Cardiac troponins and adverse outcomes in European patients with atrial fibrillation: A report from the ESC-EHRA EORP atrial fibrillation general long-term registry.

AF registry Atrial fibrillation Biomarkers Death Major adverse cardiovascular events Troponins outcomes

Journal

European journal of internal medicine
ISSN: 1879-0828
Titre abrégé: Eur J Intern Med
Pays: Netherlands
ID NLM: 9003220

Informations de publication

Date de publication:
05 2022
Historique:
received: 31 10 2021
revised: 10 01 2022
accepted: 12 01 2022
pubmed: 19 2 2022
medline: 28 4 2022
entrez: 18 2 2022
Statut: ppublish

Résumé

Cardiac troponins (cTn) have been reported to be predictors for adverse outcomes in atrial fibrillation (AF), patients, but their actual use is still unclear. To assess the factors associated with cTn testing in routine practice and evaluate the association with outcomes. Patients enrolled in the ESC-EHRA EORP-AF General Long-Term Registry were stratified into 3 groups according to cTn levels as (i) cTn not tested, (ii) cTn in range (≤99th percentile), (iii) cTn elevated (>99th percentile). The composite outcome of any thromboembolism /any acute coronary syndrome/cardiovascular (CV) death, defined as Major Adverse Cardiovascular Events (MACE) and all-cause death were the main endpoints. Among 10 445 AF patients (median age 71 years, 40.3% females) cTn were tested in 2834 (27.1%). cTn was elevated in 904/2834 (31.9%) and in-range in 1930/2834 (68.1%) patients. Female sex, in-hospital enrollment, first-detected AF, CV risk factors, history of coronary artery disease, and atypical AF symptoms were independently associated with cTn testing. Elevated cTn were independently associated with a higher risk for MACE (Model 1, hazard ratio [HR] 1.74, 95% confidence interval [CI] 1.40-2.16, Model 2, HR 1.62, 95% CI 1.28-2.05; Model 3 HR 1.76, 95% CI 1.37-2.26) and all-cause death (Model 1, HR 1.45, 95% CI 1.21-1.74; Model 2, HR 1.36, 95% CI 1.12-1.66; Model 3, HR 1.38, 95% CI 1.12-1.71). Elevated cTn levels were associated with an increased risk of all-cause mortality and adverse CV events. Clinical factors that might enhance the need to rule out CAD were associated with cTn testing.

Sections du résumé

BACKGROUND
Cardiac troponins (cTn) have been reported to be predictors for adverse outcomes in atrial fibrillation (AF), patients, but their actual use is still unclear.
AIM
To assess the factors associated with cTn testing in routine practice and evaluate the association with outcomes.
METHODS
Patients enrolled in the ESC-EHRA EORP-AF General Long-Term Registry were stratified into 3 groups according to cTn levels as (i) cTn not tested, (ii) cTn in range (≤99th percentile), (iii) cTn elevated (>99th percentile). The composite outcome of any thromboembolism /any acute coronary syndrome/cardiovascular (CV) death, defined as Major Adverse Cardiovascular Events (MACE) and all-cause death were the main endpoints.
RESULTS
Among 10 445 AF patients (median age 71 years, 40.3% females) cTn were tested in 2834 (27.1%). cTn was elevated in 904/2834 (31.9%) and in-range in 1930/2834 (68.1%) patients. Female sex, in-hospital enrollment, first-detected AF, CV risk factors, history of coronary artery disease, and atypical AF symptoms were independently associated with cTn testing. Elevated cTn were independently associated with a higher risk for MACE (Model 1, hazard ratio [HR] 1.74, 95% confidence interval [CI] 1.40-2.16, Model 2, HR 1.62, 95% CI 1.28-2.05; Model 3 HR 1.76, 95% CI 1.37-2.26) and all-cause death (Model 1, HR 1.45, 95% CI 1.21-1.74; Model 2, HR 1.36, 95% CI 1.12-1.66; Model 3, HR 1.38, 95% CI 1.12-1.71).
CONCLUSIONS
Elevated cTn levels were associated with an increased risk of all-cause mortality and adverse CV events. Clinical factors that might enhance the need to rule out CAD were associated with cTn testing.

