TY - JOUR A1 - Traub, Jan A1 - Grondey, Katja A1 - Gassenmaier, Tobias A1 - Schmitt, Dominik A1 - Fette, Georg A1 - Frantz, Stefan A1 - Boivin-Jahns, Valérie A1 - Jahns, Roland A1 - Störk, Stefan A1 - Stoll, Guido A1 - Reiter, Theresa A1 - Hofmann, Ulrich A1 - Weber, Martin S. A1 - Frey, Anna T1 - Sustained increase in serum glial fibrillary acidic protein after first ST-elevation myocardial infarction JF - International Journal of Molecular Sciences N2 - 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. KW - myocardial infarction KW - STEMI KW - glial fibrillary acidic protein KW - GFAP KW - neurofilament light chain KW - NfL KW - glial damage KW - cardiac magnetic resonance imaging KW - MRI KW - infarction size Y1 - 2022 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-288261 SN - 1422-0067 VL - 23 IS - 18 ER - TY - JOUR A1 - Frey, Anna A1 - Gassenmaier, Tobias A1 - Hofmann, Ulrich A1 - Schmitt, Dominik A1 - Fette, Georg A1 - Marx, Almuth A1 - Heterich, Sabine A1 - Boivin-Jahns, Valérie A1 - Ertl, Georg A1 - Bley, Thorsten A1 - Frantz, Stefan A1 - Jahns, Roland A1 - Störk, Stefan T1 - Coagulation factor XIII activity predicts left ventricular remodelling after acute myocardial infarction JF - ESC Heart Failure N2 - Aims Acute myocardial infarction (MI) is the major cause of chronic heart failure. The activity of blood coagulation factor XIII (FXIIIa) plays an important role in rodents as a healing factor after MI, whereas its role in healing and remodelling processes in humans remains unclear. We prospectively evaluated the relevance of FXIIIa after acute MI as a potential early prognostic marker for adequate healing. Methods and results This monocentric prospective cohort study investigated cardiac remodelling in patients with ST-elevation MI and followed them up for 1 year. Serum FXIIIa was serially assessed during the first 9 days after MI and after 2, 6, and 12 months. Cardiac magnetic resonance imaging was performed within 4 days after MI (Scan 1), after 7 to 9 days (Scan 2), and after 12 months (Scan 3). The FXIII valine-to-leucine (V34L) single-nucleotide polymorphism rs5985 was genotyped. One hundred forty-six patients were investigated (mean age 58 ± 11 years, 13% women). Median FXIIIa was 118 % (quartiles, 102–132%) and dropped to a trough on the second day after MI: 109%(98–109%; P < 0.001). FXIIIa recovered slowly over time, reaching the baseline level after 2 to 6 months and surpassed baseline levels only after 12 months: 124 % (110–142%). The development of FXIIIa after MI was independent of the genotype. FXIIIa on Day 2 was strongly and inversely associated with the relative size of MI in Scan 1 (Spearman’s ρ = –0.31; P = 0.01) and Scan 3 (ρ = –0.39; P < 0.01) and positively associated with left ventricular ejection fraction: ρ = 0.32 (P < 0.01) and ρ = 0.24 (P = 0.04), respectively. Conclusions FXIII activity after MI is highly dynamic, exhibiting a significant decline in the early healing period, with reconstitution 6 months later. Depressed FXIIIa early after MI predicted a greater size of MI and lower left ventricular ejection fraction after 1 year. The clinical relevance of these findings awaits to be tested in a randomized trial. KW - blood coagulation factor XIII KW - ST-elevation myocardial infarction KW - healing and remodelling processes KW - cardiac magnetic resonance imaging Y1 - 2020 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-236013 VL - 7 IS - 5 ER - TY - JOUR A1 - Gassenmaier, Tobias A1 - Petritsch, Bernhard A1 - Kunz, Andreas S. A1 - Gkaniatsas, Spyridon A1 - Gaudron, Philipp D. A1 - Weidemann, Frank A1 - Nordbeck, Peter A1 - Beer, Meinrad T1 - Long term evolution of MRI characteristics in a case of atypical left lateral wall hypertrophic cardiomyopathy JF - World Journal of Cardiology N2 - We are reporting a long-time magnetic resonance imaging (MRI) follow-up in a rare case of cardiac left lateral wall hypertrophy. Hypertrophic cardiomyopathy (HCM) is the most common genetic cardiovascular disorder and a significant cause of sudden cardiac death. Cardiac magnetic resonance (CMR) imaging can be a valuable tool for assessment of detailed information on size, localization, and tissue characteristics of hypertrophied myocardium. However, there is still little knowledge of long-term evolution of HCM as visualized by magnetic resonance imaging. Recently, our group reported a case of left lateral wall HCM as a rare variant of the more common forms, such as septal HCM, or apical HCM. As we now retrieved an old cardiac MRI acquired in this patient more than 20 years ago, we are able to provide the thrilling experience of an ultra-long MRI follow-up presentation in this rare case of left lateral wall hypertrophy. Furthermore, this case outlines the tremendous improvements in imaging quality within the last two decades of CMR imaging. KW - cardiac magnetic resonance imaging KW - hypertrophic cardiomyopathy KW - follow-up KW - atypical KW - left lateral wall Y1 - 2015 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-124934 VL - 7 IS - 6 ER -