Plasma glial fibrillary acidic protein and tau: predictors of neurological outcome after cardiac arrest.

Biomarkers GFAP Heart arrest In-hospital cardiac arrest Out-of-hospital cardiac arrest Prognostication Tau

Journal

Critical care (London, England)
ISSN: 1466-609X
Titre abrégé: Crit Care
Pays: England
ID NLM: 9801902

Informations de publication

Date de publication:
09 Apr 2024
Historique:
received: 30 12 2023
accepted: 23 03 2024
medline: 10 4 2024
pubmed: 10 4 2024
entrez: 9 4 2024
Statut: epublish

Résumé

The purpose was to evaluate glial fibrillary acidic protein (GFAP) and total-tau in plasma as predictors of poor neurological outcome after out-of-hospital (OHCA) and in-hospital cardiac arrest (IHCA), including comparisons with neurofilament light (NFL) and neuron-specific enolase (NSE). Retrospective multicentre observational study of patients admitted to an intensive care unit (ICU) in three hospitals in Sweden 2014-2018. Blood samples were collected at ICU admission, 12 h, and 48 h post-cardiac arrest. Poor neurological outcome was defined as Cerebral Performance Category 3-5 at 2-6 months after cardiac arrest. Plasma samples were retrospectively analysed for GFAP, tau, and NFL. Serum NSE was analysed in clinical care. Prognostic performances were tested with the area under the receiver operating characteristics curve (AUC). Of the 428 included patients, 328 were OHCA, and 100 were IHCA. At ICU admission, 12 h and 48 h post-cardiac arrest, GFAP predicted neurological outcome after OHCA with AUC (95% CI) 0.76 (0.70-0.82), 0.86 (0.81-0.90) and 0.91 (0.87-0.96), and after IHCA with AUC (95% CI) 0.77 (0.66-0.87), 0.83 (0.74-0.92) and 0.83 (0.71-0.95). At the same time points, tau predicted outcome after OHCA with AUC (95% CI) 0.72 (0.66-0.79), 0.75 (0.69-0.81), and 0.93 (0.89-0.96) and after IHCA with AUC (95% CI) 0.61 (0.49-0.74), 0.68 (0.56-0.79), and 0.77 (0.65-0.90). Adding the change in biomarker levels between time points did not improve predictive accuracy compared to the last time point. In a subset of patients, GFAP at 12 h and 48 h, as well as tau at 48 h, offered similar predictive value as NSE at 48 h (the earliest time point NSE is recommended in guidelines) after both OHCA and IHCA. The predictive performance of NFL was similar or superior to GFAP and tau at all time points after OHCA and IHCA. GFAP and tau are promising biomarkers for neuroprognostication, with the highest predictive performance at 48 h after OHCA, but not superior to NFL. The predictive ability of GFAP may be sufficiently high for clinical use at 12 h after cardiac arrest.

Sections du résumé

BACKGROUND BACKGROUND
The purpose was to evaluate glial fibrillary acidic protein (GFAP) and total-tau in plasma as predictors of poor neurological outcome after out-of-hospital (OHCA) and in-hospital cardiac arrest (IHCA), including comparisons with neurofilament light (NFL) and neuron-specific enolase (NSE).
METHODS METHODS
Retrospective multicentre observational study of patients admitted to an intensive care unit (ICU) in three hospitals in Sweden 2014-2018. Blood samples were collected at ICU admission, 12 h, and 48 h post-cardiac arrest. Poor neurological outcome was defined as Cerebral Performance Category 3-5 at 2-6 months after cardiac arrest. Plasma samples were retrospectively analysed for GFAP, tau, and NFL. Serum NSE was analysed in clinical care. Prognostic performances were tested with the area under the receiver operating characteristics curve (AUC).
RESULTS RESULTS
Of the 428 included patients, 328 were OHCA, and 100 were IHCA. At ICU admission, 12 h and 48 h post-cardiac arrest, GFAP predicted neurological outcome after OHCA with AUC (95% CI) 0.76 (0.70-0.82), 0.86 (0.81-0.90) and 0.91 (0.87-0.96), and after IHCA with AUC (95% CI) 0.77 (0.66-0.87), 0.83 (0.74-0.92) and 0.83 (0.71-0.95). At the same time points, tau predicted outcome after OHCA with AUC (95% CI) 0.72 (0.66-0.79), 0.75 (0.69-0.81), and 0.93 (0.89-0.96) and after IHCA with AUC (95% CI) 0.61 (0.49-0.74), 0.68 (0.56-0.79), and 0.77 (0.65-0.90). Adding the change in biomarker levels between time points did not improve predictive accuracy compared to the last time point. In a subset of patients, GFAP at 12 h and 48 h, as well as tau at 48 h, offered similar predictive value as NSE at 48 h (the earliest time point NSE is recommended in guidelines) after both OHCA and IHCA. The predictive performance of NFL was similar or superior to GFAP and tau at all time points after OHCA and IHCA.
CONCLUSION CONCLUSIONS
GFAP and tau are promising biomarkers for neuroprognostication, with the highest predictive performance at 48 h after OHCA, but not superior to NFL. The predictive ability of GFAP may be sufficiently high for clinical use at 12 h after cardiac arrest.

