The long-term success of coronary artery bypass surgery is limited by intimal thickening (IT) along the graft and at the graft/artery junction (distal anastomosis). It is well documented that hemodynamic forces, in particular wall shear stress, are linked to the cellular and molecular processes associated with vascular disease, and these forces have been hypothesized as a cause of bypass graft failure. The objective of this thesis is to gain further insights on the role of wall shear stress in the stenosis of human coronary artery bypass grafts (CABGs).

Histologic data, collected from 74 human coronary artery bypass grafts, were used to quantify the intimal response in early (1 week to 2 months in situ) and late (>2 month in situ) saphenous vein (SV) and left internal thoracic artery (LITA) grafts. A visible intimal thickening response at the suture line begins one-week post surgery and became significant by two months. After two months, the greatest thickening occurred on the hood in both types of grafts. Focal thickening on the floor of the distal anastomosis was variable.

Quantitative flow visualization analysis of two anatomically correct human CABGs models revealed a large spatial gradient in shear stress on the hood. This gradient was created by the significant curvature of the surgically constructed distal anastomosis. Similar hood geometry was evident in 5 of 6 casts collected. The pattern of wall shear on the floor of the distal anastomosis was unique for each model.

The development of hood intimal hyperplasia and the presence of a large spatial gradient in shear stress on the hood suggest shear-induced stenosis may cause bypass graft failure at the distal anastomosis.