Platelet FcγRIIa as a Marker of Cardiovascular Risk After Myocardial Infarction
- PMID: 39443015
- DOI: 10.1016/j.jacc.2024.08.051
Platelet FcγRIIa as a Marker of Cardiovascular Risk After Myocardial Infarction
Abstract
Background: A previous single-center study of patients with myocardial infarction (MI) showed that platelet FcγRIIa (pFCG) can distinguish patients at higher and lower risk of subsequent MI, stroke, and death.
Objectives: The authors performed an 800-patient 25-center study to validate the prognostic implications of pFCG.
Methods: Patients with type 1 MI (ST-segment elevation and non-ST-segment elevation) were enrolled in a prospective noninterventional trial during their index hospitalization. Enrolled patients had at least 2 of the following characteristics: age ≥65 years, multivessel coronary artery disease, previous MI, chronic kidney disease, or diabetes mellitus. Flow cytometry was used to quantify pFCG at a core laboratory. A predefined threshold was used to identify high and low pFCG. Patients were queried every 6 months by telephone with a standardized questionnaire. Events were confirmed by review of medical records.
Results: Treatment with antithrombotic therapy (aspirin, P2Y12 inhibitors, and anticoagulants) was similar in patients with high and low pFCG. The primary composite endpoint (MI, stroke, death) occurred more frequently in patients with high pFCG (HR: 2.09; 95% CI: 1.34-3.26; P = 0.001). Among individual components of the composite, both death (HR: 2.57; 95% CI: 1.50-4.40; P = 0.001) and MI (HR: 3.24; 95% CI: 1.64-6.37; P = 0.001) were more frequent in patients with high pFCG.
Conclusions: Quantifying pFCG identifies patients at higher and lower risk of subsequent cardiovascular events. This prognostic information will be useful in clinical decisions regarding the intensity and duration of antiplatelet therapy. (Assessment of Individual Risk of Cardiovascular Events by Platelet FcγRIIa; NCT05175261).
Keywords: biomarker; cardiovascular; platelet; prognosis.
Copyright © 2024 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.
Conflict of interest statement
Funding Support and Author Disclosures This study was supported by Prolocor. Dr Schneider is named inventor on patents (U.S. 10,502,737, U.S. 11,747,335 B2) that propose the use of FcγRIIa for assaying platelet reactivity and treatment selection. Drs Schneider and DiBattiste are co-founders of Prolocor. Dr Angiolillo has received consulting fees or honoraria from Abbott, Amgen, AstraZeneca, Bayer, Biosensors, Boehringer Ingelheim, Bristol Myers Squibb, Chiesi, CSL Behring, Daiichi-Sankyo, Eli Lilly, Faraday, Haemonetics, Janssen, Merck, Novartis, Novo Nordisk, PhaseBio, PLx Pharma, Pfizer, Sanofi, and Vectura, outside of the present work; and his institution has received research grants from Amgen, AstraZeneca, Bayer, Biosensors, CeloNova, CSL Behring, Daiichi-Sankyo, Eisai, Eli Lilly, Faraday, Gilead, Janssen, Matsutani Chemical Industry Co, Merck, Novartis, Osprey Medical, Renal Guard Solutions, and the Scott R. MacKenzie Foundation. Dr Effron has received retirement income and equity from Eli Lilly. All other authors have no relationships relevant to the contents of this paper to disclose.