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Mitigation of Shear-Induced Blood Damage in Mechanical Heart Valves using Passive Flow Control

Heart valves regulate the flow in and out of the heart cavities.  Diseased valves are replaced with artificial heart valves, from which 60% of the implants are done using mechanical heart valves.  The strong transitory shear stress generated during the time-periodic closing of the mechanical prosthetic bi-leaflet aortic heart valve, is considered to be one of the main factors responsible for complications, associated with thrombosis and thromboembolism.  These regions of high shear stress (~ 600 dyn/cm2 along the B-datum line of the valve) cause the initiation of the coagulation cascade and the blood damage that ultimately will form blood clots on the valve leaflets.  To avoid the formation of these blood clots, patients with BMHV have to be on anticoagulation therapy their entire lives, which can also develop other type of health problems.

These flow transients are investigated using phase-averaged PIV in a low-volume (about 150 ml) test setup that simulates the pulsatile physiological conditions associated with a 23 mm diameter St. Jude Medical valve. The PIV measurements are accompanied by continuous monitoring of the ventricular and aortic pressures and valve flow rate.  Following the valve closure, the leakage flow between the valve leaflets is caused by the pressure buildup across the leaflets, leading to the formation of a regurgitation jet starting from the BMHV B-datum line.  As in a typical starting jet, a counter-rotating vortex pair is formed along each leaflet edge and the vorticity sheet is associated with high shear stress that may be result in blood platelet activation.  The present investigation demonstrates that the placement of arrays of mm-scale vortex generators (VG’s) near the edges of the leaflets diffuses the vortex sheet by introducing secondary streamwise vortex pairs.  The interaction of the secondary streamwise vortices with the primary counter-rotating vortices leads to a rapid diffusion of the primary vortex pair, weakening the velocity gradients and the local shear stress near the leaflets.  Preliminary biological using the VG’s shows a conservative blood damage reduction of 30% with respect to the baseline BMHV.

Supported by NIH and NSF