Estimation of Shear-Induced Blood Damage in Artificial Heart Valve Components

Shear-induced blood damage is a prominent failure mode in cardiovascular devices. This failure mode results from structural and/or functional damage of formed elements of blood like red blood cells, platelets, white blood cells, etc., due to exposure in an environment where shear stresses are relatively high. Simplified models are required to allow computations to be employed in flow analysis of mechanical heart valve. Common simplifications include two-dimensional approximations, steady flow approximations, simplifications of configuration, or assuming fixed rather than moving occluder in valves. Studies have shown that shear stresses in excess of 17.5 Pa can result in the initiation of shear-induced cell damage. So, it is important for medical device designers to ensure that extremely high shear stresses are not occurring on the device surfaces in the design of an optimal heart valve from point of view of hemodynamics. TTK Chitra heart valve, Model TC2 is a mechanical heart valve being developed jointly by TTK Healthcare Limited and Sree Chitra Tirunal Institute for Medical Sciences and Technology (SCTIMST). This study attempts to develop a model for estimating shear stress levels during different steady flow rates corresponding to varying velocity profiles of a typical cardiac cycle on mitral valve components. A computational model was employed to study the distribution of velocity profiles and shear stress distributions in and around structural elements of the TTK Chitra heart valve. The shear stress estimates on the surface of the valve components were obtained for varying cardiac output conditions. Results indicate that the turbulent shear stresses in excess of 17.5 Pa, acceptance range for hemolysis behavior, was observed only in less than 5% area of the components. Most of these zones where turbulence stresses are high are in corners and edges where the resident time of blood cells are extremely low, of the order of few milliseconds.