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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2004;24:1147.)
© 2004 American Heart Association, Inc.

Editorials

Origin of Neointimal Cells in Autologous Vein Graft

Masataka Sata; Ryozo Nagai

From the Department of Cardiovascular Medicine, University of Tokyo, Graduate School of Medicine, Tokyo, Japan.

Correspondence to Dr Masataka Sata, Department of Cardiovascular Medicine, University of Tokyo, Graduate School of Medicine, 7-3-1 Hongo Bunkyo-ku, Tokyo 113-8655 Japan. E-mail msata-circ@umin.ac.jp

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Since the first aortocoronary vein graft implantation was performed in 1967,¹ vascular bypass surgery using saphenous vein grafts has become an established therapeutic procedure for patients with ischemic coronary or peripheral arterial diseases. Despite increasing use of arterial grafts in coronary bypass surgery,² autologous vein remains an important and convenient conduit for surgical revascularization.³ However, vein grafts are associated with poor long-term patencies.⁴ During the first year after bypass surgery, up to 15% of venous grafts occlude. Between 1 and 6 years, the graft attrition rate is 1% to 2% per year, which increases to 4% between 6 and 10 years after surgery.⁵ By 10 years, only 60% of vein grafts are patent and only 50% of patent vein grafts are free of significant stenosis.⁵

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Graft occlusion arises either from early thrombosis or from the later onset of graft narrowing.³ After implantation, the vein graft is exposed to immediate increases in flow, shear stress, circumferential stress, radial deformation, and pulsatile stress.⁶ Progressive thickening of vein grafts, mainly caused by neointima formation in the inner layer, is supposed to be the adaptation of these vessels from the low-pressure venous system to the arterial circulation. Smooth muscle cell (SMC) accumulation^7,8 and matrix biosynthesis by SMCs^4,9 are key events in the pathogenesis of neointima formation in vein grafts. However, the molecular mechanism of SMC hyperplasia is largely unknown. Consequently, no effective therapy has been established to prevent vein graft failure.

Experimental models of venous bypass graft have been described in . . . [Full Text of this Article]

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				Q. Xu, M. Sata, and R. Nagai Mouse Models of Vein Grafts Arterioscler Thromb Vasc Biol, November 1, 2004; 24(11): e185 - e187. [Full Text] [PDF]