Association of Pulse Pressure With Clinical Outcomes in Patients Under Different Antiplatelet Strategies After Percutaneous Coronary Intervention: Analysis of GLOBAL LEADERS.


Journal

The Canadian journal of cardiology
ISSN: 1916-7075
Titre abrégé: Can J Cardiol
Pays: England
ID NLM: 8510280

Informations de publication

Date de publication:
05 2020
Historique:
received: 21 08 2019
revised: 08 10 2019
accepted: 14 10 2019
pubmed: 7 3 2020
medline: 16 2 2021
entrez: 7 3 2020
Statut: ppublish

Résumé

We evaluated the association of pulse pressure (PP) and different antiplatelet regimes with clinical and safety outcomes in an all-comers percutaneous coronary intervention (PCI) population. In this analysis of GLOBAL LEADERS (n = 15,936) we compared the experimental therapy of 23 months of ticagrelor after 1 month of dual-antiplatelet therapy (DAPT) vs standard DAPT for 12 months followed by aspirin monotherapy in subjects who underwent PCI and were divided into 2 groups according to the median PP (60 mm Hg). The primary end point (all-cause death or new Q-wave myocardial infarction) and the composite end points: patient-oriented composite end points (POCE), Bleeding Academic Research Consortium (BARC) 3 or 5, and net adverse clinical events (NACE) were evaluated. At 2 years, subjects in the high-PP group (n = 7971) had similar rates of the primary end point (4.3% vs 3.9%; P = 0.058), POCE (14.9% vs 12.7%; P = 0.051), and BARC 3 or 5 (2.5% vs 1.7%; P = 0.355) and higher rates of NACE (16.4% vs 13.7%; P = 0.037) compared with the low-PP group (n = 7965). Among patients with PP < 60 mm Hg, the primary end point (3.4% vs 4.4%, adjusted hazard ratio [aHR] 0.77, 95% confidence interval [CI] 0.61-0.96), POCE (11.8% vs 13.5%, aHR 0.86, 95% CI 0.76-0.98), NACE (12.8% vs 14.7%, aHR 0.85, 95% CI 0.76-0.96), and BARC 3 or 5 (1.4% vs 2.1%, aHR 0.69, 95% CI 0.49-0.97) were lower with ticagrelor monotherapy compared with DAPT. The only significant interaction was for BARC 3 or 5 (P = 0.008). After contemporary PCI, subjects with high PP levels experienced high rates of NACE at 2 years. In those with low PP, ticagrelor monotherapy led to a lower risk of bleeding events compared with standard DAPT.

Sections du résumé

BACKGROUND
We evaluated the association of pulse pressure (PP) and different antiplatelet regimes with clinical and safety outcomes in an all-comers percutaneous coronary intervention (PCI) population.
METHODS
In this analysis of GLOBAL LEADERS (n = 15,936) we compared the experimental therapy of 23 months of ticagrelor after 1 month of dual-antiplatelet therapy (DAPT) vs standard DAPT for 12 months followed by aspirin monotherapy in subjects who underwent PCI and were divided into 2 groups according to the median PP (60 mm Hg). The primary end point (all-cause death or new Q-wave myocardial infarction) and the composite end points: patient-oriented composite end points (POCE), Bleeding Academic Research Consortium (BARC) 3 or 5, and net adverse clinical events (NACE) were evaluated.
RESULTS
At 2 years, subjects in the high-PP group (n = 7971) had similar rates of the primary end point (4.3% vs 3.9%; P = 0.058), POCE (14.9% vs 12.7%; P = 0.051), and BARC 3 or 5 (2.5% vs 1.7%; P = 0.355) and higher rates of NACE (16.4% vs 13.7%; P = 0.037) compared with the low-PP group (n = 7965). Among patients with PP < 60 mm Hg, the primary end point (3.4% vs 4.4%, adjusted hazard ratio [aHR] 0.77, 95% confidence interval [CI] 0.61-0.96), POCE (11.8% vs 13.5%, aHR 0.86, 95% CI 0.76-0.98), NACE (12.8% vs 14.7%, aHR 0.85, 95% CI 0.76-0.96), and BARC 3 or 5 (1.4% vs 2.1%, aHR 0.69, 95% CI 0.49-0.97) were lower with ticagrelor monotherapy compared with DAPT. The only significant interaction was for BARC 3 or 5 (P = 0.008).
CONCLUSIONS
After contemporary PCI, subjects with high PP levels experienced high rates of NACE at 2 years. In those with low PP, ticagrelor monotherapy led to a lower risk of bleeding events compared with standard DAPT.

