Histological study of the internal mammary artery with emphasis on its suitability as a coronary artery bypass graft

1993 ◽  
Vol 55 (1) ◽  
pp. 106-113 ◽  
Author(s):  
Jacques A.M. van Son ◽  
Frank Smedts ◽  
Peter C.M. de Wilde ◽  
Nico H.J. Pijls ◽  
Luthy Wong-Alcala ◽  
...  
1974 ◽  
Vol 33 (1) ◽  
pp. 167
Author(s):  
Stephen J. Rossiter ◽  
William R. Brody ◽  
Jon C. Kosek ◽  
Martin J. Lipton ◽  
William W. Angell

2019 ◽  
Vol 132 (3) ◽  
pp. 377-378 ◽  
Author(s):  
Mi Chen ◽  
Fang-Jiong Huang ◽  
Qiang Wu ◽  
Yi-Xi Zou ◽  
En-Jun Zhu ◽  
...  

1988 ◽  
Vol 22 (3) ◽  
pp. 179-184
Author(s):  
P. Aarnio ◽  
A. Harjula ◽  
A. Lehtola ◽  
H. Sariola ◽  
E. Merikallio ◽  
...  

2014 ◽  
Vol 92 (7) ◽  
pp. 531-545 ◽  
Author(s):  
Swastika Sur ◽  
Jeffrey T. Sugimoto ◽  
Devendra K. Agrawal

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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