Vascular Myointimal Proliferation
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Vascular myointimal hyperplasia is a response to injury. The initial injury can be caused by different factors, such as radiation, viral infections, development of immune complexes, and hyperlipidemia. Vascular injuries may also be caused by invasive procedures, such as percutaneous transluminal coronary angioplasty, organ transplantation and vascular bypass surgery. It is thought that injury to the endothelium allows platelets and leukocytes to adhere to the underlying internal elastic lamina and smooth muscle and promote the release of mitogenic and chemo-attractant factors, such as platelet derived growth factors, thromboglobulin, and others. The injury may allow monocytes and leukocytes to pass into the vascular wall. Monocytes also release platelet derived growth factor and other growth factors, such as tumor necrosis factor, and probably fibroblast growth factor, epidermal growth factor, and insulin-like growth factor. The leukocytes which adhere to the injured endothelium also release powerful chemo-attracting factors like leukotriene B4, as well as oxygen free radicals which, in turn, lead to release of growth factors. A great deal of basic research and clinical effort is now focused on inhibiting growth factor expression and chemo-attractants released during vascular injury which all are factors leading to myointimal proliferation. This effort is directed to the unacceptably high restenosis rate (>30%) following coronary angioplasty and organ transplantation, as well as the stenosis present in coronary and peripheral atherosclerosis.
KeywordsIntimal Hyperplasia Internal Elastic Lamina Coronary Arteriosclerosis Peripheral Atherosclerosis Saphenous Vein Bypass Graft
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- 12.Serruys, P. W., Luijten, H. E., Bentt, K. J., Genshens, R., de Feyter P. J., Van de Brand, M., Reiber, J. H. C, Tenkaten, H.J., Van Es, G.A., Hugenholtz, P. G.: Incidence of restenosis after successful coronary angioplasty: A time-related phenomena: A quantitative angiographic follow up study. Circulation. (1988) 77, 361-374.PubMedCrossRefGoogle Scholar
- 13.Billingham, M. E., Cardiac transplant atherosclerosis. Transpl. Proc. 19 (Suppl. 5) (1987) 19.Google Scholar
- 14.Hess, M., Lipid mediators in organ transplantation: does cyclosporine accelerate coronary atherosclerosis. Transpl. Proc. 19 (Suppl. 5) (1987) 71.Google Scholar
- 18.Foegh, M. L, Khirabadi, B. S., Nakanishi, T., Vargas, R., and Ramwell, P. W. Estradiol protects against experimental cardiac transplant atherosclerosis. Transpl. Proc. 19 (Suppl. 5) (1987) 90-95.Google Scholar
- 20.Conte, J. V., Foegh, M. L, Calcagno, D., Wallace, R. B., and Ramwell, P. W. Peptide inhibition of myointimal proliferation following angioplasty in rabbits. Transpl Proc. 21 (1989) 3686-3688.Google Scholar
- 22.Abbott, W. M., Wieland, S., and Austen, W. G. Structural changes during preparation of autogenous venous grafts. Surgery. 76 (1974) 1032-1040.Google Scholar
- 24.Robbs, J. V., Human, R. R., Rajaruthnam, P. Operative treatment non-specific aorto-arteritis (Takayasu’s disease). J. Vasc. Surg. 3, (1980) 605-609.Google Scholar
- 27.Foegh, M. L, Khirabadi, B. S., Chambers, E., and Ramwell, P. W. Peptide inhibition of accelerated transplant atherosclerosis. Transpl. Proc. 21 (1989) 3674-3676.Google Scholar