OBJECTIVE: Studies of animal and human below-knee anastomoses with Miller cuffs indicate that improved graft patency results from redistribution of intimal hyperplasia away from areas critical to flow delivery, such as the arterial toe. We hypothesize that particle hemodynamic conditions are a biophysical mechanism potentially responsible for the clinically observed shift in intimal hyperplasia localization associated with better patency of the Miller configuration. METHODS: Computational fluid dynamics analysis of vortical flow patterns, wall shear stress fields, and potential for platelet interaction with the vascular surface was performed for realistic three-dimensional conventional and Miller cuff distal end-to-side anastomoses. Sites of significant platelet-wall interaction, including elevated near-wall particle concentrations and stasis, were identified with a validated near-wall residence time model, which includes shear stress-based factors for particle activation and surface reactivity. RESULTS: Particle hemodynamics largely coincide with the observed redistribution of intimal hyperplasia away from the critical arterial toe region. Detrimental changes in wall shear stress vector magnitude and direction are significantly reduced along the arterial suture line of the Miller cuff, largely as a result of increased anastomotic area available for flow redirection. However, because of strong particle-wall interaction, resulting high near-wall residence time contours indicate significant intimal hyperplasia along the graft-vein suture line and in the vicinity of the arterial heel. CONCLUSIONS: While a number of interacting mechanical, biophysical, and technical factors may be responsible for improved Miller cuff patency, our results imply that particle hemodynamics conditions engendered by Miller cuff geometry provide a mechanism that may account for redistribution of intimal hyperplasia. In particular, it appears that a focal region of significant particle-wall interaction at the arterial toe is substantially reduced with the Miller cuff configuration.
OBJECTIVE: Studies of animal and human below-knee anastomoses with Miller cuffs indicate that improved graft patency results from redistribution of intimal hyperplasia away from areas critical to flow delivery, such as the arterial toe. We hypothesize that particle hemodynamic conditions are a biophysical mechanism potentially responsible for the clinically observed shift in intimal hyperplasia localization associated with better patency of the Miller configuration. METHODS: Computational fluid dynamics analysis of vortical flow patterns, wall shear stress fields, and potential for platelet interaction with the vascular surface was performed for realistic three-dimensional conventional and Miller cuff distal end-to-side anastomoses. Sites of significant platelet-wall interaction, including elevated near-wall particle concentrations and stasis, were identified with a validated near-wall residence time model, which includes shear stress-based factors for particle activation and surface reactivity. RESULTS: Particle hemodynamics largely coincide with the observed redistribution of intimal hyperplasia away from the critical arterial toe region. Detrimental changes in wall shear stress vector magnitude and direction are significantly reduced along the arterial suture line of the Miller cuff, largely as a result of increased anastomotic area available for flow redirection. However, because of strong particle-wall interaction, resulting high near-wall residence time contours indicate significant intimal hyperplasia along the graft-vein suture line and in the vicinity of the arterial heel. CONCLUSIONS: While a number of interacting mechanical, biophysical, and technical factors may be responsible for improved Miller cuff patency, our results imply that particle hemodynamics conditions engendered by Miller cuff geometry provide a mechanism that may account for redistribution of intimal hyperplasia. In particular, it appears that a focal region of significant particle-wall interaction at the arterial toe is substantially reduced with the Miller cuff configuration.