Sustained Increase in Serum Glial Fibrillary Acidic Protein after First ST-Elevation Myocardial Infarction

doi:10.3390/ijms231810304

. 2022 Sep 7;23(18):10304.

doi: 10.3390/ijms231810304.

Sustained Increase in Serum Glial Fibrillary Acidic Protein after First ST-Elevation Myocardial Infarction

Jan Traub^{1

2}, Katja Grondey³, Tobias Gassenmaier⁴, Dominik Schmitt¹, Georg Fette⁵, Stefan Frantz^{1

2}, Valérie Boivin-Jahns^{2

6}, Roland Jahns⁷, Stefan Störk^{1

2}, Guido Stoll⁸, Theresa Reiter^{1

2}, Ulrich Hofmann^{1

2}, Martin S Weber^{3

9

10}, Anna Frey^{1

2}

Affiliations

¹ Medical Clinic and Policlinic 1, University Hospital Würzburg, 97080 Würzburg, Germany.
² German Comprehensive Heart Failure Center, University and University Hospital Würzburg, 97080 Würzburg, Germany.
³ Institute of Neuropathology, University Medical Center Göttingen, 37075 Göttingen, Germany.
⁴ Department of Diagnostic and Interventional Radiology, University Hospital Würzburg, 97080 Würzburg, Germany.
⁵ Data Integration Center, University Hospital Würzburg, 97080 Würzburg, Germany.
⁶ Institute for Virology and Immunobiology, University of Würzburg, 97080 Würzburg, Germany.
⁷ Interdisciplinary Bank of Biomaterials and Data Würzburg, University and University Hospital Würzburg, 97080 Würzburg, Germany.
⁸ Department of Neurology, University Hospital Würzburg, 97080 Würzburg, Germany.
⁹ Department of Neurology, University Medical Center Göttingen, 37075 Göttingen, Germany.
¹⁰ Fraunhofer-Institute for Translational Medicine and Pharmacology, 37075 Göttingen, Germany.

PMID: 36142218
PMCID: PMC9499398
DOI: 10.3390/ijms231810304

Sustained Increase in Serum Glial Fibrillary Acidic Protein after First ST-Elevation Myocardial Infarction

Jan Traub et al. Int J Mol Sci. 2022.

. 2022 Sep 7;23(18):10304.

doi: 10.3390/ijms231810304.

Authors

Affiliations

¹ Medical Clinic and Policlinic 1, University Hospital Würzburg, 97080 Würzburg, Germany.
² German Comprehensive Heart Failure Center, University and University Hospital Würzburg, 97080 Würzburg, Germany.
³ Institute of Neuropathology, University Medical Center Göttingen, 37075 Göttingen, Germany.
⁴ Department of Diagnostic and Interventional Radiology, University Hospital Würzburg, 97080 Würzburg, Germany.
⁵ Data Integration Center, University Hospital Würzburg, 97080 Würzburg, Germany.
⁶ Institute for Virology and Immunobiology, University of Würzburg, 97080 Würzburg, Germany.
⁷ Interdisciplinary Bank of Biomaterials and Data Würzburg, University and University Hospital Würzburg, 97080 Würzburg, Germany.
⁸ Department of Neurology, University Hospital Würzburg, 97080 Würzburg, Germany.
⁹ Department of Neurology, University Medical Center Göttingen, 37075 Göttingen, Germany.
¹⁰ Fraunhofer-Institute for Translational Medicine and Pharmacology, 37075 Göttingen, Germany.

PMID: 36142218
PMCID: PMC9499398
DOI: 10.3390/ijms231810304

Abstract

Acute ischemic cardiac injury predisposes one to cognitive impairment, dementia, and depression. Pathophysiologically, recent positron emission tomography data suggest astroglial activation after experimental myocardial infarction (MI). We analyzed peripheral surrogate markers of glial (and neuronal) damage serially within 12 months after the first ST-elevation MI (STEMI). Serum levels of glial fibrillary acidic protein (GFAP) and neurofilament light chain (NfL) were quantified using ultra-sensitive molecular immunoassays. Sufficient biomaterial was available from 45 STEMI patients (aged 28 to 78 years, median 56 years, 11% female). The median (quartiles) of GFAP was 63.8 (47.0, 89.9) pg/mL and of NfL 10.6 (7.2, 14.8) pg/mL at study entry 0-4 days after STEMI. GFAP after STEMI increased in the first 3 months, with a median change of +7.8 (0.4, 19.4) pg/mL (p = 0.007). It remained elevated without further relevant increases after 6 months (+11.7 (0.6, 23.5) pg/mL; p = 0.015), and 12 months (+10.3 (1.5, 22.7) pg/mL; p = 0.010) compared to the baseline. Larger relative infarction size was associated with a higher increase in GFAP (ρ = 0.41; p = 0.009). In contrast, NfL remained unaltered in the course of one year. Our findings support the idea of central nervous system involvement after MI, with GFAP as a potential peripheral biomarker of chronic glial damage as one pathophysiologic pathway.

