David Erlinge1, Elmir Omerovic1, Ole Fröbert1, Rikard Linder1, Mikael Danielewicz1, Mehmet Hamid1, Eva Swahn1, Loghman Henareh1, Henrik Wagner1, Peter Hårdhammar1, Iwar Sjögren1, Jason Stewart1, Per Grimfjärd1, Jens Jensen1, Mikael Aasa1, Lotta Robertsson1, Pontus Lindroos1, Jan Haupt1, Helena Wikström1, Anders Ulvenstam1, Pallonji Bhiladvala1, Bo Lindvall1, Anders Lundin1, Tim Tödt1, Dan Ioanes1, Truls Råmunddal1, Thomas Kellerth1, Leszek Zagozdzon1, Matthias Götberg1, Jonas Andersson1, Oskar Angerås1, Ollie Östlund1, Bo Lagerqvist1, Claes Held1, Lars Wallentin1, Fredrik Scherstén1, Peter Eriksson1, Sasha Koul1, Stefan James1. 1. From the Department of Cardiology, Clinical Sciences, Lund University, Lund (D.E., P.B., A.L., T.T., M.G., F.S., S.K.), the Department of Cardiology, Sahlgrenska University Hospital, Gothenburg (E.O., D.I., T.R., O.A.), the Department of Cardiology, Faculty of Health, Örebro University, Örebro (O.F., T.K., L.Z.), the Department of Cardiology, Danderyd Hospital (R.L.), and the Department of Cardiology, Karolinska University Hospital (L.H.), Karolinska Institutet, the Department of Cardiology, Capio St. Görans Hospital (J.J., P.L.), and the Department of Cardiology, Södersjukhuset AB (M.A.), Stockholm, PCI-Unit at Karlstad Hospital, Karlstad (M.D.), the Department of Cardiology, Mälarsjukhuset, Eskilstuna (M.H.), the Department of Cardiology, Linköping University Hospital, Linköping (E.S.), the Department of Cardiology, Helsingborg Lasarett, Helsingborg (H. Wagner), the Department of Cardiology, Halmstad Hospital, Halmstad (P.H.), the Department of Cardiology, Falun Hospital, Falun (I.S.), the Department of Cardiology, Skaraborgs Hospital, Skövde (J.S.), the Department of Internal Medicine, Västmanlands Sjukhus, Västerås (P.G.), the Department of Cardiology, Södra Älvsborgs Sjukhus, Borås (L.R.), the Department of Cardiology, Sunderby Sjukhus, Luleå (J.H.), the Department of Cardiology, Kristianstad Hospital, Kristianstad (H. Wikström), the Department of Cardiology, Östersund Hospital, Östersund (A.U.), the Department of Cardiology, Sundsvall Hospital, Sundsvall (B. Lindvall), the Department of Cardiology, Umeå University, Umeå (J.A., P.E.), and the Department of Medical Sciences and Uppsala Clinical Research Center, Uppsala University, Uppsala (O.Ö., B. Lagerqvist, C.H., L.W., S.J.) - all in Sweden.
Abstract
BACKGROUND: The comparative efficacy of various anticoagulation strategies has not been clearly established in patients with acute myocardial infarction who are undergoingpercutaneous coronary intervention (PCI) according to current practice, which includes the use of radial-artery access for PCI and administration of potent P2Y12 inhibitors without the planned use of glycoprotein IIb/IIIa inhibitors. METHODS: In this multicenter, randomized, registry-based, open-label clinical trial, we enrolled patients with either ST-segment elevation myocardial infarction (STEMI) or non-STEMI (NSTEMI) who were undergoingPCI and receiving treatment with a potent P2Y12 inhibitor (ticagrelor, prasugrel, or cangrelor) without the planned use of glycoprotein IIb/IIIa inhibitors. The patients were randomly assigned to receive bivalirudin or heparin during PCI, which was performed predominantly with the use of radial-artery access. The primary end point was a composite of death from any cause, myocardial infarction, or major bleeding during 180 days of follow-up. RESULTS: A total of 6006 patients (3005 with STEMI and 3001 with NSTEMI) were enrolled in the trial. At 180 days, a primary end-point event had occurred in 12.3% of the patients (369 of 3004) in the bivalirudin group and in 12.8% (383 of 3002) in the heparin group (hazard ratio, 0.96; 95% confidence interval [CI], 0.83 to 1.10; P=0.54). The results were consistent between patients with STEMI and those with NSTEMI and across other major subgroups. Myocardial infarction occurred in 2.0% of the patients in the bivalirudin group and in 2.4% in the heparin group (hazard ratio, 0.84; 95% CI, 0.60 to 1.19; P=0.33), major bleeding in 8.6% and 8.6%, respectively (hazard ratio, 1.00; 95% CI, 0.84 to 1.19; P=0.98), definite stent thrombosis in 0.4% and 0.7%, respectively (hazard ratio, 0.54; 95% CI, 0.27 to 1.10; P=0.09), and death in 2.9% and 2.8%, respectively (hazard ratio, 1.05; 95% CI, 0.78 to 1.41; P=0.76). CONCLUSIONS: Among patients undergoing PCI for myocardial infarction, the rate of the composite of death from any cause, myocardial infarction, or major bleeding was not lower among those who received bivalirudin than among those who received heparin monotherapy. (Funded by the Swedish Heart-Lung Foundation and others; VALIDATE-SWEDEHEART ClinicalTrialsRegister.eu number, 2012-005260-10 ; ClinicalTrials.gov number, NCT02311231 .).
