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
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.