Platelet inhibition by aspirin is diminished in patients during carotid surgery: a form of transient aspirin resistance?

David A. Payne; Chris I. Jones; Paul D. Hayes; Sally E. Webster; A. Ross Naylor; Alison H. Goodall

doi:10.1160/TH03-12-0758

Thrombosis and Haemostasis, Table of Contents

Thromb Haemost 2004; 92(01): 89-96
DOI: 10.1160/TH03-12-0758

Platelets and Blood Cells

Schattauer GmbH

Platelet inhibition by aspirin is diminished in patients during carotid surgery: a form of transient aspirin resistance?

David A. Payne

¹The Department of Cardiovascular Sciences, University of Leicester, Leicester, UK

,

Chris I. Jones

¹The Department of Cardiovascular Sciences, University of Leicester, Leicester, UK

,

Paul D. Hayes

¹The Department of Cardiovascular Sciences, University of Leicester, Leicester, UK

,

Sally E. Webster

¹The Department of Cardiovascular Sciences, University of Leicester, Leicester, UK

,

A. Ross Naylor

¹The Department of Cardiovascular Sciences, University of Leicester, Leicester, UK

,

Alison H. Goodall

¹The Department of Cardiovascular Sciences, University of Leicester, Leicester, UK

› Author Affiliations

Abstract

Summary

The majority of patients who suffer peri-operative thromboembolic complication while undergoing vascular procedures do so despite taking aspirin. This study examined the antiplatelet effect of aspirin during surgery in patients undergoing carotid endarterectomy (CEA). Fifty patients undergoing CEA were standardised to 150 mg aspirin daily for ≥2 weeks. Platelet aggregation in response to arachidonic acid (AA) was measured in platelet rich plasma prepared from blood taken prior to, during, and at the end of surgery. Spontaneous platelet aggregation was also studied, as was the role of physiological agonists (ADP, collagen, thrombin, and epinephrine) in mediating the in vivo and in vitro responses to AA. Eighteen patients undergoing leg angioplasty, also on 150 mg aspirin, without general anaesthesia, served as a control group. In the CEA patients aggregation induced by AA (5 mM) increased significantly from 7.6 ± 5.5% pre-surgery to 50.8 ± 29.5% at the end of surgery (p <0.0001). Aggregation to AA was even greater in samples taken mid-surgery from a sub-set of patients (73.8 ± 7.2%; p = 0.0001), but fell to 45.9 ± 7.4% by the end of surgery. The increased aggregation in response to AA was not due to intra-operative release of physiological platelet agonists since addition of agents that block/neutralise the effects of ADP (apyrase; 4 µg/ml), thrombin (hirudin; 10 units/ml), or epinephrine (yohimbine; 10 µM/l) to the samples taken at the end of surgery did not block the increased aggregation.The patients undergoing angioplasty also showed a significant rise in the response to AA (5 mM), from 5.6 ± 5.5% pre-angioplasty to 32.4 ± 24.9% at the end of the procedure (p <0.0001), which fell significantly to 11.0 ± 8.1% 4 hours later. The antiplatelet activity of aspirin, mediated by blockade of platelet arachidonic acid metabolism, diminished significantly during surgery, but was partially restored by the end of the procedure without additional aspirin treatment.This rapidly inducible and transient effect may explain why some patients undergoing cardiovascular surgery remain at risk of peri-operative stroke and myocardial infarction.

Keywords

Aspirin - platelets - surgery - carotid artery - aspirin resistance

Full Text

References

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