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ANTIPLATELET ACTION OF CLOPIDOGREL AND PRASUGREL IN PATIENTS WITH ACUTE MYOCARDIAL INFARCTION COMPLICATED BY CARDIOGENIC SHOCK
E24 JACC March 12, 2013 Volume 61, Issue 10
Acute Coronary Syndromes Antiplatelet Action of Clopidogrel and Prasugrel in Patients with Acute Myocardial Infarction Complicated by Cardiogenic Shock Poster Contributions Poster Sessions, Expo North Saturday, March 09, 2013, 10:00 a.m.-10:45 a.m.
Session Title: MI Complications: Shock, Arrest and Cardiac Rupture Abstract Category: 1. Acute Coronary Syndromes: Clinical Presentation Number: 1126-194 Authors: Martin Orban, Isabell Bernlochner, Mathias Orban, Katharina Mayer, Martin Hadamitzky, Siegmund Braun, Joerg Hausleiter, Karl-Ludwig Laugwitz, Klaus Tiroch, Steffen Massberg, Julinda Mehilli, Dirk Sibbing, Adnan Kastrati, Department of Medicine I, Klinikum Großhadern, University of Munich, Munich, Germany, Deutsches Herzzentrum München & 1. Medizinische Klinik, Technische Universität, Munich, Germany Background: According to current guidelines clopidogrel is still the oral antiplatelet drug of choice in the setting of acute myocardial infarction complicated by cardiogenic shock. Systematic analysis on the antiplatelet action of clopidogrel in patients (pts) suffering from myocardial infarction complicated by cardiogenic shock are limited. Furthermore it is not clear if prasugrel achieves sufficient platelet inhibition compared to clopidogrel in this setting. Methods: Between January 2009 and May 2012, platelet reactivity was analysed using multiple electrode aggregometry on a Multiplate analyzer in a registry of 137 pts with cardiogenic shock and urgent percutaneous coronary intervention (PCI). Initially, all pts received a clopidogrel loading dose before PCI (600 mg in 132 pts, 450 mg in 1 pt and 300 mg in 4 pts). A part of the study cohort was switched to prasugrel according to platelet function results. Results: 42% of all 137 pts showed high on-treatment platelet reactivity (HPR) after the administration of the first clopidogrel loading dose according to consensus definitions (≥468 AU x min). 39 pts with HPR after administration of repeated (up to three) clopidogrel loading doses were switched over to prasugrel. Compared to clopidogrel, prasugrel showed a significant reduction of platelet aggregation values (median [IQR] of 597 AU x min [489 to 799] vs. 251 [148-337], p<0.0001). Even after the first prasugrel loading dose, a status of HPR was found in 15% of the pts. Conclusion: In pts suffering from a cardiogenic shock HPR on clopidogrel was detected in 42% of the pts. Prasugrel loading dose abolished this status in the majority of pts. However, even prasugrel resistance was detected in 15%. The clinicial outcome of cardiogenic shock pts with regard to antiplatelet drug responsiveness will be presented at the congress.
Acute Coronary Syndromes Antiplatelet Action of Clopidogrel and Prasugrel in Patients with Acute Myocardial Infarction Complicated by Cardiogenic Shock Poster Contributions Poster Sessions, Expo North Saturday, March 09, 2013, 10:00 a.m.-10:45 a.m.
Session Title: MI Complications: Shock, Arrest and Cardiac Rupture Abstract Category: 1. Acute Coronary Syndromes: Clinical Presentation Number: 1126-194 Authors: Martin Orban, Isabell Bernlochner, Mathias Orban, Katharina Mayer, Martin Hadamitzky, Siegmund Braun, Joerg Hausleiter, Karl-Ludwig Laugwitz, Klaus Tiroch, Steffen Massberg, Julinda Mehilli, Dirk Sibbing, Adnan Kastrati, Department of Medicine I, Klinikum Großhadern, University of Munich, Munich, Germany, Deutsches Herzzentrum München & 1. Medizinische Klinik, Technische Universität, Munich, Germany Background: According to current guidelines clopidogrel is still the oral antiplatelet drug of choice in the setting of acute myocardial infarction complicated by cardiogenic shock. Systematic analysis on the antiplatelet action of clopidogrel in patients (pts) suffering from myocardial infarction complicated by cardiogenic shock are limited. Furthermore it is not clear if prasugrel achieves sufficient platelet inhibition compared to clopidogrel in this setting. Methods: Between January 2009 and May 2012, platelet reactivity was analysed using multiple electrode aggregometry on a Multiplate analyzer in a registry of 137 pts with cardiogenic shock and urgent percutaneous coronary intervention (PCI). Initially, all pts received a clopidogrel loading dose before PCI (600 mg in 132 pts, 450 mg in 1 pt and 300 mg in 4 pts). A part of the study cohort was switched to prasugrel according to platelet function results. Results: 42% of all 137 pts showed high on-treatment platelet reactivity (HPR) after the administration of the first clopidogrel loading dose according to consensus definitions (≥468 AU x min). 39 pts with HPR after administration of repeated (up to three) clopidogrel loading doses were switched over to prasugrel. Compared to clopidogrel, prasugrel showed a significant reduction of platelet aggregation values (median [IQR] of 597 AU x min [489 to 799] vs. 251 [148-337], p<0.0001). Even after the first prasugrel loading dose, a status of HPR was found in 15% of the pts. Conclusion: In pts suffering from a cardiogenic shock HPR on clopidogrel was detected in 42% of the pts. Prasugrel loading dose abolished this status in the majority of pts. However, even prasugrel resistance was detected in 15%. The clinicial outcome of cardiogenic shock pts with regard to antiplatelet drug responsiveness will be presented at the congress.