Plasma Soluble Glycoprotein VI, Platelet Function, Bleeding, and Ischemic Events in Patients Undergoing Elective Percutaneous Coronary Intervention.


Journal

Thrombosis and haemostasis
ISSN: 2567-689X
Titre abrégé: Thromb Haemost
Pays: Germany
ID NLM: 7608063

Informations de publication

Date de publication:
17 Aug 2023
Historique:
medline: 18 8 2023
pubmed: 18 8 2023
entrez: 17 8 2023
Statut: aheadofprint

Résumé

 Glycoprotein VI (GPVI) is the major platelet-specific collagen receptor. GPVI shedding with generation of soluble GPVI (sGPVI) is an endogenous feedback mechanism preventing platelet overstimulation. sGPVI has not been investigated in patients with chronic coronary syndrome (CCS) undergoing percutaneous coronary intervention (PCI), especially regarding its potential value as a predictor of ischemic and bleeding risk.  Baseline plasma sGPVI levels were available in 318 patients with CCS undergoing PCI. Platelet function was assessed by measuring both adenosine diphosphate (ADP) and collagen-induced platelet aggregation. Co-primary endpoints were a composite of death or myocardial injury at 48 hours after PCI, and Bleeding Academic Research Consortium (BARC) type 1 to 5 bleeding at 30 days.  There was no significant correlation between sGPVI and platelet function at baseline or at 48 hours after PCI and loading with antiplatelet drugs. Baseline plasma sGPVI levels were not associated with the ischemic risk: the incidence of the ischemic endpoint was 25.0% in the lower, 22.9% in the middle, and 26.7% in the upper sGPVI tertile (  In patients with CCS undergoing PCI, plasma levels of sGPVI did not correlate with ADP- or collagen-induced platelet aggregation. Patients with higher baseline levels of sGPVI may carry an increased risk of bleeding at 30 days after PCI but no excess risk of ischemic events.

Sections du résumé

BACKGROUND AND AIMS OBJECTIVE
 Glycoprotein VI (GPVI) is the major platelet-specific collagen receptor. GPVI shedding with generation of soluble GPVI (sGPVI) is an endogenous feedback mechanism preventing platelet overstimulation. sGPVI has not been investigated in patients with chronic coronary syndrome (CCS) undergoing percutaneous coronary intervention (PCI), especially regarding its potential value as a predictor of ischemic and bleeding risk.
METHODS METHODS
 Baseline plasma sGPVI levels were available in 318 patients with CCS undergoing PCI. Platelet function was assessed by measuring both adenosine diphosphate (ADP) and collagen-induced platelet aggregation. Co-primary endpoints were a composite of death or myocardial injury at 48 hours after PCI, and Bleeding Academic Research Consortium (BARC) type 1 to 5 bleeding at 30 days.
RESULTS RESULTS
 There was no significant correlation between sGPVI and platelet function at baseline or at 48 hours after PCI and loading with antiplatelet drugs. Baseline plasma sGPVI levels were not associated with the ischemic risk: the incidence of the ischemic endpoint was 25.0% in the lower, 22.9% in the middle, and 26.7% in the upper sGPVI tertile (
CONCLUSION CONCLUSIONS
 In patients with CCS undergoing PCI, plasma levels of sGPVI did not correlate with ADP- or collagen-induced platelet aggregation. Patients with higher baseline levels of sGPVI may carry an increased risk of bleeding at 30 days after PCI but no excess risk of ischemic events.

Identifiants

pubmed: 37591289
doi: 10.1055/s-0043-1772221
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Informations de copyright

Thieme. All rights reserved.

