To elucidate the mechanisms of localisation of intimal hyperplasia in anastomosed arteries, the effects of flow disturbances on the transport of low-density lipoproteins (LDLs) from the flowing blood to the wall of end-to-end anastomosed arteries, with and without a moderate stenosis, were studied theoretically by means of a computer simulation under the condition of steady flow. In an artery with moderate stenosis at the anastomotic junction and intimal thickening distal to it, we found that, owing to the water-permeable nature of the arterial wall, the surface concentration of LDL was elevated up to 20% higher than that of the bulk flow distal to the stenosis, where a recirculation zone was formed and wall shear stresses were low. In contrast to this, no significant elevation of surface concentration of LDLs occurred in another anastomosed vessel in which no stenosis was formed and no intimal thickening was observed. These results suggest that flow-dependent concentration polarisation of LDLs plays a causative role in the localisation of anastomotic intimal hyperplasia in the human arterial system by locally elevating the surface concentration of LDLs, thus augmenting their uptake by endothelial cells.

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