Background Aortocoronary saphenous vein grafts (SVGs) undergo structural changes that render them susceptible to atherosclerosis. Accordingly, the origin of neointimal hyperplasia was examined in porcine arterialized SVGs to determine the mechanism of vein graft remodeling.

Methods and Results At 2 to 4 days after surgery, the percentage of cells lacking differentiation markers characteristic for smooth muscle (SM) cells (ie, α-SM actin, desmin, and SM myosin) increased within the media of SVGs interposed in the carotid arteries (P<.001). At 7 to 14 days, these cells acquired a differentiated phenotype (ie, α-SM-actin positive/variable desmin/SM-myosin negative) and accumulated in the neointima. At 3 months, the neointima was positive for α-SM actin but mostly negative for desmin, which contrasted with medial SMCs that were invariably positive for α-SM actin, desmin, and SM myosin. To determine the role of nonmuscle cells in the above process, perivascular wound fibroblasts were selectively labeled and found to translocate through the media of newly placed SVGs, contributing to neointimal formation. These migrating cells differentiated to myofibroblasts exhibiting sustained α-SM-actin expression. The intima of human SVGs, retrieved during repeat aortocoronary bypass surgery, exhibited the profile of cytoskeletal proteins that resembled myofibroblasts seen in porcine SVGs.

Conclusions Perivascular fibroblasts may infiltrate injured media of arterialized SVGs, differentiate to myofibroblasts (acquiring α-SM actin), and contribute to vein graft remodeling. The similarities between porcine and human SVGs regarding the repertoire of cytoskeletal proteins suggest the involvement of myofibroblasts in graft remodeling in the clinical setting.