J. L. Ferreiro (1), S. Homs (1), J. Berdejo (1), G. Roura (1), J. Gómez-Lara (1), R. Romaguera (1), L. Teruel (1), G. Sánchez-Elvira (1), A. L. Marcano (1), J. A. Gómez-Hospital (1), D. J. Angiolillo (2), Á. Cequier (1)
(1) Heart Diseases Institute, Bellvitge University Hospital – IDIBELL, University of Barcelona, L’Hospitalet de Llobregat, Barcelona, Spain; (2) University of Florida College of Medicine-Jacksonville, Jacksonville, Florida, USA
To date, there is limited data on levels of platelet inhibition achieved in patients with ST-elevation myocardial infarction (STEMI) who are loaded with clopidogrel and aspirin (ASA) prior to undergoing primary percutaneous coronary intervention (P-PCI). The aim of this investigation was to evaluate the percentage of STEMI patients with high on-treatment platelet reactivity (HPR) to clopidogrel at the time of initiating P-PCI and its association with the initial patency of the infarct-related artery (IRA). This prospective pharmacodynamic study included 50 STEMI patients, previously naïve to oral antiplatelet agents, who received 500-mg ASA and 600-mg clopidogrel loading doses prior to P-PCI. Platelet function assessment was performed at the beginning of the procedure using various assays, including VerifyNow™ system (primary endpoint), light transmission aggregometry and multiple electrode aggregometry. The percentage of patients with suboptimal response to clopidogrel and ASA assessed with the VerifyNow™ system was 88.0% and 28.6%, respectively. Similar results were obtained with the other assays used. A higher percentage of patients with initial patency of the IRA was observed among those patients without HPR compared with those with HPR to clopidogrel (66.7% vs 15.9%; p=0.013), while no differences were observed regarding postprocedural angiographic or electrocardiographic outcomes. In conclusion, this study shows that a high percentage of STEMI patients have inadequate levels of clopidogrel-induced and, to a lesser extent, aspirin-mediated platelet inhibition when starting a P-PCI procedure, and suggests that a poor response to clopidogrel might be associated with impaired initial TIMI flow in the IRA.
Antiplatelet therapy, ST-elevation myocardial infarction, Clopidogrel responsiveness
Francesca Cesari1, Rossella Marcucci1, Roberto Caporale2, Rita Paniccia1, Eloisa Romano1, Gian Franco Gensini3, Rosanna Abbate1, Anna Maria Gori1
Thromb Haemost 2008 99 5: 930-935
Haemodialysis impairs clopidogrel but not aspirin responsiveness in patients with end stage renal disease
Results of a pilot study
P. Htun (1), T. Kan (2), E. Mueller (2), C. Pohle (3), R. Schindler (4), T. Geisler (5), M. Gawaz (5), W. Bocksch (5), S. Fateh-Moghadam (5)
Thromb Haemost 2014 111 4: -
S. Kilic (1), J. P. Ottervanger (1), J.-H. E. Dambrink (1), J. C. A. Hoorntje (1), P. C. Koopmans (1), A. T. M. Gosselink (1), H. Suryapranata (1, 2), A. W. J. van ‘t Hof (1), on behalf of the Zwolle Myocardial Infarction Study Group
Thromb Haemost 2014 111 1: 165-171
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