Localization of atherosclerosis in arterial junctions. Modeling the release rate of low density lipoprotein and its breakdown products accumulated in blood vessel walls.

Arterial bifurcations and surgically created junctions at anastomoses are places where blood flow may be disturbed and slow recirculation may occur. To address the hypothesis that such disturbances in flow may result in atherogenesis, the transfer of atherogenic substances from vessel wall to flowing blood was studied theoretically using a two dimensional T-junction model. Calculations showed that the transfer of atherogenic substances from vessel wall into flowing blood was suppressed in the two regions of disturbed flow, one in the main vessel, the other in the subsidiary vessel. The lowest release rates were at the points of flow separation and were found to be much lower than those in the undisturbed flow regions. Therefore, our mathematical model predicts that locally disturbed blood flows at arterial bifurcations and surgically created junctions are responsible for two distinct phenomena. First, they provide favorable conditions for the accumulation of LDL at the luminal surface, thus increasing the potential for lipid infiltration into the vessel wall, and second, they impair the transfer into blood of atherogenic substances accumulated in the vessel wall. Such mass transfer abnormalities may account for atherogenesis and late failures of arterial grafts at these sites.