scholarly journals TCT-655 Evaluation of Aortocoronary Saphenous Vein Graft Disease Using Serial Intravascular Ultrasound Imaging. Insights From The Cardiac CAtheterization For Bypass Graft Patency Rate Optimization (CABG-PRO) Study

2013 ◽  
Vol 62 (18) ◽  
pp. B199
Author(s):  
Anna Kotsia ◽  
Tesfadelt Michael ◽  
Bavana Rangan ◽  
Carlos DiMaio ◽  
Matthias Peltz ◽  
...  
2021 ◽  
Vol 8 (10) ◽  
pp. 601-607
Author(s):  
Cihan Aydın ◽  
Mustafa Abanoz

Objective: Coronary artery bypass graft (CABG) surgery is a common treatment method in which saphenous vein grafts (SVG) and arterial grafts are used together in severe coronary artery disease. The CHA2DS2-VASc score is used to predict thromboembolic events in nonvalvular atrial fibrillation as well as to predict prognosis in cardiovascular events.  In this study, we planned to research the relation between CHA2DS2-VASc score and postoperative SVG patency rates in patients undergoing CABG. Materials and Methods: One hundred seventeen patients with angina after CABG surgery who underwent coronary angiography were analyzed retrospectively. Stenosis of 50% or more in at least one saphenous vein graft was accepted as saphenous vein graft disease (SVGD). We compared these patients in two groups concerning the presence of 50% or more stenosis in the SVG. These two groups were; Group 1 (n = 66); with saphenous vein graft disease, Group 2 (n = 51) without saphenous vein graft disease, respectively. Results: A total of 117 patients participating in the study. Sixty-six patients in group 1 had SVGD (Mean age: 68,13±8,22, 60,6% male). Fifty-one patients in group 2 did not have SVGD (Mean age: 66,92±9,44, 72,5% male ). The mean CHA2DS2-VASc score was significantly higher in group 1 compared to group 2. [5 (2-7) vs.  2 (1-7), respectively, P<0,001]. As a result of multivariate analysis, CHA2DS2-VASc score (OR: 5,263, CI 95%: 2,176- 12,728, P<0.001) and SII (OR: 1,236, CI 95%: 1,120-2,955, P=0.007) were determined as independent predictors for predicting SVGD Conclusion: In the light of the results we have found, the CHA2DS2-VASc score and SII, which are easy to calculate in daily practice, can help us in predicting SVGD.


2015 ◽  
Vol 24 (6) ◽  
pp. 544-547 ◽  
Author(s):  
Ibrahim Kocaoglu ◽  
Ugur Arslan ◽  
Yavuzer Koza ◽  
Mustafa M�cahit Balci ◽  
Gizem �elik ◽  
...  

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Swastika Sur ◽  
Songcang Chen ◽  
Jeffrey T Sugimoto ◽  
Devendra K Agrawal

Coronary revascularization by coronary artery bypass grafting (CABG) is the choice of procedure in patients with multi-vessel or left main coronary artery disease. Concerns have been raised on the long term result of CABG using saphenous vein graft (SVG) as its patency significantly declines following surgery, compared to internal mammary artery (IMA), which is almost immune to restenosis. Proliferation of smooth muscle cells (SMCs) is the key event in the pathogenesis of intimal hyperplasia leading to SVG failure. PDGF-BB is a major growth factor released at the site of pulsatile stretch- and shear stress-induced graft injury. Here, we examined, for the first time, the expression of PLK1 and its phosphorylation/activation in isolated human bypass graft conduits. Human SV and IMA vessels were freshly collected, SMCs isolated and cultured up to 5th passage. In cultured SMCs, effect of PDGF-BB was examined on total and phosphorylated PLK1 (pPLK1) by Western blot analysis. Cell proliferation was measured using thymidine incorporation, MTT method and cell count. We found significantly higher expression of pPLK1 and total PLK1 in PDGF-stimulated SV SMCs than IMA. SV SMCs had 5-fold increase in the density of pPLK1 and had 2-fold increase in the density of total PLK1. While in the IMA SMCs, increase in pPLK1 was significantly lower than in SV SMCs. Also, this increase was not sustained. These data suggest a greater and sustained sensitivity of SV SMCs to PDGF-BB induced PLK1 activity than that of IMA. A PLK1 blocker inhibited PDGF-induced proliferation in both IMA and SV SMCs. These data demonstrate differential activity of PDGF-induced PLK1 activation, which was greater in SV SMCs than in IMA. This could explain the development of intimal hyperplasia in SV conduits than the IMA following CABG. Thus, inhibition of PLK1 could be a target in developing better therapeutic approach to prevent vein-graft disease.


Sign in / Sign up

Export Citation Format

Share Document