physiological flow and pressure conditions in an in vitro setup. 11,22,[40][41][42] Compliance and resistance elements were adjusted to achieve desired flow and pressure conditions. The cardiac output, ventricular pressure and aortic pressure were measured at 500 Hz using a custom LabView program for 15 cycles, to obtain statistically converged ensemble averaged flow and pressure curves.…”

Cyclic strain induces dual-mode endothelial-mesenchymal transformation of the cardiac valve

“…VECs typically align perpendicular to flow (23,24), resulting in an anisotropic alignment on the inflow surface that is oriented circumferential to the valve leaflet (23,25). VECs in the outflow surface generally exhibit no preferred orientation and are isotropic (23) due to oscillatory blood flow patterns (26). Mechanical stresses are oriented circumferentially in the healthy valve and are altered from increased hemodynamic pressures or aberrant deformations due to altered wall stresses during the contractile cycle during ischemic cardiomyopathy.…”

Hemodynamic and Cellular Response Feedback in Calcific Aortic Valve Disease

“…For example, the normal tricuspid valve requires some amount of vorticity to facilitate rapid valve closure after systole. 71 Using a similar particle tracking and aortic valve explantation technique, Yap et al 75,76 were also able to demonstrate that the shear stresses on the ventricular side of the valve are higher than those on the aortic side. The ventricular side shear stress peaked at 64 to 71 dynes/cm 2 during systole and reversed in direction at the end of systole for only 15 to 25 milliseconds at 40 to 51 dynes/cm 2 .…”

“…These cues can be mechanical or biochemical and are critical in directing proper function of not only the vasculature system but also the surrounding tissues. For example, conditions associated with valve disease such as hypertension-related tachycardia can lead to reduced levels of aortic side shear stress, 76 which has been implicated in changes in VlvEC gene expression, function, and viability. 78,79 Hypertensive hemodynamic conditions can also increase the stretch of the vasculature system, which can lead to increased fibrosis of surrounding tissue.…”