Gilles Montalescot1, Grégoire Rangé2, Johanne Silvain2, Jean-Louis Bonnet2, Ziad Boueri2, Olivier Barthélémy2, Guillaume Cayla2, Loic Belle2, Eric Van Belle2, Thomas Cuisset2, Simon Elhadad2, Christophe Pouillot2, Patrick Henry2, Pascal Motreff2, Didier Carrié2, Hélène Rousseau2, Pierre Aubry2, Jacques Monségu2, Pierre Sabouret2, Stephen A O'Connor2, Jérémie Abtan2, Mathieu Kerneis2, Christophe Saint-Etienne2, Farzin Beygui2, Eric Vicaut2, Jean-Philippe Collet2. 1. From the ACTION Study Group, Institut de Cardiologie (AP-HP), INSERM UMRS 1166, Université Paris 6, Paris, France (G.M., J.S., O.B., P.S., S.A.O., M.K., J.-P.C.); Hôpital Louis Pasteur, Le Coudray, France (G.R.); Hôpital de la Timone, Marseille, France (J.-L.B., T.C.); CH de Bastia, Bastia, France (Z.B.); CHU Carémeau, Nîmes, France (G.C.); CH de la Région Annecienne, Annecy, France (L.B.); Hôpital Cardiologique, Lille, France (E.V.B.); CH de Lagny, Marne-la-Vallée, France (S.E.); Clinique Sainte-Clothilde, La Réunion, France (C.P.); Hôpital Lariboisière, Paris, France (P.H.); CHU Clermont-Ferrand, Clermont-Ferrand, France (P.M.); Hôpital de Rangueil, Toulouse, France (D.C.); Unite de Recherche Clinique, Hôpital Lariboisière, ACTION Study Group, Paris, France (H.R., E.V.); Hôpital Bichat, Paris, France (P.A.); HIA du Val-du-Grâce, Paris, France (J.M.); Hôpital Bichat, ACTION Study Group, Paris, France (J.A.); Hôpital Trousseau, Chambray-lès-Tours, ACTION Study Group, Paris, France (C.S.-E.); and CHU Côte de Nacre, Caen, ACTION Study Group, Caen, France (F.B.). gilles.montalescot@psl.aphp.fr. 2. From the ACTION Study Group, Institut de Cardiologie (AP-HP), INSERM UMRS 1166, Université Paris 6, Paris, France (G.M., J.S., O.B., P.S., S.A.O., M.K., J.-P.C.); Hôpital Louis Pasteur, Le Coudray, France (G.R.); Hôpital de la Timone, Marseille, France (J.-L.B., T.C.); CH de Bastia, Bastia, France (Z.B.); CHU Carémeau, Nîmes, France (G.C.); CH de la Région Annecienne, Annecy, France (L.B.); Hôpital Cardiologique, Lille, France (E.V.B.); CH de Lagny, Marne-la-Vallée, France (S.E.); Clinique Sainte-Clothilde, La Réunion, France (C.P.); Hôpital Lariboisière, Paris, France (P.H.); CHU Clermont-Ferrand, Clermont-Ferrand, France (P.M.); Hôpital de Rangueil, Toulouse, France (D.C.); Unite de Recherche Clinique, Hôpital Lariboisière, ACTION Study Group, Paris, France (H.R., E.V.); Hôpital Bichat, Paris, France (P.A.); HIA du Val-du-Grâce, Paris, France (J.M.); Hôpital Bichat, ACTION Study Group, Paris, France (J.A.); Hôpital Trousseau, Chambray-lès-Tours, ACTION Study Group, Paris, France (C.S.-E.); and CHU Côte de Nacre, Caen, ACTION Study Group, Caen, France (F.B.).
