Downstream anastomotic hyperplasia. A mechanism of failure in Dacron arterial grafts.

The precise location and progression of anastomotic hyperplasia and its possible relationship to flow disturbances was investigated in femoro-femoral Dacron grafts in 28 dogs. In 13 grafts, the outflow from the end-to-side downstream anastomosis was bidirectional (BDO), and in 15 it was unidirectional (UDO) (distally). Grafts were electively removed at intervals of two to 196 days or at the time of thrombosis. Each anastomosis and adjacent artery was perfusion-fixed and sectioned sagittally. The mean sagittal section was projected onto a digitized pad, and the total area of hyperplasia internal to the arterial internal elastic lamina and within the adjacent graft was integrated by computer. The location of the hyperplasia was compared with previously established sites of flow separation and stagnation. The observation was made that hyperplasia is significantly greater at the downstream, as compared with the upstream, anastomosis in both groups (BDO = p less than 0.001 and UDO = p less than 0.001) (analysis of variance for independent groups). Furthermore, this downstream hyperplasia was progressive with time (BDO p less than 0.01) (UDO p less than 0.01); Spearman Rank Correlation. There was no significant increase in the extent of downstream hyperplasia where flow separation was known to be greater (BDO). Five grafts failed (three BDO, two UDO), as a result of complete occlusion of the downstream anastomosis by fibrous hyperplasia. Transmission electron microscopy showed the hyperplasia to consist of collagen-producing smooth muscle cells. Anastomotic hyperplasia is significantly greater at the downstream anastomosis, is progressive with time, and is the primary cause of failure of Dacron arterial grafts in this model. Quantitative analysis of downstream anastomotic hyperplasia may be a valuable measure of the biocompatibility of Dacron grafts.

An improved technique for preservation of endothelial morphology in vein grafts.

Scanning electron microscopy was performed on 29 canine and two human veins prepared for vein grafting by means of various techniques. Endothelial morphology was best preserved when veins were pretreated with papaverine before excision, when a warm solution was used for dilatation, when the grafts were stored up to 1 hour either in a warm, nutritive medium (Dulbecco's modified eagles) or a cold, nonnutritive solution (saline), and when the grafts were maintained in the distended state. Distending pressure up to 500 mm Hg did not cause injury to veins prepared by these techniques. The use of cold solutions to distend veins was especially harmful.

Effect of flow split on separation and stagnation in a model vascular bifurcation.

This is a study of the flow disturbance in a plastic model of an asymmetric vascular bifurcation. A sidearm was attached to the mainlimb at an angle of 15 degrees to the inlet flow axis. Water at steady flow was used and flow patterns were demonstrated by a dye injection technique. The proportion of inlet flow (Qi) exiting from the sidearm (Qs) was varied and flow patterns were recorded photographically. A laser Doppler anemometer (LDA) was used to measure near-wall velocity. At a physiologic Reynolds' number of 500, no flow disturbance occurred in the mainlimb when the sidearm was completely occluded. When the fraction of flow exiting from the sidearm (Qs/Qi) reached 0.19, a region of boundary layer separation developed along the wall of the mainlimb opposite the flow divider. This region of nearly static fluid spread circumferentially around the mainlimb as Qs/Qi increased. Near-wall velocity within the separation decreased and became negative when Qs/Qi = 0.31. When Qs/Qi reached 0.38, the separation enveloped the wall of the entire bifurcation with a shell of slowly moving fluid. At the same time, the rapidly moving mainstream impinged directly on the flow divider. There is a similarity between the region of separation seen in this model and the site of formation of atherosclerotic plaque at the carotid bifurcation. Separation may contribute to atherogenesis by creating a region of low wall shear at bifurcations.

Flow studies in a model carotid bifurcation.

Boundary layer separation in a plexiglass model carotid bifurcation was investigated in relation to the origin of atherosclerotic plaque clinically found in this region. Our model was comparable to a human carotid in both dimensions and geometry. Water flowed through the model at Reynolds numbers from 200 to 1200 under steady and pulsatile flow conditions, with outflow through the external and internal branches varied. The near-wall flow was visualized by slow injection of dye through ports machined in the model. Under steady flow at a physiological Reynolds number of 500 and a flow split at the bifurcation similar to that of a human carotid at rest, boundary layer separation was found to occur in a carotid sinus across from the external carotid origin, forming a shell of slowly moving fluid around the bifurcation. The rapidly moving mainstream impinged directly on the flow divider. The location of atherosclerotic plaque correlates best with the low shear region of separation and not with the region of high shear at the flow divider. Preliminary studies with pulsatile flow demonstrated little change from the steady flow results.

Flow disturbance at the distal end-to-side anastomosis. Effect of patency of the proximal outflow segment and angle of anastomosis.

We investigated the flow disturbance that occurs at the distal end-to-side anastomosis. Clear plastic model end-to-side anastomoses were constructed with inlet angles of 15 degrees and 45 degrees. Flow patterns were visualized with steady and pulsatile flow using a dye-injection technique. Multiple lateral pressure measurements were made in the region of the anastomosis. A laser Doppler anemometer was used to measure near-wall velocity. Flow disturbance was minimal when the inlet angle was low and the proximal outflow segment occluded. Patency of the proximal outflow segment or a high inlet angle may result in areas of boundary-layer separation, with corresponding adverse pressure gradients at the anastomosis. These separation regions are characterized by low near-wall velocity, which may contribute to anastomotic hyperplasia.