Identifiants

pubmed: 32139280
pii: S0828-282X(19)31350-9
doi: 10.1016/j.cjca.2019.10.015
pii:
doi:

Substances chimiques

Platelet Aggregation Inhibitors 0
Ticagrelor GLH0314RVC

Types de publication

Equivalence Trial Journal Article Multicenter Study Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

747-755

Commentaires et corrections

Type : CommentIn

Informations de copyright

Copyright © 2019 Canadian Cardiovascular Society. Published by Elsevier Inc. All rights reserved.

Auteurs

Ana Paula de Faria (AP)

School of Medical Sciences, University of Campinas, Campinas, Brazil.

Rodrigo Modolo (R)

Department of Cardiology, Amsterdam University Medical Centre, Amsterdam, The Netherlands; Cardiology Division. Department of Internal Medicine, University of Campinas, Campinas, Brazil.

Ply Chichareon (P)

Department of Cardiology, Amsterdam University Medical Centre, Amsterdam, The Netherlands; Division of Cardiology, Department of Internal Medicine, Faculty of Medicine, Prince of Songkla University, Songkhla, Thailand.

Chun-Chin Chang (CC)

Erasmus Medical Centre, Erasmus University, Rotterdam, The Netherlands.

Norihiro Kogame (N)

Department of Cardiology, Amsterdam University Medical Centre, Amsterdam, The Netherlands.

Mariusz Tomaniak (M)

Erasmus Medical Centre, Erasmus University, Rotterdam, The Netherlands; First Department of Cardiology, Medical University of Warsaw, Warsaw, Poland.

Kuniaki Takahashi (K)

Department of Cardiology, Amsterdam University Medical Centre, Amsterdam, The Netherlands.

Tessa Rademaker-Havinga (T)

Cardialysis Clinical Trials Management and Core Laboratories, Rotterdam, The Netherlands.

Joanna Wykrzykowska (J)

Department of Cardiology, Amsterdam University Medical Centre, Amsterdam, The Netherlands.

Rob J de Winter (RJ)

Department of Cardiology, Amsterdam University Medical Centre, Amsterdam, The Netherlands.

Rui C Ferreira (RC)

Serviço de Cardiologia, Hospital de Santa Marta, Centro Hospitalar Universitário Lisboa Central, Lisbon, Portugal.

Amanda Sousa (A)

Department of Interventional Cardiology, Instituto Dante Pazzanese de Cardiologia, São Paulo, Brazil.

Pedro A Lemos (PA)

Instituto do Coração, Hospital das Clínicas da Faculdade de Medicina, Universidade de São Paulo, São Paulo, Brazil.

Scot Garg (S)

East Lancashire Hospitals NHS Trust, Blackburn, Lancashire, United Kingdom.

Christian Hamm (C)

Kerckhoff Heart Center, Campus University of Giessen, Bad Nauheim, Germany.

Peter Juni (P)

Applied Health Research Centre, Li Ka Shing Knowledge Institute, St Michael's Hospital, University of Toronto, Toronto, Canada.

Pascal Vranckx (P)

Department of Cardiology and Critical Care Medicine, Hartcentrum Hasselt, Jessa Ziekenhuis, Hasselt, Belgium.

Marco Valgimigli (M)

Department of Cardiology, Bern University Hospital, Inselspital, University of Bern, Switzerland.

Stephan Windecker (S)

Department of Cardiology, Bern University Hospital, Inselspital, University of Bern, Switzerland.

Yoshinobu Onuma (Y)

Galway University Hospital, National University of Ireland, Galway, Ireland.

Philippe Gabriel Steg (PG)

French Alliance for Cardiovascular Trials, Hopital Bichat, Assistance Publique-Hopitaux de Paris, Universite Paris-Diderot, and Institut National de la Sante et de la Recherche Medicale U-1148, Paris, France; Royal Brompton Hospital, Imperial College, London, United Kingdom.

Patrick W Serruys (PW)

Galway University Hospital, National University of Ireland, Galway, Ireland. Electronic address: patrick.w.j.c.serruys@gmail.com.

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