Plasma protein signatures for high on-treatment platelet reactivity to aspirin and clopidogrel in peripheral artery disease.

Antiplatelet therapy Atherosclerosis Atherothrombosis High on-treatment platelet reactivity Peripheral artery disease Proteomics

Journal

Thrombosis research
ISSN: 1879-2472
Titre abrégé: Thromb Res
Pays: United States
ID NLM: 0326377

Informations de publication

Date de publication:
Oct 2023
Historique:
received: 19 05 2023
revised: 31 07 2023
accepted: 31 08 2023
pubmed: 15 9 2023
medline: 15 9 2023
entrez: 14 9 2023
Statut: ppublish

Résumé

A significant proportion of patients with peripheral artery disease (PAD) displays a poor response to aspirin and/or the platelet P2Y This study aimed to elucidate specific plasma protein signatures associated with HTPR to aspirin and clopidogrel in PAD patients. Based on targeted plasma proteomics, 184 proteins from two cardiovascular Olink panels were measured in 105 PAD patients. VerifyNow ASPI- and P2Y A plasma protein signature, including eight targets involved in proatherogenic dysfunction of blood cell-vasculature interaction, coagulation and cell death, is associated with HTPR (aspirin and/or clopidogrel) in PAD. This may serve as important systems-based determinants of poor platelet responsiveness to aspirin and/or clopidogrel in PAD and other cardiovascular diseases and may contribute to identify novel treatment strategies.

Sections du résumé

BACKGROUND BACKGROUND
A significant proportion of patients with peripheral artery disease (PAD) displays a poor response to aspirin and/or the platelet P2Y
OBJECTIVE OBJECTIVE
This study aimed to elucidate specific plasma protein signatures associated with HTPR to aspirin and clopidogrel in PAD patients.
METHODS AND RESULTS RESULTS
Based on targeted plasma proteomics, 184 proteins from two cardiovascular Olink panels were measured in 105 PAD patients. VerifyNow ASPI- and P2Y
CONCLUSIONS CONCLUSIONS
A plasma protein signature, including eight targets involved in proatherogenic dysfunction of blood cell-vasculature interaction, coagulation and cell death, is associated with HTPR (aspirin and/or clopidogrel) in PAD. This may serve as important systems-based determinants of poor platelet responsiveness to aspirin and/or clopidogrel in PAD and other cardiovascular diseases and may contribute to identify novel treatment strategies.

Identifiants

pubmed: 37708596
pii: S0049-3848(23)00252-9
doi: 10.1016/j.thromres.2023.08.017
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

105-118

Informations de copyright

Copyright © 2023. Published by Elsevier Ltd.

Déclaration de conflit d'intérêts

Declaration of competing interest SH is an employee of Bayer AG. The study was sponsored inter alia by Bayer AG. The sponsors had no role in the design or conduct of the research. HtC received research funding outside the present study from Bayer and received outside the present study honoraria for consultation and/or advisory board participation, from Bayer, Alveron, Galapagos, Portola and Alexion. All reimbursements were transferred to the CARIM institute. HtC and HMHS are shareholders with Coagulation Profile, a university spinoff small diagnostic company not involved in the present study. PSW has received research funding outside the present study from Boehringer Ingelheim, Sanofi-Aventis, Bayer Healthcare, Daiichi Sankyo Europe and Novartis and received outside the present study honoraria for lectures or consulting from Boehringer Ingelheim, Bayer HealthCare, Evonik, AstraZeneca and Sanofi-Aventis. PSW is principal investigator of the DIASyM research core (BMBF 161L0217A). All other authors declare no conflict of interest.

Auteurs

G Baidildinova (G)

Departments of Biochemistry and Internal Medicine, Cardiovascular Research Institute Maastricht (CARIM), Maastricht University, Maastricht, Netherlands; Center for Thrombosis and Hemostasis (CTH), University Medical Center of the Johannes Gutenberg-University Mainz, Mainz, Germany.

A Pallares Robles (A)

Departments of Biochemistry and Internal Medicine, Cardiovascular Research Institute Maastricht (CARIM), Maastricht University, Maastricht, Netherlands; Center for Thrombosis and Hemostasis (CTH), University Medical Center of the Johannes Gutenberg-University Mainz, Mainz, Germany.

V Ten Cate (V)

Center for Thrombosis and Hemostasis (CTH), University Medical Center of the Johannes Gutenberg-University Mainz, Mainz, Germany; Preventive Cardiology and Preventive Medicine, Department of Cardiology, University Medical Center of the Johannes Gutenberg-University Mainz, Mainz, Germany; German Center for Cardiovascular Research (DZHK), Partner Site Rhine-Main, Mainz, Germany.

B M M Kremers (BMM)

Laboratory for Clinical Thrombosis and Hemostasis, Department of Biochemistry, Cardiovascular Research, Maastricht University, Netherlands.

S Heitmeier (S)

Division Pharmaceuticals, Bayer AG, Wuppertal, Germany.

H Ten Cate (H)

Departments of Biochemistry and Internal Medicine, Cardiovascular Research Institute Maastricht (CARIM), Maastricht University, Maastricht, Netherlands; Center for Thrombosis and Hemostasis (CTH), University Medical Center of the Johannes Gutenberg-University Mainz, Mainz, Germany; Thrombosis Expertise Center, Heart and Vascular Center, Maastricht University Medical Center, Maastricht, Netherlands.

B M E Mees (BME)

Department of Vascular Surgery, Maastricht University Medical Center, Maastricht, Netherlands.

H M H Spronk (HMH)

Departments of Biochemistry and Internal Medicine, Cardiovascular Research Institute Maastricht (CARIM), Maastricht University, Maastricht, Netherlands; Thrombosis Expertise Center, Heart and Vascular Center, Maastricht University Medical Center, Maastricht, Netherlands.

P S Wild (PS)

Center for Thrombosis and Hemostasis (CTH), University Medical Center of the Johannes Gutenberg-University Mainz, Mainz, Germany; Preventive Cardiology and Preventive Medicine, Department of Cardiology, University Medical Center of the Johannes Gutenberg-University Mainz, Mainz, Germany; German Center for Cardiovascular Research (DZHK), Partner Site Rhine-Main, Mainz, Germany; Institute of Molecular Biology (IMB), Mainz, Germany.

A J Ten Cate-Hoek (AJ)

Laboratory for Clinical Thrombosis and Hemostasis, Department of Biochemistry, Cardiovascular Research, Maastricht University, Netherlands; Thrombosis Expertise Center, Heart and Vascular Center, Maastricht University Medical Center, Maastricht, Netherlands.

K Jurk (K)

Center for Thrombosis and Hemostasis (CTH), University Medical Center of the Johannes Gutenberg-University Mainz, Mainz, Germany; Preventive Cardiology and Preventive Medicine, Department of Cardiology, University Medical Center of the Johannes Gutenberg-University Mainz, Mainz, Germany; German Center for Cardiovascular Research (DZHK), Partner Site Rhine-Main, Mainz, Germany. Electronic address: kerstin.jurk@unimedizin-mainz.de.

Classifications MeSH