title: Numerical model of full-cardiac cycle hemodynamics in a total artificial heart and the effect of its size on platelet activation.
abstract: The SynCardia total artificial heart (TAH) is the only Food and Drug Administration (FDA) approved device for replacing hearts in patients with congestive heart failure. It pumps blood via pneumatically driven diaphragms and controls the flow with mechanical valves. While it has been successfully implanted in more than 1300 patients, its size precludes implantation in smaller patients. This study's aim was to evaluate the viability of scaled-down TAHs by quantifying thrombogenic potentials from flow patterns. Simulations of systole were first conducted with stationary valves, followed by an advanced full-cardiac cycle model with moving valves. All the models included deforming diaphragms and platelet suspension in the blood flow. Flow stress accumulations were computed for the platelet trajectories and thrombogenic potentials were assessed. The simulations successfully captured complex flow patterns during various phases of the cardiac cycle. Increased stress accumulations, but within the safety margin of acceptable thrombogenicity, were found in smaller TAHs, indicating that they are clinically viable.
authors.affiliation: Department of Biomedical Engineering, Stony Brook University, Stony Brook, NY, USA.
authors.forename: Gil
authors.initials: G
authors.lastname: Marom
authors.forename: Wei-Che
authors.initials: WC
authors.lastname: Chiu
authors.forename: Jessica R
authors.initials: JR
authors.lastname: Crosby
authors.forename: Katrina J
authors.initials: KJ
authors.lastname: DeCook
authors.forename: Saurabh
authors.initials: S
authors.lastname: Prabhakar
authors.forename: Marc
authors.initials: M
authors.lastname: Horner
authors.forename: Marvin J
authors.initials: MJ
authors.lastname: Slepian
authors.forename: Danny
authors.initials: D
authors.lastname: Bluestein
mesh_terms: D004867:Equipment Design; D006354:Heart, Artificial / Q000009:adverse effects; D006439:Hemodynamics / Q000502:physiology*; D057446:Hydrodynamics; D008954:Models, Biological; D015539:Platelet Activation / Q000502:physiology*; D013314:Stress, Mechanical; D013927:Thrombosis / Q000209:etiology