The molecular biology of vein graft atherosclerosis and myointimal hyperplasia
Current Opinion in Cardiology
Vein graft atherosclerosis and myointimal hyperplasia can result in critical stenosis and subsequent graft failure. Injury to the vein wall and the healing response to this injury appear to underlie the formation of these graft lesions. Although the exact nature of the injury remains controversial, loss of endothelial integrity with exposure of the subendothelial intima are believed to stimulate cellular adhesion with smooth muscle migration, proliferation, and phenotypic transformation. Recent progress has been made in understanding the molecular and cellular events involved in this process. The roles of endothelial cells, smooth muscle cells, macrophages, and T lymphocytes continue to be defined as does the role of peptide growth factors such as platelet-derived growth factor, fibroblast growth factor, transforming growth factor, and insulin-like growth factor. Additional regulation by cytokines, adhesion molecules, proteoglycans of the extracellular matrix, and hemodynamic flow patterns helps determine the response of the vein wall to injury. A thorough understanding of this multifactorial process will permit molecular techniques to genetically modify vascular cells in order to deliver appropriate peptides or pharmacologic agents, thereby improving the function of vein bypass grafts.
Neville, R., Sidawy, A., & Foegh, M. (1992). The molecular biology of vein graft atherosclerosis and myointimal hyperplasia. Current Opinion in Cardiology, 7 (6). http://dx.doi.org/10.1097/00001573-199212000-00002