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Eur J Cardiothorac Surg 2005;27:606-610
© 2005 Elsevier Science NL

Is cardiopulmonary bypass a reason for aspirin resistance after coronary artery bypass grafting?

^a Department of Thoracic and Cardiovascular Surgery, Heinrich-Heine-University, Düsseldorf, Germany
^b Department of Pharmacology and Clinical Pharmacology, Heinrich-Heine-University, Düsseldorf, Germany

Received 30 September 2004; received in revised form 24 November 2004; accepted 13 December 2004.

^* Corresponding author. Address: Heinrich Heine Universität, Klinik für Thorax- und Kardiovaskuläre Chirurgie, Moorenstraße 5, Düsseldorf D-40225, Germany. Tel.: +49 211 8118332; fax: +49 211 8118333. (E-mail: hohlfeld{at}uni-duesseldorf.de).

Objective: ‘Off-pump’ coronary artery bypass grafting (OPCAB) is an alternative to conventional coronary artery bypass grafting (CABG) using cardiopulmonary bypass (CPB). While midterm results after OPCAB have become available, systematic studies of changes in platelet function after OPCAB are still missing. Since we have previously shown that oral aspirin treatment (100mg) does not achieve sufficient platelet inhibition in the majority of patients operated on with CPB, we hypothesized that bypass surgery without CPB (off-pump coronary artery bypass, OPCAB) causes less impairment of platelet inhibition by aspirin. The aim of this study was to investigate platelet function and the antiplatelet effect of aspirin after off-pump coronary artery bypass grafting in comparison with conventional on-pump surgery. Methods: We compared platelet function (in vitro aggregation and thromboxane formation) before and at days 1 and 5 after coronary artery bypass grafting, performed with (n=15) or without (n=14) CPB. Oral aspirin treatment (100mg/d) was started at day 1 after surgery. Results: After a 5 day oral treatment with aspirin, platelet aggregation was inhibited significantly in OPCAB-patients to 55.7±16.3% of control before surgery (P<0.05), whereas aggregation remained unchanged after CPB (105.8±26.9% of control before surgery; P>0.05). Since aspirin primarily inhibits platelet thromboxane formation, thromoboxane was determined after in vitro aggregation. According to platelet aggregation, thromboxane formation was only inhibited significantly after OPCAB (29.2±13.0% of control before surgery, P<0.05), but not after CPB (74.5±21.4% of control before surgery, P>0.05). This resistance to aspirin after CPB may be caused by an increased release of new platelets which are competent to form thromboxane, since the number of platelets decreased from 237±11x10³/µl before CPB to 174±13x10³/µl at day 1 after surgery and increased significantly the following days reaching 303±17x10³/µl at day 5. Platelet counts of patients operated on without CPB showed no significant changes (236±16x10³/µl before OPCAB, 220±16x10³/µl at day 1 and 266±31x10³/µl at day 5 after surgery). Conclusions: The antiplatelet effect of aspirin is largely impaired after CPB, but not after CABG without CPB. Hence, increased platelet turnover after CPB seems to contribute to aspirin resistance, since an increased number of platelets might be competent to form thromboxane within the dosing intervals.

Key Words: Off-pump coronary artery bypass grafting • Aspirin • Aspirin resistance • Platelet function

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