Gilles Montalescot1, Arnoud W van 't Hof2, Leonardo Bolognese3, Warren J Cantor4, Angel Cequier5, Mohamed Chettibi6, Jean-Philippe Collet7, Shaun G Goodman8, Christopher J Hammett9, Kurt Huber10, Magnus Janzon11, Frédéric Lapostolle12, Jens Flensted Lassen13, Muriel Licour14, Béla Merkely15, Néjoua Salhi16, Johanne Silvain7, Robert F Storey17, Jurriën M Ten Berg18, Anne Tsatsaris14, Uwe Zeymer19, Eric Vicaut20, Christian W Hamm21. 1. Université Paris 6, ACTION Study Group, Institut de Cardiologie (AP-HP), Centre Hospitalier Universitaire Pitié-Salpêtrière, INSERM UMRS 1166, Paris, France. Electronic address: gilles.montalescot@psl.aphp.fr. 2. Department of Cardiology, Isala Clinics, Zwolle, the Netherlands. 3. Cardiovascular and Neurological Department, Azienda Ospedaliera Arezzo, Arezzo, Italy. 4. Southlake Regional Health Centre, University of Toronto, Newmarket, Ontario, Canada. 5. Heart Disease Institute, Hospital Universitario de Bellvitge, University of Barcelona, L'Hospitalet de Llobregat, Barcelona, Spain. 6. Centre Hospito-universitaire Frantz Fanon, Blida, Algeria. 7. Université Paris 6, ACTION Study Group, Institut de Cardiologie (AP-HP), Centre Hospitalier Universitaire Pitié-Salpêtrière, INSERM UMRS 1166, Paris, France. 8. Canadian Heart Research Centre, Division of Cardiology, St. Michael's Hospital, University of Toronto, Toronto, Canada. 9. Department of Cardiology, Royal Brisbane and Women's Hospital, Brisbane, Queensland, Australia. 10. 3rd Department of Medicine, Cardiology and Intensive Care Medicine, Wilhelminenhospital, Vienna, Austria. 11. Department of Cardiology and Department of Medical and Health Sciences, Linköping University, Linköping, Sweden. 12. SAMU 93 Hôpital Avicenne, Bobigny, France. 13. Department of Cardiology B, Aarhus University Hospital, Aarhus N, Denmark. 14. AstraZeneca, Rueil Malmaison, France. 15. Heart and Vascular Center, Semmelweis University, Budapest, Hungary. 16. AstraZeneca, Luton, UK. 17. Department of Cardiovascular Science, University of Sheffield, Sheffield, United Kingdom. 18. Department of Cardiology, St. Antonius Hospital Nieuwegein, Nieuwegein, the Netherlands. 19. Klinikum Ludwigshafen and Institut für Herzinfarktforschung Ludwigshafen, Ludwigshafen, Germany. 20. Unite de Recherche Clinique, Université Paris 7, Hôpital Lariboisière, ACTION Study Group, Paris, France. 21. Department of Cardiology, Kerckhoff Heart Center, Bad Nauheim, Germany.
Abstract
OBJECTIVES: The aim of this landmark exploratory analysis, ATLANTIC-H(24), was to evaluate the effects of pre-hospital ticagrelor during the first 24 h after primary percutaneous coronary intervention (PCI) in the ATLANTIC (Administration of Ticagrelor in the cath Lab or in the Ambulance for New ST elevation myocardial infarction to open the Coronary artery) study. BACKGROUND: The ATLANTIC trial in patients with ongoing ST-segment elevation myocardial infarction showed that pre-hospital ticagrelor was safe but did not improve pre-PCI coronary reperfusion compared with in-hospital ticagrelor. We hypothesized that the effect of pre-hospital ticagrelor may not have manifested until after PCI due to the rapid transfer time (31 min). METHODS: The ATLANTIC-H(24) analysis included 1,629 patients who underwent PCI, evaluating platelet reactivity, Thrombolysis In Myocardial Infarction flow grade 3, ≥ 70% ST-segment elevation resolution, and clinical endpoints over the first 24 h. RESULTS: Following PCI, largest between-group differences in platelet reactivity occurred at 1 to 6 h; coronary reperfusion rates numerically favored pre-hospital ticagrelor, and the degree of ST-segment elevation resolution was significantly greater in the pre-hospital group (median, 75.0% vs. 71.4%; p = 0.049). At 24 h, the composite ischemic endpoint was lower with pre-hospital ticagrelor (10.4% vs. 13.7%; p = 0.039), as were individual endpoints of definite stent thrombosis (p = 0.0078) and myocardial infarction (p = 0.031). All endpoints except death (1.1% vs. 0.2%; p = 0.048) favored pre-hospital ticagrelor, with no differences in bleeding events. CONCLUSIONS: The effects of pre-hospital ticagrelor became apparent after PCI, with numerical differences in platelet reactivity and immediate post-PCI reperfusion, associated with reductions in ischemic endpoints, over the first 24 h, whereas there was a small excess of mortality. (Administration of Ticagrelor in the cath Lab or in the Ambulance for New ST elevation myocardial infarction to open the Coronary artery [ATLANTIC, NCT01347580]).
RCT Entities:
OBJECTIVES: The aim of this landmark exploratory analysis, ATLANTIC-H(24), was to evaluate the effects of pre-hospital ticagrelor during the first 24 h after primary percutaneous coronary intervention (PCI) in the ATLANTIC (Administration of Ticagrelor in the cath Lab or in the Ambulance for New ST elevation myocardial infarction to open the Coronary artery) study. BACKGROUND: The ATLANTIC trial in patients with ongoing ST-segment elevation myocardial infarction showed that pre-hospital ticagrelor was safe but did not improve pre-PCI coronary reperfusion compared with in-hospital ticagrelor. We hypothesized that the effect of pre-hospital ticagrelor may not have manifested until after PCI due to the rapid transfer time (31 min). METHODS: The ATLANTIC-H(24) analysis included 1,629 patients who underwent PCI, evaluating platelet reactivity, Thrombolysis In Myocardial Infarction flow grade 3, ≥ 70% ST-segment elevation resolution, and clinical endpoints over the first 24 h. RESULTS: Following PCI, largest between-group differences in platelet reactivity occurred at 1 to 6 h; coronary reperfusion rates numerically favored pre-hospital ticagrelor, and the degree of ST-segment elevation resolution was significantly greater in the pre-hospital group (median, 75.0% vs. 71.4%; p = 0.049). At 24 h, the composite ischemic endpoint was lower with pre-hospital ticagrelor (10.4% vs. 13.7%; p = 0.039), as were individual endpoints of definite stent thrombosis (p = 0.0078) and myocardial infarction (p = 0.031). All endpoints except death (1.1% vs. 0.2%; p = 0.048) favored pre-hospital ticagrelor, with no differences in bleeding events. CONCLUSIONS: The effects of pre-hospital ticagrelor became apparent after PCI, with numerical differences in platelet reactivity and immediate post-PCI reperfusion, associated with reductions in ischemic endpoints, over the first 24 h, whereas there was a small excess of mortality. (Administration of Ticagrelor in the cath Lab or in the Ambulance for New ST elevation myocardial infarction to open the Coronary artery [ATLANTIC, NCT01347580]).
Authors: Enrico Fabris; Serge Korjian; Barry S Coller; Jurrien M Ten Berg; Christopher B Granger; C Michael Gibson; Arnoud W J van 't Hof Journal: Thromb Haemost Date: 2021-04-30 Impact factor: 6.681