Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2023 Aug 28;3(4):oead078.
doi: 10.1093/ehjopen/oead078. eCollection 2023 Jul.

Predicting poor neurological outcomes following out-of-hospital cardiac arrest using neuron-specific enolase and neurofilament light chain in patients with and without haemolysis

Yusuf Abdi Isse  1 , Ruth Frikke-Schmidt  2   3 , Sebastian Wiberg  1 , Johannes Grand  1 , Laust E R Obling  1 , Anna Sina Pettersson Meyer  1 , Jesper Kjaergaard  1   3 , Christian Hassager  1   3 , Martin A S Meyer  1
Affiliations

Predicting poor neurological outcomes following out-of-hospital cardiac arrest using neuron-specific enolase and neurofilament light chain in patients with and without haemolysis

Yusuf Abdi Isse et al. Eur Heart J Open. .

Abstract

Aims: Hypoxic-ischaemic brain injury following out-of-hospital cardiac arrest (OHCA) is a common complication and a major cause of death. Neuron-specific enolase (NSE) and neurofilament light chain (NfL) are released after brain injury and elevated concentrations of both are associated with poor neurological outcome. We explored the influence of haemolysis on the prognostic performance of NSE and NfL.

Methods and results: The study is based on post hoc analyses of a randomized, single-centre, double-blinded, controlled trial (IMICA), where comatose OHCA patients of presumed cardiac cause were included. Free-haemoglobin was measured at admission to quantify haemolysis. NSE and NfL were measured after 48 h to estimate the extent of brain injury. Montreal Cognitive Assessment score (MoCA) was assessed to evaluate neurocognitive impairments. Seventy-three patients were included and divided into two groups by the median free-haemoglobin at admission. No group differences in mortality or poor neurological outcome were observed. The high-admission free-haemoglobin group had a significantly higher concentration of NSE compared to the low-admission free-haemoglobin group (27.4 µmol/L vs. 19.6 µmol/L, P = 0.03), but no differences in NfL. The performance of NSE and NfL in predicting poor neurological outcome were high for both, but NfL was numerically higher [area under the ROC (AUROC) 0.90 vs. 0.96, P = 0.09]. Furthermore, NfL, but not NSE, was inversely correlated with MoCA score, R2 = 0.21, P = 0.006.

Conclusion: High free-haemoglobin at admission was associated with higher NSE concentration after 48 h, but, the performance of NSE and NfL in predicting poor neurological outcome among OHCA patients were good regardless of early haemolysis. Only elevated NfL concentrations were associated with cognitive impairments.

Keywords: Free-haemoglobin; Haemolysis; MoCA; Neurofilament light chain; Neuron-specific enolase; Out-of-hospital cardiac arrest.

PubMed Disclaimer

Conflict of interest statement

Conflicts of interest: All authors declare no conflict of interest except Anna Sina Petterson Meyer which has been employed at Novo Nordisk after the completion of the trial.

Figures

Graphical abstract
Graphical abstract
Figure 1
Figure 1
Prognostic performance of neuron-specific enolase and neurofilament light chain in predicting poor neurological outcome after out-of-hospital cardiac arrest. Receiver operating characteristic plot showing the predictive ability of neuron-specific enolase and neurofilament light chain measured at 48 h after admission to predict poor neurological outcome (Cerebral performance category ≥3) at 180 days after out-of-hospital cardiac arrest in comatose patients. The sample size is divided into two groups: a non-haemolysis group (< median haemolysis) and a haemolysis group (≥ median haemolysis). (A) All patients. (B) Non-haemolysis group. (C) Haemolysis group.
See this image and copyright information in PMC

Similar articles

See all similar articles

Cited by

References

    1. Lemiale V, Dumas F, Mongardon N, Giovanetti O, Charpentier J, Chiche JD, Carli P, Mira JP, Nolan J, Cariou A. Intensive care unit mortality after cardiac arrest: the relative contribution of shock and brain injury in a large cohort. Intensive Care Med 2013;39:1972–1980. - PubMed
    1. Sendelbach S, Hearst MO, Johnson PJ, Unger BT, Mooney MR. Effects of variation in temperature management on cerebral performance category scores in patients who received therapeutic hypothermia post cardiac arrest. Resuscitation 2012;83:829–834. - PubMed
    1. Mongardon N, Dumas F, Ricome S, Grimaldi D, Hissem T, Pène F, Cariou A. Postcardiac arrest syndrome: from immediate resuscitation to long-term outcome. Ann Intensive Care 2011;1:45. - PMC - PubMed
    1. Nolan JP, Neumar RW, Adrie C, Aibiki M, Berg RA, Böttiger BW, Callaway C, Clark RS, Geocadin RG, Jauch EC, Kern KB, Laurent I, Longstreth WT, Merchant RM, Morley P, Morrison LJ, Nadkarni V, Peberdy MA, Rivers EP, Rodriguez-Nunez A, Sellke FW, Spaulding C, Sunde K, Hoek TV. Post-cardiac arrest syndrome: epidemiology, pathophysiology, treatment, and prognostication. A scientific statement from the international liaison committee on resuscitation; the American heart association emergency cardiovascular care committee; the council on cardiovascular surgery and anesthesia; the council on cardiopulmonary, perioperative, and critical care; the council on clinical cardiology; the council on stroke. Resuscitation 2008;79:350–379. - PubMed
    1. Sekhon MS, Ainslie PN, Griesdale DE. Clinical pathophysiology of hypoxic ischemic brain injury after cardiac arrest: a “two-hit” model. Crit Care 2017;21:90. - PMC - PubMed