Venerdì 28/7/2006 presso l’aula seminari del Dipartimento di Bioingegneria alle ore 11:00. si svolgerà un seminario di studio sulla biomeccanica della attivazione piastrinica e dei fenomeni di trombogenesi con la partecipazione del Prof. Danny Bluestein, della Stony Brook University di New York e direttore del Corso di Studi in Biomedical Engineering.
Pubblichiamo un breve abstract dell’intervento
Thrombus formation in prosthetic cardiovascular devices and in arterial pathologies is associated with elevated hemodynamic stresses that may induce platelet activation, thrombus formation, and potentiate their interaction with the endothelium. In vitro studies were conducted to estimate the thrombogenic potential of various Prosthetic Heart Valve (PHV) designs. A new polymer trileaflet design was tested for its thrombogenic potential and compared to that of existing prosthetic heart valves (PHVs) routinely implanted in patients: a St. Jude Medical bileaflet mechanical heart valve (MHV) and a St. Jude porcine bioprosthetic tissue valve. The valves were mounted in a left ventricular assist device (LVAD) and the procoagulant activity of the platelets was measured using an innovative platelet activation state (PAS) assay.
Complementary in vivo studies were conducted in the sheep model to study the effects of valve implantation on platelet activity and the risk of cardioembolic stroke. Sheep with implanted valves had increased level of platelet activity, as measured with the PAS assay. Transcranial Doppler measurements indicated a significant increase in the amount of microembolic signals, as measured in the carotid artery of the sheep after valve implantation.
Mechanisms of thrombus formation were investigated using numerical simulations of transient non-Newtonian blood flow patterns in various PHVs, using advanced turbulence models. Platelet damage accumulation model incorporating damage history (senescence) was developed to estimate platelet activation resulting from the combined effect of flow induced stresses and exposure time in the device. Additionally, Fluid Structure Interaction (FSI) simulations of flow past ATS and SJM bileaflet valves were conducted and platelet activation damage averaged over a large number of trajectories within the flow field.
FSI simulations were also conducted in a model of a vulnerable plaque- a pathology that prompts strokes and fatal heart attacks (sudden cardiac death), and in abdominal aortic aneurysms (AAA) reconstructed from patients CT images, in order to predict plaque vulnerability and AAA risk of rupture. For the vulnerable plaque the analysis indicates regions where a combination of elevated strains in the vessel wall and shear stresses induced by the flow, combined with the fibrous cap thickness, enhance the plaque vulnerability and may lead to rapid thrombus formation. The role of calcification in the plaque was examined, indicating that it significantly increases the plaque vulnerability. For the AAA, the role of intraluminal (ILT) thrombus in the AAA was examined and used to predict potential rupture locations.
A discrete multiple particles dynamics multiscale approach, which widely departs from the traditional continuum approach, is being developed to study flow induced thrombosis. The multiscale modeling concentrates on flow regions in devices and pathologies that have a high propensity to activate platelets and to form aggregates. Forces and potentials around particles representing platelets are characterized using Lennard-Jones equations and a summation of viscosity forces, to calculate the motion of particles representing the different phases in the domain.