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Disease Progression After CABG

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Coronary Graft Failure

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Abstract

Patients with clinical post- coronary artery bypass grafting (CABG) deterioration manifest angiographic disease progression in both the native coronary arteries and aortocoronary conduits. Although clinical results suggest more pronounced impact of failed revascularization in comparison to progression in the native coronary circulation, the latter one is also of clinical importance. Coronary artery disease (CAD) progression in the ungrafted coronaries mimics pathophysiology of atherosclerosis, thus strict control of the commonest risk factors for its development is the therapeutic target. Otherwise, angiographic disease deterioration in the target coronary arteries is a net result of negative remodeling and plaque progression. Analysis of the angiographic post-CABG follow-up indicates that vessel shrinkage (i.e., negative remodeling) dominates. Low endothelial shrear stress resulted from diminished blood flow seems to be the most powerful pathogenetic factor of negative remodeling.

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References

  1. Windecker S, Kolh PH, Alfonso F, et al. 2014 ESC/EACTS Guidelines on myocardial revascularization. The Task Force on Myocardial Revascularization of the European Society of Cardiology (ESC) and the European Association for Cardio-Thoracic Surgery (EACTS) developed with the special contribution of the European Association of Percutaneous Cardiovascular Interventions (EAPCI). Eur Heart J. 2014. doi:10.1093/eurheartj/ehu278.

    Google Scholar 

  2. Javaid A, Steinberg DH, Buch AN, et al. Outcomes of coronary artery bypass grafting versus percutaneous coronary intervention with drug-eluting stents for patients with multivessel coronary artery disease. Circulation. 2007;116(11 Suppl):I200–6.

    CAS  PubMed  Google Scholar 

  3. Deb S, Wijeysundera HC, Ko DT, et al. Coronary artery bypass graft surgery vs percutaneous interventions in coronary revascularization: a systematic review. JAMA. 2013;310:2086–95.

    Article  CAS  PubMed  Google Scholar 

  4. Loponen P, Korpilahti K, Luther M, et al. Repeat intervention after invasive treatment of coronary arteries. Eur J Cardiothorac Surg. 2009;35:43–7.

    Article  PubMed  Google Scholar 

  5. Eifert S, Rasch A, Beiras-Fernandez A, et al. Gene polymorphisms in APOE, NOS3, and LIPC genes may be risk factors for cardiac adverse events after primary CABG. J Cardiothorac Surg. 2009;4:46.

    Article  PubMed  PubMed Central  Google Scholar 

  6. Beiras-Fernandez A, Angele MK, Koutang C, et al. Genetic polymorphisms of TP53 and FAS promoter modulate the progression of coronary artery disease after coronary artery bypass grafting: a gender-specific view. Inflamm Res. 2011;60:439–45.

    Article  CAS  PubMed  Google Scholar 

  7. The Post Coronary Artery Bypass Graft Trial investigations. The effect of aggressive lowering of low-density lipoprotein cholesterol levels and low-dose anticoagulation on obstructive changes in saphenous-vein coronary artery bypass grafts. N Engl J Med. 1997;336:153–62.

    Article  Google Scholar 

  8. Alderman EL, Kip KE, Whitlow PL, et al. Native coronary disease progression exceeds failed revascularization as cause of angina five years in the bypass angioplasty revascularization investigation (BARI). J Am Coll Cardiol. 2004;44:766–74.

    Article  PubMed  Google Scholar 

  9. Chen L, Théroux P, Lespérance J, et al. Angiographic features of vein grafts versus ungrafted coronary arteries in patients with unstable angina and previous bypass surgery. J Am Coll Cardiol. 1996;28:1493–9.

    Article  CAS  PubMed  Google Scholar 

  10. Preston LM, Calvin JE, Class S, et al. Coronary angiographic morphology in unstable angina: comparative observations of culprit lesions in saphenous vein grafts versus native coronary arteries. J Invasive Cardiol. 2002;14:81–6.

    PubMed  Google Scholar 

  11. Halabi AR, Alexander JH, Shaw LK, et al. Relation of early sapehnous vein graft failure to outcomes following coronary artery bypass surgery. Am J Cardiol. 2005;96:1254–9.

    Article  PubMed  Google Scholar 

  12. Bourassa MG, Enjalbert M, Campeau L, et al. Progression of atherosclerosis in coronary arteries and bypass grafts: ten years later. Am J Cardiol. 1984;53:102C–7.

    Article  CAS  PubMed  Google Scholar 

  13. Rupprecht HJ, Hamm C, Ischinger T, et al. On behalf of the GABI study group. Angiographic follow-up results of a randomized study on angioplasty versus bypass surgery (GABI trial). Eur Heart J. 1996;17:1192–8.

