Changes in circulating ApoJ-Glyc levels in patients with suspected acute coronary syndrome: The EDICA trial.

Acute coronary syndrome Acute myocardial ischemia Angina Glycosylated ApoJ Ischemia

Journal

International journal of cardiology
ISSN: 1874-1754
Titre abrégé: Int J Cardiol
Pays: Netherlands
ID NLM: 8200291

Informations de publication

Date de publication:
15 Nov 2023
Historique:
received: 15 05 2023
revised: 08 08 2023
accepted: 20 08 2023
pubmed: 25 8 2023
medline: 25 8 2023
entrez: 24 8 2023
Statut: ppublish

Résumé

Myocardial ischemia induces intracellular accumulation of non-glycosylated apolipoprotein J that results in a reduction of circulating glycosylated ApoJ (ApoJ-Glyc). The latter has been suggested to be a marker of transient myocardial ischemia. This proof-of-concept clinical study aimed to assess whether changes in circulating ApoJ-Glyc could detect myocardial ischemia in patients attending the emergency department (ED) with chest pain suggestive of acute coronary syndrome (ACS). In suspected ACS patients, EDICA (Early Detection of Myocardial Ischemia in Suspected Acute Coronary Syndromes by ApoJ-Glyc a Novel Pathologically based Ischemia Biomarker), a multicentre, international, cohort study assessed changes in 2 glycosylated variants of ApoJ-Glyc, (ApoJ-GlycA2 and ApoJ-GlycA6), in serum samples obtained at ED admission (0 h), and 1 h and 3 h thereafter, blinded to the clinical diagnosis (i.e. STEMI, NSTEMI, unstable angina, non-ischemic). 404 patients were recruited; 291 were given a clinical diagnosis of "non-ischemic" chest pain and 113 were considered to have had an ischemic event. ApoJ-GlycA6 was lower on admission in ischemic compared with "non-ischemic" patients (66 [46-90] vs. 73 [56-95] μg/ml; P = 0.04). 74% of unstable angina patients (all with undetectable hs-Tn), had ischemic changes in ApoJ-Glyc at 0 h and 89% at 1 h. Initially low ApoJ-Glyc levels in 62 patients requiring coronary revascularization increased significantly after successful percutaneous intervention. Circulating ApoJ-Glyc concentrations decrease early in ED patients with myocardial ischemia compared with "non-ischemic" patients, even in the absence of troponin elevations. ApoJ-Glyc may be a useful marker of myocardial ischemia in the ED setting.

Sections du résumé

BACKGROUND BACKGROUND
Myocardial ischemia induces intracellular accumulation of non-glycosylated apolipoprotein J that results in a reduction of circulating glycosylated ApoJ (ApoJ-Glyc). The latter has been suggested to be a marker of transient myocardial ischemia.
OBJECTIVE OBJECTIVE
This proof-of-concept clinical study aimed to assess whether changes in circulating ApoJ-Glyc could detect myocardial ischemia in patients attending the emergency department (ED) with chest pain suggestive of acute coronary syndrome (ACS).
METHODS METHODS
In suspected ACS patients, EDICA (Early Detection of Myocardial Ischemia in Suspected Acute Coronary Syndromes by ApoJ-Glyc a Novel Pathologically based Ischemia Biomarker), a multicentre, international, cohort study assessed changes in 2 glycosylated variants of ApoJ-Glyc, (ApoJ-GlycA2 and ApoJ-GlycA6), in serum samples obtained at ED admission (0 h), and 1 h and 3 h thereafter, blinded to the clinical diagnosis (i.e. STEMI, NSTEMI, unstable angina, non-ischemic).
RESULTS RESULTS
404 patients were recruited; 291 were given a clinical diagnosis of "non-ischemic" chest pain and 113 were considered to have had an ischemic event. ApoJ-GlycA6 was lower on admission in ischemic compared with "non-ischemic" patients (66 [46-90] vs. 73 [56-95] μg/ml; P = 0.04). 74% of unstable angina patients (all with undetectable hs-Tn), had ischemic changes in ApoJ-Glyc at 0 h and 89% at 1 h. Initially low ApoJ-Glyc levels in 62 patients requiring coronary revascularization increased significantly after successful percutaneous intervention.
CONCLUSIONS CONCLUSIONS
Circulating ApoJ-Glyc concentrations decrease early in ED patients with myocardial ischemia compared with "non-ischemic" patients, even in the absence of troponin elevations. ApoJ-Glyc may be a useful marker of myocardial ischemia in the ED setting.

