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European Heart Journal Advance Access originally published online on December 16, 2004
European Heart Journal 2005 26(6):567-575; doi:10.1093/eurheartj/ehi071
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© The European Society of Cardiology 2004. All rights reserved. For Permissions, please e-mail: journals.permissions{at}oupjournals.org

Does pre-treatment with aspirin and loading dose clopidogrel obviate the need for glycoprotein IIb/IIIa antagonists during elective coronary stenting? A focus on peri-procedural myonecrosis{dagger}

Marc J. Claeys1,*, Marc G. Van der Planken2, Johan M. Bosmans1, Jan J. Michiels2, Francine Vertessen2, Peter Van Der Goten1, Floris L. Wuyts3 and Chris J. Vrints1

1Department of Cardiology, Antwerp University Hospital, Wilrijkstraat 10, B-2650 Edegem, Belgium
2Laboratory of Haematology and Haemostatis, Antwerp University Hospital, Antwerp, Belgium
3Dept of Biomedical Physics and Biostatistics, Antwerp University Hospital, Antwerp, Belgium

Received 16 April 2004; revised 7 October 2004; accepted 4 November 2004; online publish-ahead-of-print 16 December 2004.

* Corresponding author. Tel:+32 3 821 30 00; fax: +32 3 825 08 48. E-mail address: marc.claeys{at}ua.ac.be

Aims Although full platelet inhibition with aspirin and thienopyridines before coronary stenting has significantly reduced the risk of acute stent thrombosis, peri-procedural myonecrosis still occurs frequently and is associated with increased death rate. Whether further inhibition of platelet aggregation by a glycoprotein IIb/IIIa antagonist may provide an additional cardioprotection is unknown.

Methods and results A total of 200 patients pre-treated with aspirin and a loading dose of clopidogrel (450 mg) were randomized just before coronary intervention (percutaneous coronary intervention, PCI) to treatment with or without abciximab. Platelet aggregation was assessed in samples collected during the procedure and the degree of platelet aggregation inhibition was correlated with cardiac enzyme release post-PCI. Abciximab treatment achieved a more complete inhibition of aggregation than dual oral antiplatelet therapy alone (median value of 1 vs. 50%, normal 100%). Any pathological increase in creatinine kinase-MB (CK-MB) post-PCI was present in 21% of the abciximab group and in 22% of the no-abciximab group (P=0.9). Also the occurrence of clinically relevant myonecrosis [myocardial infarction (MI)=CK-MB >3x upper limit of normal] was not significantly influenced by treatment assignment: 9 vs. 10% (P=0.9). In a multiple logistic regression model including clinical, angiographic, and procedural characteristics, post-PCI myonecrosis was not correlated with the degree of platelet aggregation inhibition but with procedural features (such as long inflation time) and with the presence of multi-vessel disease. There were no cases of acute or subacute stent thrombosis. At 6 months, major adverse cardiac events, including cardiac death, non-fatal MI, or target lesion revascularization occurred in 13% of abciximab patients and in 16% of the control patients (P=0.6).

Conclusions In the studied patients scheduled for elective coronary stenting and pre-treated with aspirin and a loading dose of clopidogrel, further inhibition of platelet aggregation by abciximab does not afford additional cardioprotection. Our data suggest that distal athero-embolization rather than thrombo-embolization is involved in the phenomenon of myonecrosis post-elective stenting.

Key Words: Stents • Platelets • Glycoprotein • Creatinine kinase


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