Mechanisms of arterial graft failure. II. Chronic endothelial and smooth muscle cell proliferation in healing polytetrafluoroethylene prostheses.

In a previous study of arterial bypass grafts (4 mm polytetrafluoroethylene [PTFE]) in baboons we observed that endothelial and smooth muscle cells (SMCs) formed the neointima and were derived from the cut edges of adjacent artery. The purpose of this study was to determine at late times whether endothelial cells would continue to migrate and to proliferate to cover the graft surface and whether the underlying proliferating SMCs would produce a progressively thickened intima, graft stenosis, and eventual thrombosis. At 6 and 12 months after grafts were placed, endothelial coverage by ingrowth from the anastomoses was more advanced than at 3 months, and by 12 months 60% of grafts (7 to 9 cm in length) were covered. Endothelial cells proliferated in association with the growing edge and focally in other regions. Underlying SMCs proliferated in the region of the growing edge of the endothelial cells and also at anastomoses. Intimal cross-sectional area was greatest at anastomoses and at late times was principally due to an increase in connective tissue; actual SMC mass remained constant after 3 months. These results demonstrated slow but progressive healing of the grafts by ingrowth of endothelium. There was also an increased turnover rate of SMCs and endothelial cells in established intima at late times, which might be the consequence of chronic endothelial injury. This condition represents a stable state since it does not produce further intimal thickening and accumulation of SMCs and does not lead to a high rate of thrombosis.