Keywords: GFAP; MRI; NfL; STEMI; cardiac magnetic resonance imaging; glial damage; glial fibrillary acidic protein; infarction size; myocardial infarction; neurofilament light chain.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

**Figure 1**
Course of serum GFAP (**top**) and NfL (**bottom**) serum levels after first myocardial infarction. Different colored lines connect the values of individual patients. Each dot represents the value of a patient at one time point. Wilcoxon signed-rank test (n = 45). * = outlier.

**Figure 2**
Spearman’s correlation of serum biomarkers and change over 12 months (Δ). Dots represent single patients (n = 45). CK = creatine kinase; ρ = Spearman’s rho. Solid trend lines and standard deviation (thin lines) are shown.

See this image and copyright information in PMC

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[1] Disease G.B.D., Injury I., Prevalence C. Global, regional, and national incidence, prevalence, and years lived with disability for 310 diseases and injuries, 1990–2015: A systematic analysis for the Global Burden of Disease Study. Lancet. 2016;388:1545–1602. doi: 10.1016/S0140-6736(16)31678-6. - DOI - PMC - PubMed

[2] Disease G.B.D., Injury I., Prevalence C. Global, regional, and national incidence, prevalence, and years lived with disability for 310 diseases and injuries, 1990–2015: A systematic analysis for the Global Burden of Disease Study. Lancet. 2016;388:1545–1602. doi: 10.1016/S0140-6736(16)31678-6. - DOI - PMC - PubMed

[3] Zhang W., Luo P. Myocardial Infarction Predisposes Neurodegenerative Diseases. J. Alzheimers Dis. 2020;74:579–587. doi: 10.3233/JAD-191225. - DOI - PubMed

[4] Zhang W., Luo P. Myocardial Infarction Predisposes Neurodegenerative Diseases. J. Alzheimers Dis. 2020;74:579–587. doi: 10.3233/JAD-191225. - DOI - PubMed

[5] Wolters F.J., Segufa R.A., Darweesh S.K.L., Bos D., Ikram M.A., Sabayan B., Hofman A., Sedaghat S. Coronary heart disease, heart failure, and the risk of dementia: A systematic review and meta-analysis. Alzheimers Dement. 2018;14:1493–1504. doi: 10.1016/j.jalz.2018.01.007. - DOI - PubMed

[6] Wolters F.J., Segufa R.A., Darweesh S.K.L., Bos D., Ikram M.A., Sabayan B., Hofman A., Sedaghat S. Coronary heart disease, heart failure, and the risk of dementia: A systematic review and meta-analysis. Alzheimers Dement. 2018;14:1493–1504. doi: 10.1016/j.jalz.2018.01.007. - DOI - PubMed

[7] Liu H., Luiten P.G., Eisel U.L., Dejongste M.J., Schoemaker R.G. Depression after myocardial infarction: TNF-alpha-induced alterations of the blood-brain barrier and its putative therapeutic implications. Neurosci. Biobehav. Rev. 2013;37:561–572. doi: 10.1016/j.neubiorev.2013.02.004. - DOI - PubMed

[8] Liu H., Luiten P.G., Eisel U.L., Dejongste M.J., Schoemaker R.G. Depression after myocardial infarction: TNF-alpha-induced alterations of the blood-brain barrier and its putative therapeutic implications. Neurosci. Biobehav. Rev. 2013;37:561–572. doi: 10.1016/j.neubiorev.2013.02.004. - DOI - PubMed

[9] Honig A., Lousberg R., Wojciechowski F.L., Cheriex E.C., Wellens H.J., van Praag H.M. Depression following a first heart infarct; similarities with and differences from ‘ordinary’ depression. Ned. Tijdschr. Geneeskd. 1997;141:196–199. - PubMed

[10] Honig A., Lousberg R., Wojciechowski F.L., Cheriex E.C., Wellens H.J., van Praag H.M. Depression following a first heart infarct; similarities with and differences from ‘ordinary’ depression. Ned. Tijdschr. Geneeskd. 1997;141:196–199. - PubMed

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Sustained Increase in Serum Glial Fibrillary Acidic Protein after First ST-Elevation Myocardial Infarction

Affiliations

Sustained Increase in Serum Glial Fibrillary Acidic Protein after First ST-Elevation Myocardial Infarction

Authors

Affiliations

Abstract

Conflict of interest statement

Figures

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Medical

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Abstract

Conflict of interest statement

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