    Article  CAS  PubMed  Google Scholar 

  14. Bourassa MG, Fisher LD, Campeau L, et al. Long-term fate of bypass grafts: the Coronary Artery Surgery Study (CASS) and Montreal Heart Institute experiences. Circulation. 1985;72:V71–8.

    CAS  PubMed  Google Scholar 

  15. Alderman EL, Corley SD, Fisher LD, et al. Five-year angiography follow-up of factors associated with progression of coronary artery disease in the Coronary Artery Surgery Study (CASS). J Am Coll Cardiol. 1993;22:1141–54.

    Article  CAS  PubMed  Google Scholar 

  16. Kroncke GM, Kosolcharoen P, Clayman JA, et al. Five-year changes in coronary arteries of medical and surgical patients of the Veterans Administration randomized study of bypass surgery. Circulation. 1988;78(Suppl I):I44–50.

    Google Scholar 

  17. Sabik III JF, Lytle W, Blackstone EH, et al. Does competitive flow reduce internal thoracic artery graft patency? Ann Thorac Surg. 2003;76:1490–7.

    Article  PubMed  Google Scholar 

  18. Kaku D, Nakahira A, Hirai H, et al. Does rich coronary collateral circulation distal to chronically occluded left anterior descending artery compete with graft flow? Interact Cardiovasc Thorac Surg. 2013;17:944–9.

    Article  PubMed  PubMed Central  Google Scholar 

  19. Nordgaard H, Nordhug D, Kirkeby-Garstad I, et al. Different graft flow patterns due to competitive flow or stenosis in the coronary anastomosis assessed by transit-time flowmetry in a porcine model. Eur J Cardiothorac Surg. 2009;36:137–42.

    Article  PubMed  Google Scholar 

  20. Sabik III JF, Lytle W, Blackstone EH, et al. Comparison of saphenous vein and internal thoracic artery graft patency by coronary system. Ann Thorac Surg. 2005;79:544–51.

    Article  PubMed  Google Scholar 

  21. Shang Y, Mintz GS, Pu J, et al. Bypass to the left coronary artery systém may accelerate left main coronary artery negative remodeling and calcification. Clin Res Cardiol. 2013;102:831–5 (mam).

    Article  PubMed  Google Scholar 

  22. Ward MR, Tsao PS, Agrotis A, et al. Low blood flow after angioplasty augments mechanisms of restenosis: inward vessel remodeling, cell migration, and activity of genes regulating migration. Arterioscler Thromb Vasc Biol. 2001;21:208–13.

    Article  CAS  PubMed  Google Scholar 

  23. Korshunov VA, Schwartz SM, Berk BC. Vascular remodeling: hemodynamic and biochemical mechanisms underlying Glagov’s phenomenon. Arterioscler Thromb Vasc Biol. 2007;27:1722–8.

    Article  CAS  PubMed  Google Scholar 

  24. Cheng C, van Haperen R, de Waard M, et al. Shear stress affects the intracellular distribution of eNOS: direct demonstration by a novel in vivo technique. Blood. 2005;106:3691–8.

    Article  CAS  PubMed  Google Scholar 

  25. Harrison DG, Widder J, Grumbach I, et al. Endothelial mechanotransduction, nitric oxide and vascular inflammation. J Intern Med. 2006;259:351–63.

    Article  CAS  PubMed  Google Scholar 

  26. Qiu Y, Tarbell JM. Interaction between wall shear stress and circumferential strain affects endothelial cell biochemical production. J Vasc Res. 2000;37:147–57.

    Article  CAS  PubMed  Google Scholar 

  27. Liu Y, Chen BP, Lu M, et al. Shear stress activation of SREBP1 in endothelial cells is mediated by integrins. Arterioscler Thromb Vasc Biol. 2002;22:76–8.

    Article  PubMed  Google Scholar 

  28. Chien S. Molecular and mechanical bases of focal lipid accumulation in arterial wall. Prog Biophys Mol Biol. 2003;83:131–51.

    Article  CAS  PubMed  Google Scholar 

  29. Himburg HA, Grzybowski DM, Hazel AZ, et al. Spatial comparison between wall shear stress measures and porcine arterial endothelial permeability. Am J Physiol Heart Circ Physiol. 2004;286:H1916–22.

    Article  CAS  PubMed  Google Scholar 

  30. Chen YL, Jan KM, Lin HS, et al. Ultrastructural studies on macromolecular permeability in relation to endothelial cell turnover. Atherosclerosis. 1995;118:89–104.

    Article  CAS  PubMed  Google Scholar 

  31. Feldman CL, Ilegbusi OJ, Hu Z, et al. Determination of in vivo velocity and endothelial shear stress patterns with phasic flow in human coronary arteries: a methodology to predict progression of coronary atherosclerosis. Am Heart J. 2002;143:931–9.

