A Novel Toroidal-Flow Left Ventricular Assist Device Minimizes Blood Trauma: Implications of Improved Ventricular Assist Device Hemocompatibility

Cardiac prostheses‐related hemolytic anemia

“…38,39 Similarly, the novel TORVAD toroidal-flow LVAD has shown negligible rates of hemolysis in preclinical testing. 40 A unique aspect of hemolysis in LVAD patients is its strong relationship with thrombotic complications. Local thrombosis increases shear stress and leads to local destruction of the red cells.…”

“…However, early experience with the third generation magnetically levitated left ventricular assist devices (LVAD) (HeartMate III) revealed very low (<1%) rates of hemolysis . Similarly, the novel TORVAD toroidal‐flow LVAD has shown negligible rates of hemolysis in pre‐clinical testing . A unique aspect of hemolysis in LVAD patients is its strong relationship with thrombotic complications.…”

Reinventing the displacement left ventricular assist device in the continuous-flow era: TORVAD, the first toroidal-flow left ventricular assist device

“…Low shear stress with the TORVAD causes minimal blood trauma. In ex vivo mock circulatory loop experiments with human blood, the TORVAD caused no platelet activation, no hemolysis, and minimal VWF degradation (2). Similarly, over 60 days, sheep implanted with a TORVAD did not demonstrate significant hemolysis or VWF degradation.…”

“…Indeed, current-generation LVADs generate peak shear stress of up to 1,500 Pa (2). For reference, physiologic levels of intravascular shear stress in mammals are approximately two to eight Pa (2).…”

Pathologic von Willebrand factor degradation is a major contributor to left ventricular assist device-associated bleeding: pathophysiology and evolving clinical management

“…VWF, a multimeric plasma clotting protein, initiates primary hemostasis. Shear stress closely regulates VWF activation for thrombogenesis (6). Normal intravascular shear stress is approximately 2 to 8 Pa. VWF activation occurs above 10 Pa. During activation, shear stress unravels inactive, globular VWF into an active, elongated conformation, which exposes binding sites for collagen and platelets to generate thrombus.…”