| description abstract | The development of intimal hyperplasia at the distal anastomosis is the major cause of long-term bypass graft failure. To evaluate the suspected role of hemodynamic factors in the pathogenesis of distal intimal hyperplasia, an understanding of anastomotic flow patterns is essential. Due to the complexity of arterial flow, model studies typically make simplifying assumptions, such as treating the artery and graft walls as rigid. In the present study this restriction is relaxed to consider the effects of vessel wall distensibility on anastomotic flow patterns. Flow was simulated in an idealized 2-D distensible end-to-side anastomosis model, using parameters appropriate for the distal circulation and assuming a purely elastic artery wall. A novel numerical approach was developed in which the wall velocities are solved simultaneously with the fluid and pressure fields, while the wall displacements are treated via an iterative update. Both the rigid and distensible cases indicated the presence of elevated temporal variations and low average magnitudes of wall shear stress at sites known to be susceptible to the development of intimal hyperplasia. At these same sites, large spatial gradients of wall shear stress were also noted. Comparison between distensible-walled and corresponding rigid-walled simulations showed moderate changes in wall shear stress at isolated locations, primarily the bed, toe and heel. For example, in the case of a distensible geometry and a physiologic pressure waveform, the heel experienced a 38 percent increase in cycle-averaged shear stress, with a corresponding 15 percent reduction in shear stress variability, both relative to the corresponding values in the rigid-walled case. However, other than at these isolated locations, only minor changes in overall wall shear stress patterns were observed. While the physiological implications of such changes in wall shear stress are not known, it is suspected that the effects of wall distensibility are less pronounced than those brought about by changes in arterial geometry and flow conditions. | |
