Hindawi Publishing Corporation Thrombosis Volume 2010, Article ID 908272, 6 pages doi:10.1155/2010/908272 Research Article The Potential Value of Near Patient Platelet Function Testing in PCI: Randomised Comparison of 600 mg versus 900 mg Clopidogrel Loading Doses Alex R. Hobson, 1 Zeshan Qureshi, 2 Phil Banks, 3 and Nicholas Curzen 2, 3 1 Cardiac Intervention Unit, Royal Bournemouth Hospital, Castle Lane East, Bournemouth, BH7 7DW, UK 2 Wessex Cardiothoracic Unit, Southampton University Hospital, Tremona Road, SO16 6YD, UK 3 Southampton University Medical School, Southampton University Hospital, Tremona Road, Southampton, SO16 6YD, UK Correspondence should be addressed to Alex R. Hobson, alexhobson1@aol.com Received 4 July 2009; Accepted 14 August 2009 Academic Editor: Karin Przyklenk Copyright © 2010 Alex R. Hobson et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Whilst poor response to clopidogrel is associated with adverse outcomes uncertainty exists as to how (a) response should be assessed and (b) poor responders managed. We utilised VerifyNow P2Y12 and short Thrombelastography (TEG) to assess 900 mg doses in (i) initial poor responders to 600 mg and (ii) in a randomised comparison with 600 mg. Blood was taken before and six hours post clopidogrel in (i) 30 volunteers receiving 600 mg (poor responders received 900 mg > two weeks later) and (ii) 60 patients randomized 1 : 1 to 600 mg or 900 mg doses. Poor response was defined as TEG %Clotting Inhibition (%CIn) or VerifyNow Platelet Response Unit (PRU) reduction <30%. (i) Poor responders to 600 mg had greater PRU reduction (45.0 versus 20.1%, P = 0.03) and greater %CIn (22.9 versus -15.1%, P = 0.01) after 900 mg but (ii) there were no significant differences between the patient groups. Near-patient assessment of response to clopidogrel is feasible and clinically useful. Whilst ineffective on a population basis 900 mg doses increase the effect of clopidogrel in initial poor responders. 1. Introduction The clinical value of dual antiplatelet therapy with aspirin and clopidogrel to reduce platelet-mediated cardiovascular events is now well established in patients with acute coronary syndromes and those receiving intracoronary stents. In the field of PCI, in particular, a large and expanding body of evidence indicates that periprocedural complication rates can be reduced by loading doses of clopidogrel given at least 6 hours before planned stenting. The superiority of 600 mg loading doses of clopidogrel over 300 mg is now widely accepted [1–4]. There remain several areas of uncertainty in relation to optimal clopidogrel therapy in PCI patients, however. First, whether the risk of periprocedural and 30 day events could be further reduced by a 900 mg loading dose. The current data are discrepant in this regard [5–7]. Second, it is clear that there is heterogeneity in the response of individual patients to clopidogrel and that poor responders are susceptible to both early events [8–10] and later stent thrombosis [11–14]. Taking these factors into account, there is a logical case to be made that all patients being treated with clopidogrel should have their platelet function assessed to ensure a therapeutic response with the intention of reducing their risk. This concept is undermined by the limitations of current options for platelet function testing. Tests that are considered to be the “gold standard” for assessment of platelet function are generally laboratory based and analyse the platelet in isolation, rather that providing the clinician with an impression of the effect of clopidogrel on the patient’s tendency to clot. The high proportion of patients labeled as “poor responders” by these assays illustrates their limited value in the clinical arena. By contrast, clinically relevant near patient tests are few and there is uncertainty about their reliability. As a result global testing of patient responses to clopidogrel still does not occur, despite the knowledge that if it did it has the potential to reduce the incidence of both periprocedural myocardial infarction and stent thrombosis.