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

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.

Chronic Neuroinflammation and Cognitive Decline in Patients with Cardiac Disease: Evidence, Relevance, and Therapeutic Implications

“…Along these lines, elevated neuronal serum biomarkers such as neurofilament light chain, phosphorylated tau protein and GFAP are associated with cognitive decline in chronic HF [ 116 , 117 ]. The recently observed increase in serum GFAP after MI might reflect the abovedescribed astroglial activation [ 118 ]. However, more studies on the mentioned biomarkers will be needed to further evaluate their relevance and potential in this currently evolving field of research.…”

A Molecular (Not Very Becoming) Picture of Stressed Arteries and Heart, with Some Therapeutic Hope

“…As the major outcome of vascular stenosis, due to underlying atherosclerosis within the coronary arteries, myocardial infarction (MI) is the major contributor to CVD-associated mortality and morbidity. Interestingly, the 1-year follow up of serum biomarkers after MI has shown an increase in the glial damage biomarker: glial fibrillary acidic protein (GFAP), but no changes in the neuronal damage biomarker: neurofilament light chain (NfL) [ 10 ]. Given that cognitive impairment after MI has been already described, this study suggests a pivotal contribution of glial cell damage in existing post-MI alterations of the central nervous system.…”