Endothelial injury and acquired aspirin resistance as promoters of regional thrombin formation and early vein graft failure after coronary artery bypass.

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Presentation transcript:

Endothelial injury and acquired aspirin resistance as promoters of regional thrombin formation and early vein graft failure after coronary artery bypass grafting Robert S. Poston, MD, Junyan Gu, MD, PhD, James M. Brown, MD, James S. Gammie, MD, Charles White, MD, Lei Nie, PhD, Richard N. Pierson, MD, Bartley P. Griffith, MD The Journal of Thoracic and Cardiovascular Surgery Volume 131, Issue 1, Pages 122-130 (January 2006) DOI: 10.1016/j.jtcvs.2005.08.058 Copyright © 2006 The American Association for Thoracic Surgery Terms and Conditions

Figure 1 Surplus segments of each vein graft were procured intraoperatively and underwent immunohistochemical testing with CD31 monoclonal antibody. EC integrity was defined as percentage luminal circumference positive for CD31 according to image analysis software. A, As illustrated in this representative SVG section, CD31 staining was inconsistent on endoluminal surface of vein, suggesting endothelial disruption. In contrast, luminal staining was consistently positive in adventitial vessels of vasa vasorum, which were less exposed to procurement trauma. B, With image analysis, percentage endoluminal surface positive for CD31 was calculated. Original magnification ×10. The Journal of Thoracic and Cardiovascular Surgery 2006 131, 122-130DOI: (10.1016/j.jtcvs.2005.08.058) Copyright © 2006 The American Association for Thoracic Surgery Terms and Conditions

Figure 2 Whole-blood flow cytometry was used to confirm diagnosis of aspirin resistance by monitoring platelets (anti-CD41a, x-axis) for change in P-selectin expression (anti-CD62P, y-axis) in response to arachidonic acid (AA, 1.0 mmol/L). These representative examples illustrate 30-fold increase in mean fluorescence intensity (MFI) for P-selectin when both TEG and WBA were positive for aspirin resistance after arachidonic acid stimulation relative to baseline. In contrast, when both functional assays showed aspirin responsiveness, there was little change in P-selectin after arachidonic acid. The Journal of Thoracic and Cardiovascular Surgery 2006 131, 122-130DOI: (10.1016/j.jtcvs.2005.08.058) Copyright © 2006 The American Association for Thoracic Surgery Terms and Conditions

Figure 3 Tissue factor was constitutively expressed in adventitia (thick arrows) of surplus vein segments taken from each bypass graft analyzed by immunohistochemistry. Subendothelial pattern of tissue factor expression (A, arrowheads) was detected in 52 vein segments with more severe disruption of EC integrity (12%, 95% CI −2% to 26%). By comparison, vein segments that did not show this pattern of tissue factor expression (B, thin arrows) showed better EC integrity (49.6%, 95% CI 34.4%-60.9%, n = 355). The Journal of Thoracic and Cardiovascular Surgery 2006 131, 122-130DOI: (10.1016/j.jtcvs.2005.08.058) Copyright © 2006 The American Association for Thoracic Surgery Terms and Conditions

Figure 4 Although aspirin (ASA) monotherapy was sole antithrombotic strategy used during this study, postoperative aspirin resistance was significantly associated with failure only in vein grafts in lowest quartile of EC integrity (<9%). Additionally, very few grafts in this lowest quartile failed if aspirin sensitivity was preserved after OPCAB. Presence of both of these risk factors dramatically increased the risk of graft failure. Synergistic interaction of ASA-R and EC disruption was confirmed by paired analysis of variance test. The Journal of Thoracic and Cardiovascular Surgery 2006 131, 122-130DOI: (10.1016/j.jtcvs.2005.08.058) Copyright © 2006 The American Association for Thoracic Surgery Terms and Conditions