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Robert S. Poston
James M. Brown
James S. Gammie
Bartley P. Griffith
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J Thorac Cardiovasc Surg 2006;131:122-130
© 2006 The American Association for Thoracic Surgery


Surgery for Acquired Cardiovascular Disease

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 a , * , Junyan Gu, MD, PhD a , James M. Brown, MD a , James S. Gammie, MD a , Charles White, MD b , Lei Nie, PhD c , Richard N. Pierson, III, MD a , Bartley P. Griffith, MD a

a Department of Surgery, University of Maryland School of Medicine and Baltimore VAMC, Baltimore, Md
b Department of Radiology, University of Maryland School of Medicine and Baltimore VAMC, Baltimore, Md
c Department of Epidemiology, University of Maryland School of Medicine and Baltimore VAMC, Baltimore, Md

Received for publication April 18, 2005; revisions received July 1, 2005; accepted for publication August 8, 2005.

* Address for reprints: Robert S. Poston, MD, Assistant Professor of Surgery, Division of Cardiac Surgery, N4W94 22 S Greene St, Baltimore, MD 21201 (Email: rposton{at}smail.umaryland.edu).

OBJECTIVE: The predominant mechanism of early graft failure after coronary artery bypass grafting remains in doubt. Aspirin administered in the initial hours after coronary artery bypass grafting improves graft patency, implicating prostanoid synthesis in the pathogenesis. We hypothesized that synergy between endothelial disruption in the venous conduit and aspirin resistance would cause vein graft failure.

METHODS: Aspirin resistance, defined by diagnostic findings on at least two of three separate assays, was serially assessed in 225 patients undergoing off-pump coronary artery bypass grafting. Endothelial cell integrity was determined in surplus segments obtained from 408 vein grafts. The deposition of intraluminal thrombin within the vein was determined by comparing serum F1.2 levels between the coronary sinus and the aorta after grafting. Intraoperative blood flow in the grafts was measured with transit-time technology, and patency was assessed with electrocardiographically gated multichannel computed tomographic coronary angiography on day 5. Aspirin was the sole antithrombotic agent used during the study.

RESULTS: Thrombosed grafts (16/408) showed more endothelial cell loss at the time of grafting than did those grafts that remained patent (10.8% ± 21.5% vs 51.4% ± 39.1% integrity, P < .01). Aspirin resistance occurred in 67 patients (30%). Graft thrombosis was associated with aspirin resistance (P < .04) and reduced endothelial integrity (P < .01). These factors coexisted in 14 of 16 grafts that failed and were associated with elevated coronary sinus F1.2 levels.

CONCLUSION: Aspirin resistance and relatively compromised venous endothelial cell integrity together marked patients whose vein grafts failed within days after off-pump coronary artery bypass grafting. These observations form a basis for identifying patients at risk and developing approaches to prevent vein injury or to selectively intervene in high-risk circumstances.



Abbreviations and Acronyms CABG = coronary artery bypass grafting; CS = coronary sinus; CT = computed tomography; EC = endothelial cell; MA = maximum amplitude; OPCAB = off-pump coronary artery bypass grafting; PFA-100 = platelet function analyzer; SVG = saphenous vein graft; TEG = thromboelastography; WBA = whole-blood aggregometry





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