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

Abstract

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.

Off‐Pump Coronary Artery Bypass Grafting: 30 Years of Debate

“…In a study by Zimmermann et al,33 the antiplatelet effect of aspirin (100 mg/day started on day 1 after surgery) evaluated at day 5 was largely impaired after CPB but not after CABG without CPB; therefore, increased platelet turnover after CPB appears to contribute to transient aspirin “resistance” because an increased number of new platelets might be competent to form Thromboxane A 2 (TXA 2 ) within the 24‐hour dosing interval 33. Consistent with this hypothesis, Cavalca et al recently reported impaired aspirin pharmacodynamics early after ONCAB that were associated with significant increases in immature platelets, total platelets, platelet mass, thrombopoieitin, IL‐6, glycocalicin, leukocytes, and high‐sensitivity CRP 32.…”

“…A limited number of studies have compared the effects of ONCAB versus OPCAB on platelet activation and aggregation and failed to demonstrate major differences between them 30, 33, 34, 35. It should be emphasized that these studies relied on measurements of platelet function ex vivo, which do not necessarily reflect the extent of platelet activation in vivo 31…”

“…A different and more clinically relevant way of assessing the potential hemostatic/prothrombotic differences related to ONCAB versus OPCAB is represented by studies of the pharmacodynamic response to antiplatelet drugs in these settings 32, 33. In a study by Zimmermann et al,33 the antiplatelet effect of aspirin (100 mg/day started on day 1 after surgery) evaluated at day 5 was largely impaired after CPB but not after CABG without CPB; therefore, increased platelet turnover after CPB appears to contribute to transient aspirin “resistance” because an increased number of new platelets might be competent to form Thromboxane A 2 (TXA 2 ) within the 24‐hour dosing interval 33.…”

Impact of aspirin resistance on outcomes among patients following coronary artery bypass grafting: exploratory analysis from randomized controlled trial (NCT01159639)

“…In addition to interindividual differences in platelet inhibitory response to aspirin, it is very important to stress out that antiplatelet effect of aspirin may vary intraindividually [11][12][13] . This is of particular relevance in patients undergoing CABG, as there is evidence that cardiopulmonary bypass contributes to hyperactivity onset in postoperative phase 2,12,14,15 . Although there is evidence on AR prevalence in patients undergoing CABG, the clinical impact of AR on outcomes among patients following CABG remains elusive.…”

“…2) Pharmacodynamic AR may be considered in cases where is incomplete (cyclooxygenase-1) COX-1 inhibition presented in spite adequate plasma concentration 12 . Early postoperative increased platelet turnover and reactivity 12 as well as COX-1 polymorphism may be underlying cause for such a phenomenon 24,25 .…”