https://onlinelibrary.wiley.com/doi/pdf/10.1111/j.1538-7836.2006.01958.x

Aspirin resistance detected with aggregometry cannot be explained by cyclooxygenase activity: involvement of other signaling pathway(s) in cardiovascular events of aspirin-treated patients.

The success of coronary artery bypass graft surgery (CABG) depends mainly on the patency of the graft vessels. Aortocoronary vein graft disease is comprised of three distinct but interrelated pathological processes: thrombosis, intimal hyperplasia and atherosclerosis. Early thrombosis is a major cause of vein graft attrition during the first month after CABG, while during the remainder of the first year, intimal hyperplasia forms a template for subsequent atherogenesis, which thereafter predominates. Platelets play a crucial role in the pathophysiology of graft thrombosis and aspirin is the primary antiplatelet drug that has been shown to improve vein graft patency within the first year after CABG. Nevertheless, a significant number of grafts still occlude in the early postoperative period despite 'appropriate' aspirin treatment. Moreover, laboratory investigations showed that the expected inhibition of platelet function is not always achieved. This has been called 'aspirin nonresponse' or 'aspirin resistance', although a uniform definition is lacking. The finding that a considerable number of patients show an impaired antiplatelet effect of aspirin after CABG brought new insight into the discussion concerning poor patency rates of bypass grafts: the early period after CABG shows a coincidence of an increased risk for bypass thrombosis (amongst others, due to platelet activation and endothelial cell disruption of the graft) and an increased prevalence of aspirin resistance. Hitherto, the underlying mechanisms of aspirin resistance are uncertain and largely hypothetical; amongst others, increased platelet turnover, enhanced platelet reactivity, systemic inflammation, and drug-drug interaction are discussed. Up to now available data concerning the clinical outcome of aspirin resistant CABG patients are limited, and there is evidence that platelets of patients with graft thrombosis are more likely to be resistant to aspirin compared with patients without thrombotic events. Many publications concerning aspirin resistance are available today, but reports addressing this topic in CABG patients are sparse. This review summarises recent insights into the antiplatelet treatment after CABG and describes the clinical benefit, but also the therapeutic failure of the well-established drug aspirin. Moreover, possible pharmacological approaches to improve antithrombotic therapy in aspirin nonresponders among CABG patients are discussed.

Aspirin in coronary artery bypass surgery: new aspects of and alternatives for an old antithrombotic agent.

Platelet reactivity and activation are important factors during the development of atherothrombotic processes and subsequent ischaemic complications. Pharmacological agents that suppress platelet function are proved to be the most efficient in the prevention and treatment of thrombotic complications. As the activation of platelets during thrombus generation involves many complex and redundant pathways, simultaneous use of different antiplatelet drugs that are directed against different targets have been effective in reducing adverse clinical events. The main antiplatelet drugs are aspirin (which inhibits thromboxane synthesis), thienopyridines (which block P2Y12 receptors) and glycoprotein IIb/IIIa antagonists (which block glycoprotein IIb/IIIa receptors). In recent years, resistance or nonresponsiveness to antiplatelet therapy has been reported and, more importantly, are linked to the occurrence of adverse cardiovascular events. New treatment strategies to overcome nonresponsiveness are being sought. A focus on the development of simple, reproducible and user friendly point-of-care methods to determine aspirin/clopidogrel responsiveness should be undertaken to assist clinicians in tailoring antiplatelet therapy to the individual patient.

Resistance to antiplatelet drugs: current status and future research

:The aim of the present study was to assess the responsiveness of blood platelets to aspirin in patients following coronary artery bypass grafting (CABG) surgery. Aspirin was administered following CABG in 24 operated patients (aged 63.2 ± 6.3 years). Platelet function was monitored on the 1

Resistance to aspirin in patients after coronary artery bypass grafting is transient: impact on the monitoring of aspirin antiplatelet therapy.

Platelet activation, myocardial ischemic events and postoperative non-response to aspirin in patients undergoing major vascular surgery.

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

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

Thromb Haemost 2004; 92: 89‐96 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.

http://www.researchgate.net/profile/Ross_Naylor/publication/8494090_Platelet_inhibition_by_aspirin_is_diminished_in_patients_during_carotid_surgery_A_form_of_transient_aspirin_resistance/links/00b7d53c7e1424815c000000.pdf

https://www.jvascsurg.org/article/S0741-5214(04)00832-8/pdf

Anti-platelet effect of aspirin is substantially reduced after administration of heparin during carotid endarterectomy.

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

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

Anti-platelet effect of aspirin is substantially reduced after administration of heparin during carotid endarterectomy.