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European Heart Journal 2004 25(6):476-483; doi:10.1016/j.ehj.2003.12.016
Copyright © 2004 by the European Society of Cardiology.
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Clinical research

Limited early antiplatelet effect of 300 mg clopidogrel in patients with aspirin therapy undergoing percutaneous coronary interventions

Aino Lepäntaloa, Kari S Virtanenb, Juhani Heikkiläb, Ulla Wartiovaarac and Riitta Lassilaa,d,*

a Wihuri Research Institute, Kalliolinnantie 4, Fin-00140 Helsinki, Finland
b Division of Cardiology, Department of Internal Medicine, Helsinki University Central Hospital, PO Box 340, Fin-00029 HUCH, Helsinki, Finland
c Laboratory Department, Helsinki University Central Hospital, PO Box 340, Fin-00029 HUCH, Helsinki, Finland
d Division of Haematology, Department of Internal Medicine, Helsinki University Central Hospital, PO Box 340, Huch, Helsinki, Finland

* Corresponding author. Tel.: +358-(9)-681411; fax: +358-(9)-637476
E-mail address: riitta.lassila{at}hus.fi

See page 454 for the editorial comment on this article1

Aim Our aim was to evaluate the early efficacy and variability of the platelet inhibition exerted by 300 mg clopidogrel for the purpose of acute percutaneous coronary interventions using platelet function tests.

Methods and results Elective percutaneous coronary intervention was used as a timely model in which clopidogrel was added to ongoing acetylsalicylic acid (aspirin) (100 mg/day) at 2.5 h prior to procedure. Blood samples were collected before administration of clopidogrel and immediately before the intervention from 50 patients. Platelet functions were assessed with traditional aggregation and PFA-100®.

At baseline, 14 (28%) patients were poor responders to aspirin according to PFA and 9 (18%) continued to show arachidonic acid-induced aggregation. After clopidogrel ADP-triggered aggregation was only modestly inhibited in 40% of the patients. Eight percent of the study population was left without any measurable antiplatelet effect. The patients with modest response to clopidogrel had higher levels of c-peptide (1.5 nmol/L) than the ones responding well (0.9 nmol/L, ).

Conclusion Neither ongoing aspirin treatment nor added clopidogrel did reach an expected extent of platelet inhibition. This study shows that aspirin-treated patients undergoing PCI gain highly variable levels of platelet inhibition with short-term clopidogrel 300 mg. At 2 h after adding clopidogrel it failed to enhance platelet inhibition in 40% of the patients. In future, targeted platelet function tests may be helpful to individually select an effective antiplatelet medication for these patients. This study suggests that for acute PTCA clopidogrel does not reach the optimal antithrombotic efficacy in all patients.

Key Words: Angioplasty • Aspirin • Clopidogrel • Platelet • Thrombosis


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