    Article  PubMed  Google Scholar 

  32. Hwang J, Ing MH, Salazar A, et al. Pulsatile versus oscillatory shear stress regulates NADPH oxidase subunit expression: implication for native LDL oxidation. Circ Res. 2003;93:1225–32.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  33. McNally JS, Davis ME, Giddens DP, et al. Role of xanthine oxidoreductase and NAD(P)H oxidase in endothelial superoxide production in response to oscillatory shear stress. Am J Physiol Heart Circ Physiol. 2003;285:H2290–7.

    Article  CAS  PubMed  Google Scholar 

  34. Mueller CF, Widder JD, McNally JS, et al. The role of the multidrug resistance protein-1 in modulation of endothelial cell oxidative stress. Circ Res. 2005;97:637–44.

    Article  CAS  PubMed  Google Scholar 

  35. Libby P. Inflammation in atherosclerosis. Nature. 2002;420:868–74.

    Article  CAS  PubMed  Google Scholar 

  36. Orr AW, Sanders JM, Bevard M, et al. The subendothelial extracellular matrix modulates NF-kappaB activation by flow: a potential role in atherosclerosis. J Cell Biol. 2005;169:191–202.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  37. Mohan S, Hamuro M, Sorescu GP, et al. Ikappa Balpha-dependent regulation of low-shear flow-induced NF-kappa B activity: role of nitric oxide. Am J Physiol Cell Physiol. 2003;284:C1039–47.

    Article  CAS  PubMed  Google Scholar 

  38. Collins T, Cybulsky MI. NF-kappaB: pivotal mediator or innocent bystander in atherogenesis? J Clin Invest. 2001;107:255–64.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  39. Hsiai TK, Cho SK, Wong PK, et al. Monocyte recruitment to endothelial cells in response to oscillatory shear stress. FASEB J. 2003;17:1648–57.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  40. Conklin BS, Zhong DS, Zhao W, et al. Shear stress regulates occludin and VEGF expression in porcine arterial endothelial cells. J Surg Res. 2002;102:13–21.

    Article  CAS  PubMed  Google Scholar 

  41. Palumbo R, Gaetano C, Antonini A, et al. Different effects of high and low shear stress on platelet-derived growth factor isoform release by endothelial cells: consequences for smooth muscle cell migration. Arterioscler Thromb Vasc Biol. 2002;22:405–11.

    Article  CAS  PubMed  Google Scholar 

  42. Redmond EM, Cullen JP, Cahill PA, et al. Endothelial cells inhibit flow-induced smooth muscle cell migration: role of plasminogen activator inhibitor-1. Circulation. 2001;103:597–603.

    Article  CAS  PubMed  Google Scholar 

  43. Grainger DJ. Transforming growth factor beta and atherosclerosis: so far, so good for the protective cytokine hypothesis. Arterioscler Thromb Vasc Biol. 2004;24:399–404.

    Article  CAS  PubMed  Google Scholar 

  44. Virmani R, Kolodgie FD, Burke AP, et al. Lessons from sudden coronary death: a comprehensive morphological classification scheme for atherosclerotic lesions. Arterioscler Thromb Vasc Biol. 2000;20:1262–75.

    Article  CAS  PubMed  Google Scholar 

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Author information

Authors and Affiliations

  1. Department of Cardiac Surgery and Transplantology, Poznan University of Medical Sciences, Poznan, Poland

    Bartłomiej Perek MD, PhD

Authors
  1. Bartłomiej Perek MD, PhD
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Correspondence to Bartłomiej Perek MD, PhD .

Editor information

Editors and Affiliations

  1. Cardiology, Army's Center for Cardiovascular Di, Bucharest, Romania

    Ion C. Ţintoiu

  2. Department of Surgery, Chinese University of Hong Kong, Sha Tin, Hong Kong

    Malcolm John Underwood

  3. University Fribourg, Hospital HFR Fribourg, Fribourg, Fribourg, Switzerland

    Stephane Pierre Cook

  4. Department of Cardiovascular Medicine, Wakayama Medical University, Wakayama, Japan

    Hironori Kitabata

  5. University Medical Center, Texas Tech Univ. Health Science Center, EL PASO, Texas, USA

    Aamer Abbas

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© 2016 Springer International Publishing Switzerland

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Perek, B. (2016). Disease Progression After CABG. In: Ţintoiu, I., Underwood, M., Cook, S., Kitabata, H., Abbas, A. (eds) Coronary Graft Failure. Springer, Cham. https://doi.org/10.1007/978-3-319-26515-5_12

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  • DOI: https://doi.org/10.1007/978-3-319-26515-5_12

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  • Publisher Name: Springer, Cham

  • Print ISBN: 978-3-319-26513-1

  • Online ISBN: 978-3-319-26515-5

  • eBook Packages: MedicineMedicine (R0)

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