Identifiants

pubmed: 35177307
pii: S0953-6205(22)00037-1
doi: 10.1016/j.ejim.2022.01.025
pii:
doi:

Substances chimiques

Troponin 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

45-56

Commentaires et corrections

Type : CommentIn

Informations de copyright

Copyright © 2022 European Federation of Internal Medicine. Published by Elsevier B.V. All rights reserved.

Auteurs

Marco Vitolo (M)

Cardiology Division, Department of Biomedical, Metabolic and Neural Sciences, University of Modena and Reggio Emilia, Policlinico di Modena, Via del Pozzo, 71, Modena 41124, Italy; Liverpool Center for Cardiovascular Science, University of Liverpool and Liverpool Heart and Chest Hospital, Liverpool, United Kingdom; Clinical and Experimental Medicine PhD Program, University of Modena and Reggio Emilia, Modena, Italy.

Vincenzo L Malavasi (VL)

Cardiology Division, Department of Biomedical, Metabolic and Neural Sciences, University of Modena and Reggio Emilia, Policlinico di Modena, Via del Pozzo, 71, Modena 41124, Italy.

Marco Proietti (M)

Liverpool Center for Cardiovascular Science, University of Liverpool and Liverpool Heart and Chest Hospital, Liverpool, United Kingdom; Department of Clinical Sciences and Community Health, University of Milan, Milan, Italy; Geriatric Unit, IRCCS Istituti Clinici Scientifici Maugeri, Milan, Italy.

Igor Diemberger (I)

Department of Experimental, Diagnostic and Specialty Medicine, Institute of Cardiology, University of Bologna, Policlinico S. Orsola-Malpighi, Bologna, Italy.

Laurent Fauchier (L)

Service de Cardiologie, Center Hospitalier Universitaire Trousseau, Tours, France.

Francisco Marin (F)

Department of Cardiology, Hospital Universitario Virgen de la Arrixaca, IMIB-Arrixaca, University of Murcia, CIBERCV, Murcia, Spain.

Michael Nabauer (M)

Department of Cardiology, Ludwig-Maximilians-University, Munich, Germany.

Tatjana S Potpara (TS)

School of Medicine, University of Belgrade, Belgrade, Serbia; Intensive Arrhythmia Care, Cardiology Clinic, Clinical Center of Serbia, Belgrade, Serbia.

Gheorghe-Andrei Dan (GA)

Carol Davila' University of Medicine, Colentina University Hospital, Bucharest, Romania.

Zbigniew Kalarus (Z)

Department of Cardiology, SMDZ in Zabrze, Silesian Center for Heart Diseases, Medical University of Silesia, Zabrze, Katowice, Poland.

Luigi Tavazzi (L)

Maria Cecilia Hospital, GVM Care and Research, Cotignola, Italy.

Aldo Pietro Maggioni (AP)

ANMCO Research Center, Firenze, Italy.

Deirdre A Lane (DA)

Liverpool Center for Cardiovascular Science, University of Liverpool and Liverpool Heart and Chest Hospital, Liverpool, United Kingdom; Department of Clinical Medicine, Aalborg University, Aalborg, Denmark.

Gregory Y H Lip (GYH)

Liverpool Center for Cardiovascular Science, University of Liverpool and Liverpool Heart and Chest Hospital, Liverpool, United Kingdom; Department of Clinical Medicine, Aalborg University, Aalborg, Denmark.

Giuseppe Boriani (G)

Cardiology Division, Department of Biomedical, Metabolic and Neural Sciences, University of Modena and Reggio Emilia, Policlinico di Modena, Via del Pozzo, 71, Modena 41124, Italy. Electronic address: giuseppe.boriani@unimore.it.

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