Identifiants

pubmed: 38594704
doi: 10.1186/s13054-024-04889-0
pii: 10.1186/s13054-024-04889-0
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

116

Subventions

Organisme : EU Joint Programme - Neurodegenerative Disease Research
ID : 2019-03401

Informations de copyright

© 2024. The Author(s).

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Auteurs

Isabelle Arctaedius (I)

Department of Clinical Sciences, Anaesthesia and Intensive Care, Skane University Hospital, Lund University, Lund, Sweden. isabelle.arctaedius@med.lu.se.

Helena Levin (H)

Department of Research and Education, Skane University Hospital and Department of Clinical Sciences, Anaesthesia and Intensive Care, Lund University, Lund, Sweden.

Bergthóra Thorgeirsdóttir (B)

Department of Clinical Sciences, Anaesthesia and Intensive Care, Skane University Hospital, Lund University, Malmö, Sweden.

Marion Moseby-Knappe (M)

Neurology and Rehabilitation Medicine, Department of Clinical Sciences Lund, Skane University Hospital, Lund University, Lund, Sweden.

Tobias Cronberg (T)

Department of Clinical Sciences, Neurology, Skane University Hospital, Lund University, Lund, Sweden.

Martin Annborn (M)

Department of Clinical Sciences, Anaesthesia and Intensive Care, Helsingborg Hospital, Lund University, Helsingborg, Sweden.

Niklas Nielsen (N)

Department of Clinical Sciences, Anaesthesia and Intensive Care, Helsingborg Hospital, Lund University, Helsingborg, Sweden.

Henrik Zetterberg (H)

Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal, Sweden.
Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
Department of Neurodegenerative Disease, UCL Institute of Neurology, Queen Square, London, UK.
UK Dementia Research Institute at UCL, London, UK.
Hong Kong Center for Neurodegenerative Diseases, Clear Water Bay, Hong Kong, China.
Wisconsin Alzheimer's Disease Research Centre, University of Wisconsin School of Medicine and Public Health, University of Wisconsin-Madison, Madison, WI, USA.

Kaj Blennow (K)

Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal, Sweden.
Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.

Nicholas J Ashton (NJ)

Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, UK.
NIHR Biomedical Research Centre for Mental Health and Biomedical Research Unit for Dementia at South London and Maudsley NHS Foundation, London, UK.
Centre for Age-Related Medicine, Stavanger University Hospital, Stavanger, Norway.

Attila Frigyesi (A)

Department of Clinical Sciences, Anaesthesia and Intensive Care, Skane University Hospital, Lund University, Lund, Sweden.

Hans Friberg (H)

Department of Clinical Sciences, Anaesthesia and Intensive Care, Skane University Hospital, Lund University, Malmö, Sweden.

Anna Lybeck (A)

Department of Clinical Sciences, Anaesthesia and Intensive Care, Skane University Hospital, Lund University, Lund, Sweden.

Niklas Mattsson-Carlgren (N)

Department of Clinical Sciences, Neurology, Skane University Hospital, Lund University, Lund, Sweden.
Clinical Memory Research Unit, Department of Clinical Sciences, Lund University, Malmö, Sweden.
Wallenberg Centre for Molecular Medicine, Lund University, Lund, Sweden.

Classifications MeSH