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Platelet aggregation plays a central role in the pathogenesis of atherothrombosis and the development of ischaemic complications following percutaneous coronary intervention (PCI). Dual antiplatelet therapy with aspirin and clopidogrel is the gold standard treatment in PCI and its beneficial effect in reducing the incidence of stent thrombosis and major adverse cardiovascular (CV) events compared with aspirin alone is well established.w1 w2 However, despite dual antiplatelet therapy, up to 20% of patients undergoing PCI experience recurrent ischaemic events and this has been attributed to antiplatelet treatment failure, the mechanisms of which are not fully understood and likely to be multifactorial.
Clinical studies have demonstrated significant heterogeneity in individual patient responses to antiplatelet therapy determined using various laboratory tests of platelet function. It is well documented that reduced responsiveness or high on-treatment platelet reactivity is associated with increased risk of adverse cardiovascular events. Nonetheless, clinical guidelines recommend standard doses of aspirin and clopidogrel in all patients undergoing PCI and routine measurement of individual responses to antiplatelet therapy has not been widely implemented. This is largely due to: (1) the need for a standardised definition of antiplatelet therapy hyporesponsiveness; (2) the lack of consensus regarding the preferred method of assessing platelet reactivity in the acute clinical setting; and (3) the lack of clarity as to whether laboratory findings of hyporesponsiveness unequivocally reflect biological hyporesponsiveness with direct clinical relevance.
In this paper, we will explore the clinical implications of antiplatelet therapy response variability in PCI, the relationship between tailored therapy and clinical outcome, and the state of play with regards to the move towards personalised antiplatelet therapy. The term ‘antiplatelet therapy response variability’ specifically refers to inter-patient differences in response to aspirin and clopidogrel as measured using various platelet function tests.
Measuring response to antiplatelet therapy
Although several platelet function assays are currently available for use in both …
Competing interests In compliance with EBAC/EACCME guidelines, all authors participating in Education in Heart have disclosed potential conflicts of interest that might cause a bias in the article. Nick Curzen has received unrestricted research funding from Haemonetics, Medtronic, Boston Scientific and Pfizer. He has also received speaker fees/consultancy from Boston Scientific, Abbott, Medtronic, AstraZeneca, Lilly and Cordis.
Provenance and peer review Commissioned; internally peer reviewed.