Martin Orban1, Katharina Mayer2, Tanja Morath3, Isabell Bernlochner3, Martin Hadamitzky4, Siegmund Braun4, Stefanie Schulz5, Petra Hoppmann3, Jörg Hausleiter6, Klaus Tiroch7, Julinda Mehilli8, Heribert Schunkert5, Steffen Massberg8, Karl-Ludwig Laugwitz9, Dirk Sibbing8, Adnan Kastrati5. 1. Department of Cardiology, Ludwig-Maximilians-Universität, Munich, Germany. Electronic address: MartinOrban@gmail.com. 2. Deutsches Herzzentrum München, Technische Universität München, Munich, Germany. Electronic address: katharina.mayer.mt@gmx.de. 3. I. Medizinische Klinik, Klinikum rechts der Isar, Technische Universität München, Munich, Germany. 4. Deutsches Herzzentrum München, Technische Universität München, Munich, Germany. 5. Deutsches Herzzentrum München, Technische Universität München, Munich, Germany; DZHK (German Center for Cardiovascular Research), partner site Munich Heart Alliance, Munich, Germany. 6. Department of Cardiology, Ludwig-Maximilians-Universität, Munich, Germany. 7. Herzzentrum Wuppertal, Helios Klinikum Wuppertal, Germany. 8. Department of Cardiology, Ludwig-Maximilians-Universität, Munich, Germany; DZHK (German Center for Cardiovascular Research), partner site Munich Heart Alliance, Munich, Germany. 9. I. Medizinische Klinik, Klinikum rechts der Isar, Technische Universität München, Munich, Germany; DZHK (German Center for Cardiovascular Research), partner site Munich Heart Alliance, Munich, Germany.
Abstract
INTRODUCTION: Mild therapeutic hypothermia (TH) is standard of care after cardiac arrest of any cause. However, its impact on on-treatment platelet reactivity and clinical outcome in patients with acute myocardial infarction (AMI) complicated by cardiogenic shock and undergoing PCI with P2Y12 receptor inhibitor treatment is less clear. METHODS AND RESULTS: For the ISAR-SHOCK registry, 145 patients with AMI, cardiogenic shock and primary PCI in two centers (Deutsches Herzzentrum München and Klinikum rechts der Isar, Technical University Munich) between January 2009-May 2012 were analysed. Of these, 64 (44%) patients received TH treatment. The median [IQR] ADP-induced platelet aggregation following thienopyridine loading dose administration (clopidogrel in 95 and prasugrel in 50 patients) did not differ between the two groups (419 [283-684] for TH vs. 355 [207-710] AU x min for non-TH patients, P=0.22). After 30days follow-up, no significant differences were observed between both groups for mortality (42 vs. 44 %, HR: 0.93, 95% CI [0.56-1.53], p=0.77), MI (6 vs. 6%, HR: 0.99 95% CI [0.27-3.7], p=0.99) and TIMI minor bleedings (17 vs. 17%, HR 0.99 95% CI [0.45-2.18], p=0.98). TIMI major bleedings were numerically higher in the TH vs. non-TH cohort (25 % vs. 12 %, HR: 2.1 95% CI [0.95-4.63], p=0.07). Three definite stent thrombosis (ST) were observed in this registry and all STs occurred in the TH group of patients (p=0.09). CONCLUSION: Results of this registry suggest that TH does not negatively impact on platelet reactivity in shock patients receiving either clopidogrel or prasugrel. The numerically higher rate of major bleedings and the clustering of STs in the TH cohort warrant further investigation.
INTRODUCTION: Mild therapeutic hypothermia (TH) is standard of care after cardiac arrest of any cause. However, its impact on on-treatment platelet reactivity and clinical outcome in patients with acute myocardial infarction (AMI) complicated by cardiogenic shock and undergoing PCI with P2Y12 receptor inhibitor treatment is less clear. METHODS AND RESULTS: For the ISAR-SHOCK registry, 145 patients with AMI, cardiogenic shock and primary PCI in two centers (Deutsches Herzzentrum München and Klinikum rechts der Isar, Technical University Munich) between January 2009-May 2012 were analysed. Of these, 64 (44%) patients received TH treatment. The median [IQR] ADP-induced platelet aggregation following thienopyridine loading dose administration (clopidogrel in 95 and prasugrel in 50 patients) did not differ between the two groups (419 [283-684] for TH vs. 355 [207-710] AU x min for non-TH patients, P=0.22). After 30days follow-up, no significant differences were observed between both groups for mortality (42 vs. 44 %, HR: 0.93, 95% CI [0.56-1.53], p=0.77), MI (6 vs. 6%, HR: 0.99 95% CI [0.27-3.7], p=0.99) and TIMI minor bleedings (17 vs. 17%, HR 0.99 95% CI [0.45-2.18], p=0.98). TIMI major bleedings were numerically higher in the TH vs. non-TH cohort (25 % vs. 12 %, HR: 2.1 95% CI [0.95-4.63], p=0.07). Three definite stent thrombosis (ST) were observed in this registry and all STs occurred in the TH group of patients (p=0.09). CONCLUSION: Results of this registry suggest that TH does not negatively impact on platelet reactivity in shockpatients receiving either clopidogrel or prasugrel. The numerically higher rate of major bleedings and the clustering of STs in the TH cohort warrant further investigation.
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