Pathophysiological features of intimal hyperplasia of the arterially implanted autovein graft and its anastomosis in dogs

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.