Aspirin resistance after coronary artery bypass grafting.

Abstract

The antiplatelet effect of aspirin may be compromised by an enhanced platelet turnover, generating an increased fraction of platelets that is able to form thromboxane within the dosing intervals (usually 1 day). This may be of particular relevance for patients undergoing CABG after cardiopulmonary bypass, when postoperative platelet turnover is increased. The present work examines whether the antiplatelet effect of aspirin, which is based on the inhibition of platelet thromboxane production, may be impaired by an increased platelet turnover. Determination of thromboxane in collagen-stimulated platelet-rich plasma after CABG showed a remarkable enhancement of the capacity for thromboxane formation, despite the fact that aspirin was administered at an antiplatelet dose (100 mg once daily) that largely suppressed thromboxane synthesis in healthy control subjects. Aspirin is widely used to reduce graft thrombosis after coronary artery bypass grafting (CABG).1 However, aspirin appears to not always be an effective inhibitor of platelet function because considerable individual variations in the antiplatelet effect of aspirin have been reported in patients assigned to CABG.2 ASPIRIN RESISTANCE AFTER CORONARY ARTERY BYPASS GRAFTING