Déclaration de conflit d'intérêts

R.H.-R. reported grants from German Center for Cardiovascular Research, Deutsches Herzzentrum München, the Federal Ministry of Education and Research, and advanceCOR GmbH during the conduct of the study. I.B. reported personal fees from Sysmex Europe GmbH outside the submitted work. S.S. reported grants from Else Kröner-Fresenius-Stiftung (Else Kröner-Memorial grant) during the conduct of the study and DZHK (German Center for Cardiovascular Research) for the Intracoronary Stenting and Antithrombotic Regimen: Lesion Platelet Adhesion as Selective Target of Endovenous Revacept in Patients with Chronic Coronary Syndromes Undergoing Percutaneous Coronary Intervention trial and personal fees from Bayer Vital GmbH, Daiichi Sankyo, and Biopas Laboratories outside the submitted work. S.H. has received research grants and honoraria from Roche Diagnostics, Bristol Myers Squibb, Merck KGaA, Sysmex Inostics, and Volition SPRL outside the submitted work. M.G. is cofounder of advanceCor, the manufacturer of Revacept. H.S. reports honoraria from AstraZeneca, Bayer Vital, MSD Sharp & Dohme, Novartis, Servier, Sanofi-Aventis, Boehringer Ingelheim, Daiichi Sankyo, Amgen, Pfizer and consulting fees from AstraZeneca, Amgen, MSD Sharp & Dohme, not related to the current work. G.M. is the founder of advanceCOR GmbH, Martinsried, Germany. K.A. is employee of advanceCOR GmbH, Martinsried, Germany.

Auteurs

Shqipdona Lahu (S)

Department of Cardiology, Deutsches Herzzentrum München, Technische Universität München, Munich, Germany.

Kristin Adler (K)

AdvanceCOR GmbH, Martinsried, Germany.

Katharina Mayer (K)

Department of Cardiology, Deutsches Herzzentrum München, Technische Universität München, Munich, Germany.
German Centre for Cardiovascular Research (DZHK), Partner Site Munich Heart Alliance, Munich, Germany.

Ralph Hein-Rothweiler (R)

German Centre for Cardiovascular Research (DZHK), Partner Site Munich Heart Alliance, Munich, Germany.
Department of Cardiology, Medizinische Klinik und Poliklinik I, Klinikum der Universität München, Ludwig-Maximilians-Universität, Munich, Germany.

Isabell Bernlochner (I)

German Centre for Cardiovascular Research (DZHK), Partner Site Munich Heart Alliance, Munich, Germany.
Klinik und Poliklinik für Innere Medizin I, Klinikum rechts der Isar, Technische Universität München, Munich, Germany.

Gjin Ndrepepa (G)

Department of Cardiology, Deutsches Herzzentrum München, Technische Universität München, Munich, Germany.

Stefanie Schüpke (S)

Department of Cardiology, Deutsches Herzzentrum München, Technische Universität München, Munich, Germany.
German Centre for Cardiovascular Research (DZHK), Partner Site Munich Heart Alliance, Munich, Germany.
Privatpraxis für Kardiologie, Kaiserstr. 10, 60311 Frankfurt am Main, Germany.

Stefan Holdenrieder (S)

Institut für Laboratoriumsmedizin, Deutsches Herzzentrum München, Technische Universität München, Munich, Germany.

Dario Bongiovanni (D)

Klinik für Kardiologie, Pneumologie, Endokrinologie, Intensivmedizin, Universitätsklinikum Augsburg, Augsburg, Germany.

Karl-Ludwig Laugwitz (KL)

German Centre for Cardiovascular Research (DZHK), Partner Site Munich Heart Alliance, Munich, Germany.
Klinik und Poliklinik für Innere Medizin I, Klinikum rechts der Isar, Technische Universität München, Munich, Germany.

Heribert Schunkert (H)

Department of Cardiology, Deutsches Herzzentrum München, Technische Universität München, Munich, Germany.
German Centre for Cardiovascular Research (DZHK), Partner Site Munich Heart Alliance, Munich, Germany.

Meinrad Gawaz (M)

Department of Cardiology and Angiology, University of Tübingen, Tübingen, Germany.

Steffen Massberg (S)

German Centre for Cardiovascular Research (DZHK), Partner Site Munich Heart Alliance, Munich, Germany.
Department of Cardiology, Medizinische Klinik und Poliklinik I, Klinikum der Universität München, Ludwig-Maximilians-Universität, Munich, Germany.

Adnan Kastrati (A)

Department of Cardiology, Deutsches Herzzentrum München, Technische Universität München, Munich, Germany.
German Centre for Cardiovascular Research (DZHK), Partner Site Munich Heart Alliance, Munich, Germany.

Götz Münch (G)

AdvanceCOR GmbH, Martinsried, Germany.

Classifications MeSH