Poor responsiveness to clopidogrel. Drug-specific or class-effect?

ABSTRACTS / Journal of Molecular and Cellular Cardiology 42 (2007) S234–S237

ponse to long-term aspirin therapy in patients with a history of coronary artery disease in 1-year follow-up. Materials and methods: 61 patients (19 women (31.1%) vs. 42 men (68.9%)) with coronary artery disease taking aspirin (mean treatment duration 4.7 ± 3.1 years) as a secondary prevention were screened by the Platelet Function Analyzer PFA − 100. Compliance was assessed by means of a self-report questionnaire designed specifically for the purpose of the present study. Results: Aspirin resistance was defined as a normal collagen/epinephrine closure time on the PFA-100 (< 189 s). The baseline EPI-CT was 212.26 ± 86.44 s and after 1 year lasting antiplatelet therapy with aspirin EPI-CT was 210.11 ± 79.57s. At baseline measurement 27 (44.3%) patients were aspirin resistant and after 1-year follow-up the 29 patients (47.5%) were resistant to antiplatelet therapy. There was a non-significant difference between the two groups (regularly taking—41 patients and not regularly taking aspirin—20 patients) in EPI-CT after 1 year observation (226.78 ± 77.13 s vs. 176.83 ± 75.18 s; NS). Mean number of aspirin pills the patients forgot to take during the previous 2 weeks were 3.6 ± 2.7. Conclusion: In the studied group non-compliance may be one of the most important factors responsible for aspirin resistance in long term treatment. Keywords: PFA-100; Aspirin resistance; Cardiology doi:10.1016/j.yjmcc.2007.03.705

Utility of platelet function analyzer Pfa-100 in assessment of platelet function in patients with stable coronary artery Marek Postula, Agnieszka Serafin, Michal Marchel, Krzysztof Filipiak, Bozena Tarchalska, Grzegorz Opolski. 1st Department of Cardiology, Warsaw Medical University, Poland Introduction: We sought to investigate the association of aspirin usage and utility of platelet function analyzer (PFA100). Materials and methods: 61 patients (19 women (31.1%) vs. 42 men (68.9%)) with coronary artery disease taking aspirin (mean treatment duration 4.7 ± 3.1 years) as a secondary prevention were screened by PFA − 100. All patients were taking aspirin in doses from 75 to 150 mg/day (mean dose 83.2 ± 21.3 mg) for at least 3 months prior to the study and during 1-year follow-up. Results: Aspirin resistance was defined as a normal collagen/ epinephrine closure time on the PFA-100 (< 189 s). The baseline EPI-CT was 212.26 ± 86.44 s and after 1 year lasting antiplatelet therapy with aspirin EPI-CT was 210.11 ± 79.57s. At baseline (group A) measurement 27 (44.3%) patients were aspirin resistant and in 1-year follow-up (group B) the 29 patients (47.5%) were resistant to antiplatelet therapy. 10 patients (16.4%) extended maximal EPI-CT in both measurements. In 9 (14.75%) patients EPI-CT in 1-year follow-up has prolonged more than 100 s (mean 162.1 ± 36.37 s) and these patients became responders to antiplatelet therapy according to our criteria. In 8 (13.1%) patients EPI-CT was lower than baseline measurement (mean

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142.2 s ± 30.1 s) and they became non-responders according to criteria. Conclusion: PFA-100 is a very useful tool to evaluate platelet activation. Closure time (CT), measured by platelet function analyzer (PFA-100) device, in one-year follow-up is stable over the time. Keywords: PFA-100; Aspirin resistance; Cardiology doi:10.1016/j.yjmcc.2007.03.706

Poor responsiveness to clopidogrel. Drug-specific or class-effect? A. Frangione, S. Luccarelli, G. Campo, M. Valgimigli, R. Ferrari. Cardiovascular Institute, University of Ferrara, and Cardiovascular Research Centre, Salvatore Maugeri, Foundation, IRCCS Gussago (BS), Italy Background: It is uncertain if poor responders to clopidogrel display inadequate platelet inhibition also after ticlopidine administration. Objectives: To investigate whether poor responders to clopidogrel do not improve their pattern of platelet inhibition after ticlopidine intake. Methods: 143 patients receiving ASA. Platelet aggregation (PA) was measured with light transmission aggregometry using adenosine diphosphate as agonist at baseline, before clopidogrel intake (T0), and at clopidogrel steady-state (T1). After T1 clopidogrel was stopped and substituted with ticlopidine, and PA assessed at ticlopidine steady-state (T2). Resistance was defined as an absolute difference between T0 and post-treatment (T1 or T2) PA ≤ 10%. Results: Clopidogrel and ticlopidine responsiveness was normally distributed. Thirty (21%) and 28 (19%) patients were clopidogrel and ticlopidine non-responders, respectively. Five patients were non-responders both clopidogrel and ticlopidine, whereas 25 clopidogrel-resistant were ticlopidine-responder and 23 clopidogrel-responder were ticlopidine-resistant. Conclusions: Poor responsiveness to either clopidogrel or ticlopidine at steady-state is common, whereas non-responders to both drugs are infrequent (3%, 95%CI 1.5%-7.9%). Keywords: Clopidogrel; Ticlopidine doi:10.1016/j.yjmcc.2007.03.707

Determination of platelet aggregation in patients with stable coronary artery disease on long-term aspirin therapy Marek Postula, Agnieszka Serafin, Krzysztof Filipiak, Bozena Tarchalska. 1st Department of Cardiology; Department of Experimental and Clinical Pharmacology, Warsaw Medical University, Poland Background: We investigated whether use of low-dose aspirin for secondary prevention of cardiovascular events has