Flow-Induced Damage to Blood Cells in Aortic Valve Stenosis.

Abstract

Valvular hemolysis and thrombosis are common complications associated with stenotic heart valves. This study aims to determine the extent to which hemodynamics induce such traumatic events. The viscous shear stress downstream of a severely calcified bioprosthetic valve was evaluated via in vitro 2D particle image velocimetry measurements. The blood cell membrane response to the measured stresses was then quantified using 3D immersed-boundary computational simulations. The shear stress level at the boundary layer of the jet flow formed downstream of the valve orifice was observed to reach a maximum of 1000-1700 dyn/cm(2), which was beyond the threshold values reported for platelet activation (100-1000 dyn/cm(2)) and within the range of thresholds reported for red blood cell (RBC) damage (1000-2000 dyn/cm(2)). Computational simulations demonstrated that the resultant tensions at the RBC membrane surface were unlikely to cause instant rupture, but likely to lead to membrane plastic failure. The resultant tensions at the platelet surface were also calculated and the potential damage was discussed. It was concluded that although shear-induced thrombotic trauma is very likely in stenotic heart valves, instant hemolysis is unlikely and the shear-induced damage to RBCs is mostly subhemolytic.