Thromb Haemost 2007; 97(02): 282-287
DOI: 10.1160/TH06-07-0362
Cardiovascular Biology and Cell Signalling
Schattauer GmbH

High post-treatment platelet reactivity is associated with a high incidence of myonecrosis after stenting for non-ST elevation acute coronary syndromes

Thomas Cuisset
1   Department of Cardiology, CHU Timone, Marseille, France
,
Corinne Frere
2   INSERM, UMR 626, Faculté de Médecine CHU Timone, Marseille, France
,
Jacques Quilici
1   Department of Cardiology, CHU Timone, Marseille, France
,
Pierre-Emmanuel Morange
2   INSERM, UMR 626, Faculté de Médecine CHU Timone, Marseille, France
,
Lyassine Nait-Saidi
1   Department of Cardiology, CHU Timone, Marseille, France
,
Christopher Mielot
1   Department of Cardiology, CHU Timone, Marseille, France
,
Laurent Bali
1   Department of Cardiology, CHU Timone, Marseille, France
,
Marc Lambert
1   Department of Cardiology, CHU Timone, Marseille, France
,
Marie-Christine Alessi
2   INSERM, UMR 626, Faculté de Médecine CHU Timone, Marseille, France
,
Jean-Louis Bonnet
1   Department of Cardiology, CHU Timone, Marseille, France
› Author Affiliations
Further Information

Publication History

Received 03 July 2006

Accepted after resubmission 10 January 2006

Publication Date:
25 November 2017 (online)

Summary

High post-treatment platelet reactivity (HPPR= adenosine diphosphate [ADP] 10 µM-induced platelet aggregation > 70%) identifies low responders to dual antiplatelet therapy with increased risk of recurrent cardiovascular (CV) events after stenting for non-ST elevation acute coronary syndromes (NSTEACS). This study was designed to compare the incidence of periprocedural myocardial infarction (MI) after stenting for NSTEACS patients between non-responders to dual antiplatelet therapy defined by HPPR and normo-responders. One hundred ninety NSTE-ACS consecutive patients undergoing coronary stenting were included in this prospective study. They received 250 mg aspirin and a 600 mg loading dose of clopidogrel at least 12 hours (h) before percutaneous coronary intervention (PCI). A single post-treatment blood sample was obtained before PCI to analyze maximal intensity of ADP-induced platelet aggregation, and troponin levels were analyzed before PCI, and 12 and 24 h after PCI. Troponin I was considered elevated if > 0.4 ng/ ml. HPPR was present in 22% of patients (n=42). Periprocedural MI occurred significantly more frequently in patients with HPPR than in the normo-responders (43% vs. 24%, p=0.014). After being correlated with recurrent ischemic events after stenting for NSTE-ACS, the HPPR seems to be also a marker of increased risk of periprocedural MI for NSTE-ACS patients.

 
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