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Coronary artery bypass graft: why is the saphenous vein prone to intimal hyperplasia?

Journal

CANADIAN JOURNAL OF PHYSIOLOGY AND PHARMACOLOGY
Volume 92, Issue 7, Pages 531-545

Publisher

CANADIAN SCIENCE PUBLISHING, NRC RESEARCH PRESS
DOI: 10.1139/cjpp-2013-0445

Keywords

coronary artery bypass graft; intimal hyperplasia; PTEN; matrix metalloproteinases; vein-graft disease

Funding

  1. National Institutes of Health

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Proliferation and migration of smooth muscle cells and the resultant intimal hyperplasia cause coronary artery bypass graft failure. Both internal mammary artery and saphenous vein are the most commonly used bypass conduits. Although an internal mammary artery graft is immune to restenosis, a saphenous vein graft is prone to develop restenosis. We found significantly higher activity of phosphatase and tensin homolog (PTEN) in the smooth muscle cells of the internal mammary artery than in the saphenous vein. In this article, we critically review the pathophysiology of vein-graft failure with detailed discussion of the involvement of various factors, including PTEN, matrix metalloproteinases, and tissue inhibitor of metalloproteinases, in uncontrolled proliferation and migration of smooth muscle cells towards the lumen, and invasion of the graft conduit. We identified potential target sites that could be useful in preventing and (or) reversing unwanted consequences following coronary artery bypass graft using saphenous vein.

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