In vivo wall shear stress distribution in the carotid artery: effect of bifurcation geometry, internal carotid artery stenosis, and recanalization therapy.

BACKGROUND the purpose of this study was to analyze the in vivo distribution of absolute wall shear stress (WSS(abs)) and oscillatory shear index (OSI) in the carotid bifurcation and to evaluate its dependence on bifurcation geometry, the presence of internal carotid artery (ICA) stenosis, and recanalization therapy. METHODS AND RESULTS time-resolved 3D blood flow was acquired with flow-sensitive 4D MRI in 64 normal carotid bifurcations and 17 carotid arteries with moderate ICA stenosis (48±6%) or after surgical recanalization. Among 64 normal arteries, atherogenic wall parameters were consistently concentrated in proximal bulb regions of the common (CCA) and internal (ICA) carotid arteries. The fraction of the carotid bulb exposed to atherosclerosis-prone wall parameters (low WSS(abs) below and high OSI above group-defined 20% and 10% thresholds) was correlated with the individual bifurcation geometry. Multiple regressions revealed significant (P<0.01) relationships (β, 0.44 to 0.48) between the areas with atherosclerosis-prone wall parameters and the d(ICA)/d(CCA) diameter ratio. The size of regions exposed to high OSI demonstrated highly significant (P≤0.01) relationships with all analyzed geometry parameters (d(ICA)/d(CCA) β, 0.48; tortuosity β, ≤-0.56; bifurcation angle β, ≥0.47). Moderate ICA stenosis altered the distribution of wall parameters (45%/61% reduction of individually low WSS(abs)/high OSI in the proximal ICA), which were relocated to segments distal to the arterial stenosis. WSS(abs)/OSI topology after recanalization was similar compared with the normal wall parameter distribution. CONCLUSIONS flow-sensitive 4D MRI identified alterations in the segmental in vivo WSS distribution associated with atherosclerotic disease, surgical therapy, and individual bifurcation geometry and could be a valuable technique to assess the individual risk of flow-mediated atherosclerosis and carotid plaque progression.