Particle motion within in vitro models of stenosed internal carotid and left anterior descending coronary arteries.
Asymmetric 75% and 95% area reduction, transparent Sylgard stenotic models were operated under internal carotid artery (ICA) [Womersley parameter, alpha=5.36, Re(mean) =213 and 180, respectively, and Re(peak)=734 and 410, respectively] and left anterior descending coronary artery (LAD) flow wave forms (alpha=2.65, Re(mean)=59 and 57, respectively, and Re(peak)= 137 and 94, respectively) to evaluate the effect of these conditions on particle residence times downstream of the stenoses. Amberlite particles (1.05 g/cm3, 400 microm) were added to the fluid to simulate platelets and their motion through the stenotic region and were traced using a laser light sheet flow visualization method with pseudo-color display. Two-dimensional (2D) particle motions were recorded and particle washout in the stenotic throat and downstream section were computed for all cases. All four model cases demonstrated jetting through the stenosis which followed an arching pattern around a large separation zone downstream. Considerable mixing was observed within these vortex regions during high flow phases. Particle washout profiles showed no clear trend between the degrees of stenosis although particles downstream of the stenoses tended to remain longer for LAD conditions. The critical washout cycle (1% of particles remaining downstream of the stenosis), however, was longer for the 95% stenoses cases under each flow condition due to the larger protected region immediately downstream and maximal for the LAD 95% case. Results of this study suggest that particle residence times downstream of 75% and 95% stenoses (approximately 3-6 s for ICA and approximately 8-10 s for LAD) exceed the minimum time for platelet adhesion (approximately 1 s) for at least 1% of cells and, thus, may be sufficient to initiate thrombus formation under resting conditions.
Cao
J
J
Department of Biomedical Engineering, The University of Akron, OH 44325-0302, USA.
Rittgers
S E
SE
D001698:Biomedical Engineering / Q000295:instrumentation; D002343:Carotid Artery, Internal; D016893:Carotid Stenosis / Q000209:etiology / Q000473:pathology / Q000503:physiopathology*; D003327:Coronary Disease / Q000209:etiology / Q000473:pathology / Q000503:physiopathology*; D018056:Hemorheology; D006801:Humans; D066298:In Vitro Techniques; D007834:Lasers; D008955:Models, Cardiovascular; D009038:Motion; D010316:Particle Size; D010973:Platelet Adhesiveness / Q000502:physiology; D011673:Pulsatile Flow / Q000502:physiology; D013927:Thrombosis / Q000209:etiology; D013997:Time Factors