RCT Entities:
BACKGROUND: The comparative efficacy of various anticoagulation strategies has not been clearly established in patients with acute myocardial infarction who are undergoing percutaneous coronary intervention (PCI) according to current practice, which includes the use of radial-artery access for PCI and administration of potent P2Y12 inhibitors without the planned use of glycoprotein IIb/IIIa inhibitors. METHODS: In this multicenter, randomized, registry-based, open-label clinical trial, we enrolled patients with either ST-segment elevation myocardial infarction (STEMI) or non-STEMI (NSTEMI) who were undergoing PCI and receiving treatment with a potent P2Y12 inhibitor (ticagrelor, prasugrel, or cangrelor) without the planned use of glycoprotein IIb/IIIa inhibitors. The patients were randomly assigned to receive bivalirudin or heparin during PCI, which was performed predominantly with the use of radial-artery access. The primary end point was a composite of death from any cause, myocardial infarction, or major bleeding during 180 days of follow-up. RESULTS: A total of 6006 patients (3005 with STEMI and 3001 with NSTEMI) were enrolled in the trial. At 180 days, a primary end-point event had occurred in 12.3% of the patients (369 of 3004) in the bivalirudin group and in 12.8% (383 of 3002) in the heparin group (hazard ratio, 0.96; 95% confidence interval [CI], 0.83 to 1.10; P=0.54). The results were consistent between patients with STEMI and those with NSTEMI and across other major subgroups. Myocardial infarction occurred in 2.0% of the patients in the bivalirudin group and in 2.4% in the heparin group (hazard ratio, 0.84; 95% CI, 0.60 to 1.19; P=0.33), major bleeding in 8.6% and 8.6%, respectively (hazard ratio, 1.00; 95% CI, 0.84 to 1.19; P=0.98), definite stent thrombosis in 0.4% and 0.7%, respectively (hazard ratio, 0.54; 95% CI, 0.27 to 1.10; P=0.09), and death in 2.9% and 2.8%, respectively (hazard ratio, 1.05; 95% CI, 0.78 to 1.41; P=0.76). CONCLUSIONS: Among patients undergoing PCI for myocardial infarction, the rate of the composite of death from any cause, myocardial infarction, or major bleeding was not lower among those who received bivalirudin than among those who received heparin monotherapy. (Funded by the Swedish Heart-Lung Foundation and others; VALIDATE-SWEDEHEART ClinicalTrialsRegister.eu number, 2012-005260-10 ; ClinicalTrials.gov number, NCT02311231 .).
Authors: Łukasz Kołtowski; Jacek Legutko; Krzysztof J Filipiak; Artur Dziewierz; Stanisław Bartuś; Paweł Buszman; Piotr Buszman; Dariusz Ciećwierz; Maciej Dąbrowski; Sławomir Dobrzycki; Robert Gil; Jarosław Gorący; Marek Grygier; Miłosz Jaguszewski; Janusz Kochman; Jacek Kubica; Wiktor Kuliczkowki; Piotr Lodziński; Andrzej Ochała; Krzysztof Reczuch; Adam Witkowski; Wojciech Wojakowski; Jarosław Wójcik; Dariusz Dudek Journal: Cardiol J Date: 2019 Impact factor: 2.737
Authors: Behnood Bikdeli; Thomas McAndrew; Aaron Crowley; Shmuel Chen; Ghazaleh Mehdipoor; Björn Redfors; Yangbo Liu; Zixuan Zhang; Mengdan Liu; Yiran Zhang; Dominic P Francese; David Erlinge; Stefan K James; Yaling Han; Yi Li; Adnan Kastrati; Stefanie Schüpke; Rod H Stables; Adeel Shahzad; Philippe Gabriel Steg; Patrick Goldstein; Enrico Frigoli; Roxana Mehran; Marco Valgimigli; Gregg W Stone Journal: Thromb Haemost Date: 2019-12-09 Impact factor: 5.249