Regular Article The risk of false results in the assessment of platelet function in the absence of antiplatelet medication: Comparision of the PFA-100, multiplate electrical impedance aggregometry and verify now assays Mehmet Mustafa Can a, ⁎, İbrahim Halil Tanboğa a , Erdem Türkyılmaz a , Can Yucel Karabay a , Taylan Akgun a , Fatih Koca a , Hacer Ceren Tokgoz a , Nursen Keles a , Alper Ozkan a , Tahir Bezgin a , Olcay Ozveren b , Kenan Sonmez a , Mustafa Sağlam a , Nihal Ozdemir a , Cihangir Kaymaz a a Department of Cardiology, Koşuyolu Heart & Research Hospital, Turkey b Department of Cardiology, Kutahya Dumlupınar University, Turkey abstract article info Article history: Received 16 September 2009 Received in revised form 22 October 2009 Accepted 6 November 2009 Available online 1 December 2009 Keywords: Platelet function tests Baseline platelet activity Objectives: Evaluation of aspirin (ASA) responsiveness with platelet function tests varies by the choice of blood mixture and functional test and cut off values for defining the the treatment used. Addition to that we also aimed to determine aggregement between three tests and to research whether there is any necessity to measure baseline platelet activity. Methods: The study group comprised of 52 patients with multiple risk factors receiving primary prophylaxis of ASA (100 mg/day). For each patient inhibition of platelet aggregation with aspirin was determined using three different whole blood tests: Multiplate electrical impedance aggregometry , Verify Now Aspirin, and collagen- epinephrine closure time PFA-100. Platelet aggregation was assessed with multiplate electrical impedance aggregometry,and was defined as the area under curve (AUC,AUxmin).Maximal 6,4 microM collagen-induced AUC were used to quantify platelet aggregation due to ASA.The ASA response was defined as > 30 % reduction in basal platelet aggregation with multiplate electrical impedance aggregometry.Collagen induced platelet aggregation at the Verify Now Aspirin assay quantitated the ASA-induced platelet inhibition as aspirin reaction units (ARU).According to manifacturer insert ARU > 550 indicates aspirin resistance. ASA platelet function studies were assessed twice at baseline (pre-aspirin), and after 7 day(post-aspirin) were performed. Results: After ASA intake none of the patients was found aspirin resistant with PFA-100. (CEPI-CT (129 ± 36 vs 289 ± 18 ). None of the patients was found aspirin resistant with PFA-100. As > 30 % reduction in bazal platelet aggregation with multiplate electrical impedance aggregometry is selected all of the patients have been stratified as responders.(COL TEST 688±230 vs 169 ± 131 AU) None of the patients with Verify Now Aspirin found resistance to ASA(594 ± 62 vs 446 ± 43).Prior to ASA intake 15 of all patients with VN(501 ± 16) and 2 of all patients with multiplate electrical impedance aggregometry (223 ± 40 AUC )aggregation levels below the cut off label before ingestion of ASA.None of the patients was above the cut off label with PFA -100 (129 ± 36). Conclusions: Verify Now ASA assay, multiplate electrical impedance aggregometry and PFA-100 seem to be reliable tests in reflecting ASA effect on platelets. Cut off labels for the defining the responsiveness given by manıfacturer may show significant interindividual variabiliy with Verify Now ASA assay and multiplate electrical impedance aggregometry, and these test may show platelet inhibition despite the absence of ASA intake. Consideration of the pretreatment values may eliminate the risk of overestimation in the assessment of platelet inhibtion by ASA. © 2009 Elsevier Ltd. All rights reserved. Introduction Primary, secondary and tertiary prevention strategies in cardio- vascular medicine aim to limit or prevent future atherothrombotic events, and acetylsalicylic acid (ASA) has been considered to be an important part of this approach [1–3]. Its antiplatelet activity is based on the irreversible inhibition of cycloxgenase enzyme activity, responsible for one of the strong platelet agonists, thromboxane A2. Although the benefits of ASA in primary and secondary prevention have been well documented in numerous recent studies, its efficacy is not uniform and ASA resistance or treatment failure continues to be an important problem. The failure of an antiplatelet agent to inhibit its targets is defined as nonresponsiveness or resistance to agent. However, resistance defined by platelet function assays may not Thrombosis Research 125 (2010) e132–e137 ⁎ Corresponding author. Department of Cardiology, Kartal Koşuyolu Heart and Research Instıtue, Denizer Street, 34860, Kartal, İstanbul, Turkey. Tel.: +90 2164594041. E-mail address: mehmetmustafacan@yahoo.com (M.M. Can). 0049-3848/$ – see front matter © 2009 Elsevier Ltd. All rights reserved. doi:10.1016/j.thromres.2009.11.005 Contents lists available at ScienceDirect Thrombosis Research journal homepage: www.elsevier.com/locate/thromres