Despite significant progress in the development of circulatory-assist devices over the last several decades, one of the major requirements for current clinical and pre-clinically tested devices remains the reduction of mechanical blood trauma. This blood trauma is associated with known complications of mechanically assisted circulation, such as thrombosis, coagulopathy, postoperative bleeding, increased susceptibility to inflammation and infection, compromised microcirculation and neurological injury, which is especially important in pediatric patients. Despite numerous experimental and computational studies of blood trauma conducted over several decades by investigators worldwide, there are still no reliable widely-accepted algorithms to minimize blood trauma at the circulatory-assist device design stage, and the mechanisms of blood damage in these devices are not completely understood. Non-physiological flow conditions such as elevated shear forces, turbulence, cavitation, prolonged contact and collision between blood cells and foreign surfaces may induce a variety of damage mechanisms: overstretching or fragmentation of a subpopulation of red blood cells (RBCs) causing release of free hemoglobin into plasma (i.e., hemolysis), functional alterations of other blood cells such as activation or dysfunction and an increase in adhesiveness of platelets and leukocytes, increased concentrations of inflammatory mediators in plasma, complement activation, etc.

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