Enhancement of stent-induced thromboembolism by residual stenoses: contribution of hemodynamics.
In vitro stent-induced thromboembolism was altered by the presence of residual stenoses placed upstream or placed upstream and downstream of the stent. Heparinized (3 micro/ml) bovine blood was gravity fed through a conduit with a deployed coronary stent. Embolism was continuously monitored using a light-scattering microemboli detector, and the thrombus accumulated on the stent at the conclusion of the experiment was assessed gravimetrically. Gaussian stenoses (75% reduction in the cross-sectional area) were placed upstream or upstream and downstream of the stent to alter flow characteristics in the stent region. The presence of stenoses enhanced embolization from the stent in all cases, while end-point thrombus accumulation on the stent decreased with only an upstream stenosis present, and increased when upstream and downstream stenoses were present. Computational fluid dynamics with and without hypothetical model thrombi were used to ascertain the alterations in the flow environment caused by the stenoses and thrombi. Combining the computed hemodynamic parameters with experimental results indicated that increased radial transport of blood components and low wall shear stress provided by the stenoses and thrombi may explain the enhancement of end-point thrombus accumulation. Analysis further showed that thrombi growing at the stenosis-induced reattachment and separation points will be subjected to high shear forces which may explain the increased embolism when stenoses are present.
Sukavaneshvar
S
S
Department of Chemical Engineering, Brigham Young University, Provo, UT 84602, USA.
Rosa
G M
GM
Solen
K A
KA
D000818:Animals; D001783:Blood Flow Velocity; D002417:Cattle; D003198:Computer Simulation; D003251:Constriction, Pathologic / Q000503:physiopathology; D006439:Hemodynamics; D008955:Models, Cardiovascular; D015607:Stents / Q000009:adverse effects*; D013314:Stress, Mechanical; D013923:Thromboembolism / Q000209:etiology* / Q000503:physiopathology*; D014783:Viscosity