Early determination of clopidogrel responsiveness by platelet reactivity indexidentifies patients at risk for cardiovascular events after myocardial infarction
Autor: | Anna Kobsar, Andreas Schäfer, Jürgen Kössler, Ulrike Flierl, Johann Bauersachs, Nora Seydelmann, Stefan Störk |
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Rok vydání: | 2011 |
Předmět: |
0301 basic medicine
Male medicine.medical_specialty Ticlopidine Platelet Function Tests Drug Resistance Myocardial Infarction 030204 cardiovascular system & hematology 03 medical and health sciences 0302 clinical medicine P2Y12 Predictive Value of Tests Reference Values Internal medicine Diabetes mellitus medicine Humans Platelet cardiovascular diseases Myocardial infarction Platelet activation Adverse effect Aged business.industry Hematology Middle Aged medicine.disease Clopidogrel Flow Cytometry Platelet Activation Prognosis Receptors Purinergic P2Y12 030104 developmental biology Endocrinology Early Diagnosis Treatment Outcome Cardiology Disease Progression Female business circulatory and respiratory physiology Lipoprotein medicine.drug |
Zdroj: | Thrombosis and haemostasis. 106(1) |
ISSN: | 2567-689X |
Popis: | SummaryWhile acute myocardial infarction (MI) is associated with impaired clopidogrel responsiveness, systematic evaluation is lacking due to the inability of functional aggregation-based assays to analyse clopidogrel responsiveness in the presence of glycoprotein IIb/IIIa inhibitors. Using the P2Y12-specific, non-aggregation-based platelet-reactivity-index (PRI) we assessed clopidogrel responsiveness in patients with acute MI. Clopidogrel responsiveness was determined 24 hours (h) after loading with 600 mg clopidogrel in 54 patients with acute MI admitted for coronary intervention. A PRI > 50% was considered as suboptimal inhibition. Overall response in MI patients was suboptimal with a median PRI of 58%. Diabetes, low high-density lipoprotein and pre-hospital clopidogrel loading were associated with impaired clopidogrel responsiveness. Patients loaded at first medical contact had a significantly weaker platelet inhibition by clopidogrel after 24 h (PRI 63%) compared to those loaded peri-interventionally (PRI 54%, p=0.014). Clinical outcome was assessed as a combination of cardiac death, non-fatal MI, stent thrombosis, ischaemic stroke, and urgent target vessel revascularisation after 12 months. The pre-selected cut-off of PRI ≤ 50% yielded a sensitivity of 87% at a specificity of 26%, whereas a PRI ≤ 57% determined by receiver-operating characteristics (ROC)-analysis yielded a sensitivity of 80% at a specificity of 56% (event rate: PRI ≤ 57%: 12.0%; PRI > 57%: 41.4%, p=0.0136). In conclusion, PRI detects clopidogrel responsiveness in acute MI patients requiring glycoprotein IIb/IIIa antagonism; and impaired clopidogrel responsiveness predisposes to clinical events. Pre-hospital clopidogrel loading was associated with impaired response and more adverse events challenging the concept of earliest oral clopidogrel loading in MI patients. |
Databáze: | OpenAIRE |
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