Abstract
We investigated pathophysiological features of intimal hyperplasia of arterially implanted
autovein graft and its distal end-to-side anastomosis under conditions of poor distal
runoff. Intimal hyperplasia of the graft was significantly evident, became 70.5 ±
38.5 μm thick at 14 days with infiltration of myofibroblasts, and increased to 420
± 199.7 μm at 6 months. The proliferated neointima was strongly positive for alpha-smooth
muscle (A-sm) actin staining. Cells in the entire layer of the graft were diffusely
labeled with BrdU at 14 days. At 3–6 months after grafting, cells in the superficial
layer of the neointima were scarcely labeled with BrdU, however, cells in the deeper
layer were strongly labeled. At the distal end-to-side anastomosis, mural thrombi
deposited on the suture line were replaced by fibrous tissues with infiltration of
fibroblast-like cells within 14 days, and proliferated considerably at 3–6 months.
The neointima at the toe portion was thickened to 82.5 ± 50.7 μm at 14 days and increased
to 370.6 ± 40.0 μm at 6 months. The superficial layer of the proliferated neointima
consisted of mature smooth muscle cells positive for A-sm actin staining and scarcely
labeled with BrdU. However, the deeper layer was negative for A-sm actin staining
and strongly labeled with BrdU. In conclusion, intimal hyperplasia is caused by infiltration
of myofibroblasts in the graft and of fibroblast-like cells at the anastomosis. Proliferation
of these cells is progressive at the deeper layer of the neointima, even at 6 months
after grafting.
