Experimental studies of physiological flows in replicated diseased carotid bifurcations.

摘要

Atherosclerosis, plaque induced arterial wall thickening, is a leading cause of mortality and morbidity in the United States. Fluid dynamics is believed to be one of the primary factors promoting atherosclerosis by predisposing sites to plaque formation, progression, and rupture. We examine diseased carotid artery flow fields flow visualization and particle image velocimetry (PIV). The findings are expected to provide clinicians with enhanced understanding of flows in diseased arteries.; We investigate flow conditions under physiological (pulsatile) and steady inputs in two atherosclerotic, stenotic carotid bifurcation lumens replicated from patients' intact excised plaques, which are cast in nearly rigid optically clear silicone models. The systolic and diastolic Reynolds numbers ( Re) (900 and 300, respectively), are obtained from pre-surgery Doppler Ultrasound scans.; The complex internal geometry of the diseased artery combined with pulsatile input gives each model unique complex flow patterns. However, both models exhibit strong jets leaving the stenosis. The vorticity and planar streamline maps, which are chaotic, three dimensional, and vary by cycle, indicates numerous separation points, recirculation zones, internal jets, three-dimensional shear layers, stagnation lines. In general, flow features at any point on the pulsatile waveform is similar to features observed at the corresponding Re steady input. However, after peak systole the stenosis jet is absent and the flow is highly unsteady and three-dimensional.; A PIV boundary treatment technique is employed to estimate WSS to first order accuracy. The arterial lumen WSS profiles are unique for each artery, but similar profiles are observed for both physiological and steady input flows. The flow details vary chaotically from cycle to cycle. Peak WSS values (typically +/-5 to +/-70 Pa) are found at the stenotic neck and jet attachment location during peak systole, suggesting endothelial cell erosion, platelet activation, and apoptosis. Minimum WSS values (less than +/-0.4 Pa) are seen at the recirculation zones downstream of the stenosis, suggesting atherogenesis. Observed high and low WSS regions are consistent with previous studies. Flow features and WSS profiles varied significantly between the two patients' models studied, suggesting that plaque rupture/atherogenesis needs to be determined in each case and not by degree stenosed.