Abstract
BACKGROUND: Individualizing antiplatelet therapy after platelet function testing did not improve outcome after coronary stenting in the Assessment by a Double Randomization of a Conventional Antiplatelet Strategy Versus a Monitoring-Guided Strategy for Drug-Eluting Stent Implantation and of Treatment Interruption Versus Continuation One Year After Stenting (ARCTIC) study. Whether results are different during the phase of secondary prevention starting after hospital discharge, when periprocedural events have been excluded, is unknown. METHODS AND RESULTS: In ARCTIC, 2440 patients were randomized beforecoronary stenting to a strategy of platelet function monitoring (VerifyNow P2Y12/aspirin point-of-care assay) with drug adjustment in suboptimal responders to antiplatelet therapy or to a conventional strategy without monitoring and without drug or dose changes. We performed a landmark analysis starting at the time of hospital discharge evaluating the primary end point of death, myocardial infarction, stent thrombosis, stroke, or urgent revascularization through 1 year. After discharge, the primary end point occurred in 8.6% of patients in the monitoring arm and 7.9% in the conventional arm (hazard ratio, 1.105; 95% confidence interval, 0.835-1.461; P=0.48). Stent thrombosis or urgent revascularization occurred in 4.4% and 4.5% in the monitoring and conventional arms, respectively (P=0.99). There was no difference for any of the other ischemic end points. Major bleeding event rates were 1.8% in the monitoring arm and 2.8% in the conventional arm (P=0.11), whereas major or minor bleeding event rates were 2.3% and 3.4%, respectively (P=0.10). CONCLUSIONS: Detection of platelet hyper-reactivity by platelet function testing in patients undergoing coronary stenting with further therapeutic adjustment does not reduce ischemic recurrences after intervention. On-treatment platelet hyperreactivity cannot be considered as a risk factor requiring intervention for secondary prevention after percutaneous coronary revascularization. CLINICAL TRIAL REGISTRATION URL: http://www.clinicaltrials.gov. Unique identifier: NCT00827411.
RCT Entities:
BACKGROUND: Individualizing antiplatelet therapy after platelet function testing did not improve outcome after coronary stenting in the Assessment by a Double Randomization of a Conventional Antiplatelet Strategy Versus a Monitoring-Guided Strategy for Drug-Eluting Stent Implantation and of Treatment Interruption Versus Continuation One Year After Stenting (ARCTIC) study. Whether results are different during the phase of secondary prevention starting after hospital discharge, when periprocedural events have been excluded, is unknown. METHODS AND RESULTS: In ARCTIC, 2440 patients were randomized before coronary stenting to a strategy of platelet function monitoring (VerifyNow P2Y12/aspirin point-of-care assay) with drug adjustment in suboptimal responders to antiplatelet therapy or to a conventional strategy without monitoring and without drug or dose changes. We performed a landmark analysis starting at the time of hospital discharge evaluating the primary end point of death, myocardial infarction, stent thrombosis, stroke, or urgent revascularization through 1 year. After discharge, the primary end point occurred in 8.6% of patients in the monitoring arm and 7.9% in the conventional arm (hazard ratio, 1.105; 95% confidence interval, 0.835-1.461; P=0.48). Stent thrombosis or urgent revascularization occurred in 4.4% and 4.5% in the monitoring and conventional arms, respectively (P=0.99). There was no difference for any of the other ischemic end points. Major bleeding event rates were 1.8% in the monitoring arm and 2.8% in the conventional arm (P=0.11), whereas major or minor bleeding event rates were 2.3% and 3.4%, respectively (P=0.10). CONCLUSIONS: Detection of platelet hyper-reactivity by platelet function testing in patients undergoing coronary stenting with further therapeutic adjustment does not reduce ischemic recurrences after intervention. On-treatment platelet hyperreactivity cannot be considered as a risk factor requiring intervention for secondary prevention after percutaneous coronary revascularization. CLINICAL TRIAL REGISTRATION URL: http://www.clinicaltrials.gov. Unique identifier: NCT00827411.
Authors: Thomas W Johnson; Andrew D Mumford; Lauren J Scott; Stuart Mundell; Mark Butler; Julian W Strange; Chris A Rogers; Barnaby C Reeves; Andreas Baumbach Journal: PLoS One Date: 2015-12-16 Impact factor: 3.240