scholarly journals The Value of Inflammation Indexes in Predicting Patency of Saphenous Vein Grafts in Patients With Coronary Artery Bypass Graft Surgery

Cureus ◽  
2021 ◽  
Author(s):  
Cihan Aydın ◽  
Mesut Engin
2019 ◽  
Vol 17 (3) ◽  
pp. 155-169 ◽  
Author(s):  
Etem Caliskan ◽  
Domingos Ramos de Souza ◽  
Andreas Böning ◽  
Oliver J. Liakopoulos ◽  
Yeong-Hoon Choi ◽  
...  

Author(s):  
Pedro D. Pedroso ◽  
Andreas S. Anayiotos ◽  
Brad L. Hershey ◽  
Evangelos Eleftheriou ◽  
William L. Holman

Coronary artery disease (CAD) is the leading cause of death in the world today. According to the American Heart Association 529,659 people in 1999 died as a result of CAD [1]. Starting in the 1960’s, surgeons have used Coronary Artery Bypass Graft (CABG) techniques in order to reestablish blood flow to the heart. Today, the procedure remains the same, using autologous grafts, such as the mammary artery and the saphenous vein. An unresolved problem, is that a significant number of CABGs reocclude months to years postoperatively. In the case of Saphenous Vein Grafts (SVGs) typically 50% of these bypasses are totally occluded months to years after the procedure, the remaining half being more than 50% occluded [2]. The re-occlusion of CABGs is due to a process labeled intimal hyperplasia (IH). Investigators have shown that IH, believed by some to be a remodeling process, occurs at branch sites, regions of curvature, and anastomotic junctions [3,4]. At these sites there are low residence times, slow secondary structures, disturbed flow, and areas of recirculation, therefore the onset of IH is believed to be hemodynamically linked. Most recently, floor IH has been attributed to four variables: time averaged wall shear stress (WSS), oscillating shear index (OSI), spatial wall shear stress gradients (WSSG), and temporal WSSG [5]. Adverse values of these parameters, in the case of SVGs, are believed to be caused by impedance mismatch at the anastomosis site. Over time this characteristic causes a bulge at the sinus. Such a morphology additionally contributes to disturbed flows which tend to propagate down the CABG and are believed to play a major role in the development of IH and the eventual failure of the graft.


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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