Identifiants

pubmed: 37619880
pii: S0167-5273(23)01170-1
doi: 10.1016/j.ijcard.2023.131291
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

131291

Informations de copyright

Copyright © 2023 Elsevier B.V. All rights reserved.

Auteurs

Juan Carlos Kaski (JC)

Molecular and Clinical Sciences Research Institute, St George's, University of London, London, United Kingdom; GlyCardial Diagnostics, S.L., Barcelona, Spain.

Nuria Lluch (N)

GlyCardial Diagnostics, S.L., Barcelona, Spain.

Jose-Luis Lopez-Sendon (JL)

IDIPAZ Research Institute, Hospital Universitario La Paz, UAM, Madrid, Spain.

Diana A Gorog (DA)

Postgraduate Medical School, University of Hertfordshire, Hertfordshire, United Kingdom; Faculty of Medicine, National Heart and Lung Institute, Imperial College, London.

Isabel Antorrena-Miranda (I)

IDIPAZ Research Institute, Hospital Universitario La Paz, UAM, Madrid, Spain.

Pablo Avanzas (P)

Interventional Cardiology Unit, Hospital Universitario Central de Asturias, Department of Medicine, University of Oviedo, Oviedo, Spain Sanitaria del Principado de Asturias, Spain.

Pablo Herrero Puente (P)

Emergency Department, University Central Hospital of Asturias, Instituto de Investigación Sanitaria del Principado de Asturias, Spain.

Alessandro Sionis (A)

Cardiology Department Hospital de la Santa Creu i Sant Pau, IIB-Sant Pau, Barcelona, Spain.

José R González-Juanatey (JR)

Cardiology Department. University Hospital Santiago de Compostela, Spain.

Andrés Íñiguez (A)

Department of Cardiology, Hospital Universitario Álvaro Cunqueiro, Vigo, Spain.

Alberto Cordero (A)

Cardiology Department, Hospital Universitario de San Juan, Alicante, Spain.

Emmanuel Ako (E)

Chelsea & Westminster Hospital, London, United Kingdom.

Francisco Fernández-Avilés (F)

Department of Cardiology, Hospital General Universitario Gregorio Marañón, Madrid, Spain; Ciber Cardiovascular (CiberCV), Madrid, Spain.

Felipe Atienza (F)

Department of Cardiology, Hospital General Universitario Gregorio Marañón, Madrid, Spain; Ciber Cardiovascular (CiberCV), Madrid, Spain.

Alejandro Recio-Mayoral (A)

Cardiology Department, Hospital Virgen Macarena, Sevilla, Spain.

Alan H B Wu (AHB)

Clinical Chemistry and Toxicology Laboratories, San Francisco General Hospital and Dept. Lab. Medicine, University of California, San Francisco, USA.

Filippo Crea (F)

Università Cattolica del Sacro Cuore, and Fondazione Policlinico Universitario A. Gemelli IRCCS, Roma, Italy.

Robert Storey (R)

Department of Infection, Immunity and Cardiovascular Disease, University of Sheffield, Sheffield, United Kingdom.

Lina Badimon (L)

GlyCardial Diagnostics, S.L., Barcelona, Spain; Cardiovascular-Program-ICCC, IR-Hospital Santa Creu i Sant Pau, IIB-Sant Pau, 08025 Barcelona, Spain; Cardiovascular Research, Universitat Autònoma de Barcelona, Barcelona, Spain.

Judit Cubedo (J)

GlyCardial Diagnostics, S.L., Barcelona, Spain. Electronic address: jcubedorafols@gmail.com.

Classifications MeSH