Clopidogrel use and bleeding after coronary artery bypass graft surgery - 08/08/11
, Robert M. Clare, MS b, Linda K. Shaw, MS b, Andrew J. Lodge, MD d, Peter K. Smith, MD d, E. Marc Jolicoeur, MD, MS b, Sunil V. Rao, MD b, c, Richard C. Becker, MD b, c, Daniel B. Mark, MD, MPH b, c, Christopher B. Granger, MD b, cRésumé |
Background |
Short-term use of clopidogrel plus aspirin among patients with acute coronary syndrome reduces ischemic events, but concerns about coronary artery bypass graft (CABG) surgery–related bleeding limit its early use.
Methods |
Using data from 4,794 consecutive CABG procedures in the Duke Databank for Cardiovascular Disease (January 1999 to December 2003), we developed multivariable models for associations with CABG-related bleeding defined as reoperation for bleeding, red cell transfusion, and a composite of reoperation/transfusion/hematocrit drop ≥15%. We examined clopidogrel use ≤5 days versus no clopidogrel ≤5 days before CABG in each model. Models were adjusted for propensity for clopidogrel use ≤5 days.
Results |
Of 4,794 CABG patients, 332 (6.9%) received clopidogrel ≤5 days before CABG, 127 (2.6%) had reoperation for bleeding, 3,277 (68.4%) received red cell transfusion, and 4,387 (91.5%) had the composite outcome. After adjustment, clopidogrel use ≤5 days was not significantly associated with reoperation (odds ratio [OR] 1.24, 95% CI 0.63-2.41) or the composite end point (OR 1.23, 95% CI 0.72-2.10). Clopidogrel ≤5 days was modestly associated with red cell transfusion (OR 1.40, 95% CI 1.04-1.89) but more weakly than other factors, including which surgeon performed the procedure.
Conclusion |
Clopidogrel administration ≤5 days before CABG was not significantly associated with reoperation for bleeding or a bleeding composite, and only weakly with red cell transfusion after surgery. The impact of withholding clopidogrel acutely in those for whom clopidogrel has proven benefits and the impact of delaying CABG to prevent bleeding among patients treated with clopidogrel should be viewed in the context of other stronger determinants of bleeding.
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| This work was supported by a research grant from Bristol Myers-Squibb/Sanofi Pharmaceuticals. The authors designed the study, had full access to the data, and drafted and revised the manuscript independently. All statistical programming and analyses were performed by co-authors (R.M.C. and L.K.S.) from the Duke Clinical Research Institute (Durham, NC). The authors take full responsibility for the integrity of this work. |
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| The paper was presented as an oral abstract on April 1, 2008, at the American College of Cardiology Scientific Sessions in Chicago, IL. |
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| John Hyung-Jun Kim, Andrew J. Lodge, Linda K. Shaw, Robert M. Clare, and E. Marc Jolicoeur have no financial disclosures to report. Financial disclosures for L. Kristin Newby and Christopher B. Granger can be found at documents/. Sunil V. Rao has received research funding from Cordis Corporation (Warren, NJ), Momenta Pharmaceuticals (Cambridge, MA), and Portola Pharmaceuticals (San Francisco, CA); and serves on speaker's bureaus for the Medicines Company, Sanofi-Aventis (Paris, France), and Bristol Myers-Squibb (Princeton, NJ). Daniel B. Mark has received research grant support from Eli Lilly (Indianapolis, IN) and Astra Zeneca (Wilmington, DE). Peter K. Smith has received consulting honoraria from Bayer Pharmaceuticals. Richard C. Becker has received research grant support from Astra Zeneca (Wilmington, DE), Bayer (Leverkusen, Germany), Bristol Myers-Squibb/Sanofi-Aventis, Regado Biosciences (Durham, NC), Schering Plough (Kenilworth, NJ), and the Medicines Company (Parsippany, NJ); and honoraria from Astra Zeneca, Bayer, and Daiichi/Eli Lilly; and serves as a consultant to Eisai Medical Research, Regado Biosciences and the Medicines Company. |
Vol 156 - N° 5
P. 886-892 - novembre 2008 Retour au numéro
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