Abstract 10581: Sustained Increase of Serum Glial Fibrillary Acidic Protein After First St-Elevation Myocardial Infarction

Abstract

Introduction: Acute ischemic cardiac injury predisposes for cognitive impairment, dementia and depression. Beyond altered cerebral blood flow and neurohumoral activation, recent positron emission tomography data pathophysiologically suggest acute and chronic neuroinflammation, which is accompanied by astroglial activation, after acute experimental myocardial infarction (MI). Hypothesis: Peripheral serum biomarkers indicating neuronal and glial involvement are altered in the year after first acute MI. Methods: Within the investigator-initiated, prospective, multicenter diagnostic ETiCS study, we quantified serum levels of neurofilament light chain (NfL) and glial fibrillary acidic protein (GFAP) using ultra-sensitive molecular immunoassays serially in the year after first ST-elevation MI (STEMI). Cardiac magnetic resonance imaging enabled precise detection of infarction volume and ejection fraction. Results: Sufficient biomaterial was available from 45 STEMI patients (aged 28 to 78 years, median 56 years, 11% female). Median serum NfL (quartiles) at hospital admission was 10.6 (7.2, 14.8 pg/ml) and median GFAP 63.8 (47.0, 89.9 pg/ml). Absolute levels of NfL (ρ=0.78; p<0.001) and GFAP (ρ=0.56; p<0.001) correlated to patient age at all time-points. While NfL remained unaltered in the course of one year, GFAP after STEMI increased in the first 3 months after MI with a mean change of +10.6±25.0 pg/ml (p=0.007), and remained elevated after 6 months (+12.4±32.9 pg/ml; p=0.015) and 12 months (+12.6±31.2 pg/ml; p=0.010) compared to baseline. Larger relative infarction volume (ρ=0.41; p=0.009) and higher peak creatine kinase levels (ρ=0.39; p<0.001), but not ejection fraction, correlated to increases of GFAP and NfL, respectively. Conclusions: Our findings suggest subtle glial damage after STEMI which correlates to infarction volume. Further studies need to evaluate the valence of serum GFAP as a peripheral biomarker of cognitive decline after MI.