Cerebro-vascular events are often related to the rupture of vulnerable atherosclerotic plaques and thrombus formation in the carotid arteries. Haemodynamically significant stenoses experience increased wall shear stress (WSS) in the entrance region but in the post-stenotic region, instead the flow decelerates and tends to become unstable, with separation and recirculation. The high WSS tends to promote processes leading to matrix degradation, with potential rupture, whilst processes stimulated in the post-stenotic zone might be expected to promote further plaque development [1].

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