Molekulare PET-Diagnostik inflammatorischer und fibrotischer Prozesse nach akutem Myokardinfarkt

Zusammenfassung

Nach akutem Myokardinfarkt entscheidet die frühe Gewebsreaktion – insbesondere die Interaktion zwischen Immunzellen und Fibroblasten – maßgeblich über das Risiko für ventrikuläres Remodeling und chronische Herzinsuffizienz. Während Standardtherapien wie RAAS-Blockade und Betablocker vorrangig in der chronischen Phase greifen, eröffnet das subakute Zeitfenster nach einem Infarkt die Möglichkeit gezielter, personalisierter Interventionen. Molekulare Bildgebung mit Radiotracern erlaubt die nicht-invasive Darstellung dieser biologischen Prozesse und kann helfen, Patienten zu identifizieren, die am ehesten von neuen antiinflammatorischen oder antifibrotischen Therapien profitieren. Der Artikel gibt einen Überblick über den klinischen Hintergrund, zentrale pathophysiologische Mechanismen und aktuelle Entwicklungen in der PET-Bildgebung bei Myokardinfarkt.

Abstract

After acute myocardial infarction, the early tissue response – in particular the interaction between immune cells and fibroblasts – has a decisive influence on the risk of ventricular remodeling and chronic heart failure. While standard therapies such as RAAS blockade and beta blockers are primarily effective in the chronic phase, the subacute window of opportunity after an infarction opens up the possibility of targeted, personalized interventions. Molecular imaging with radiotracers allows non-invasive visualization of these biological processes and can help identify patients who are most likely to benefit from new anti-inflammatory or anti-fibrotic therapies. This article provides an overview of the clinical background, key pathophysiological mechanisms, and current developments in PET imaging for myocardial infarction.

Schlüsselwörter

PET-Diagnostik - Myokardinfarkt - Remodeling

Keywords

PET diagnostics - myocardial infarction - remodeling

Publikationsverlauf

Artikel online veröffentlicht:
08. Dezember 2025

• Referenzen

• 1 Frangogiannis NG. Cardiac fibrosis. Cardiovasc Res 2021; 117: 1450-88
• 2 Rurik JG, Aghajanian H, Epstein JA. Immune Cells and Immunotherapy for Cardiac Injury and Repair. Circ Res 2021; 128: 1766-79
• 3 Bengel FM, Hess A, Diekmann J. et al. Molecular imaging of immune and fibrosis targets for guidance of therapy for repair after myocardial infarction. Nature Reviews Cardiology 2025; in press.
• 4 Weber WA, Barthel H, Bengel F. et al. What Is Theranostics?. J Nucl Med 2023; 64: 669-70
• 5 Weber WA, Czernin J, Anderson CJ. et al. The Future of Nuclear Medicine, Molecular Imaging, and Theranostics. J Nucl Med 2020; 61: 263S-72S
• 6 Prabhu SD, Frangogiannis NG. The Biological Basis for Cardiac Repair After Myocardial Infarction: From Inflammation to Fibrosis. Circ Res 2016; 119: 91-112
• 7 Kuppe C, Ramirez Flores RO, Li Z. et al. Spatial multi-omic map of human myocardial infarction. Nature 2022; 608: 766-77
• 8 Tillmanns J, Hoffmann D, Habbaba Y. et al. Fibroblast activation protein alpha expression identifies activated fibroblasts after myocardial infarction. J Mol Cell Cardiol 2015; 87: 194-203
• 9 Hess A, Renko A, Schafer A. et al. Spatial FAP Expression as Detected by (68) Ga-FAPI-46 Identifies Myofibroblasts Beyond the Infarct Scar After Reperfusion. Mol Imaging Biol 2025; 27: 173-83
• 10 Hill JA, Ardehali R, Clarke KT. et al. Fundamental Cardiovascular Research: Returns on Societal Investment: A Scientific Statement From the American Heart Association. Circ Res 2017; 121: e2-e8
• 11 Sutton MG, Sharpe N. Left ventricular remodeling after myocardial infarction: pathophysiology and therapy. Circulation 2000; 101: 2981-8
• 12 Frantz S, Hundertmark MJ, Schulz-Menger J. et al. Left ventricular remodelling post-myocardial infarction: pathophysiology, imaging, and novel therapies. Eur Heart J 2022; 43: 2549-61
• 13 Kempf T, Zarbock A, Vestweber D. et al. Anti-inflammatory mechanisms and therapeutic opportunities in myocardial infarct healing. J Mol Med (Berl) 2012; 90: 361-9
• 14 Lee WW, Marinelli B, van der Laan AM. et al. PET/MRI of inflammation in myocardial infarction. J Am Coll Cardiol 2012; 59: 153-63
• 15 Wollenweber T, Roentgen P, Schafer A. et al. Characterizing the inflammatory tissue response to acute myocardial infarction by clinical multimodality noninvasive imaging. Circ Cardiovasc Imaging 2014; 7: 811-8
• 16 Thackeray JT, Bankstahl JP, Wang Y. et al. Targeting post-infarct inflammation by PET imaging: comparison of (68)Ga-citrate and (68)Ga-DOTATATE with (18)F-FDG in a mouse model. Eur J Nucl Med Mol Imaging 2015; 42: 317-27
• 17 Hess A, Derlin T, Koenig T. et al. Molecular imaging-guided repair after acute myocardial infarction by targeting the chemokine receptor CXCR4. Eur Heart J 2020; 41: 3564-75
• 18 Thackeray JT, Derlin T, Haghikia A. et al. Molecular Imaging of the Chemokine Receptor CXCR4 After Acute Myocardial Infarction. JACC Cardiovasc Imaging 2015; 8 (12) 1417-26
• 19 Werner RA, Koenig T, Diekmann J. et al. CXCR4-Targeted Imaging of Post-Infarct Myocardial Tissue Inflammation: Prognostic Value After Reperfused Myocardial Infarction. JACC Cardiovasc Imaging 2022; 15: 372-4
• 20 Heo GS, Bajpai G, Li W. et al. Targeted PET Imaging of Chemokine Receptor 2-Positive Monocytes and Macrophages in the Injured Heart. J Nucl Med 2021; 62: 111-4
• 21 Heo GS, Kopecky B, Sultan D. et al. Molecular Imaging Visualizes Recruitment of Inflammatory Monocytes and Macrophages to the Injured Heart. Circ Res 2019; 124: 881-90
• 22 Corovic A, Gopalan D, Wall C. et al. Novel Approach for Assessing Postinfarct Myocardial Injury and Inflammation Using Hybrid Somatostatin Receptor Positron Emission Tomography/Magnetic Resonance Imaging. Circ Cardiovasc Imaging 2023; 16: e014538
• 23 Tarkin JM, Calcagno C, Dweck MR. et al. (68)Ga-DOTATATE PET Identifies Residual Myocardial Inflammation and Bone Marrow Activation After Myocardial Infarction. J Am Coll Cardiol 2019; 73: 2489-91
• 24 Lapa C, Reiter T, Li X. et al. Imaging of myocardial inflammation with somatostatin receptor based PET/CT - A comparison to cardiac MRI. Int J Cardiol 2015; 194: 44-9
• 25 Varasteh Z, Mohanta S, Robu S. et al. Molecular Imaging of Fibroblast Activity After Myocardial Infarction Using a (68)Ga-Labeled Fibroblast Activation Protein Inhibitor, FAPI-04. J Nucl Med 2019; 60: 1743-9
• 26 Diekmann J, Koenig T, Thackeray JT. et al. Cardiac Fibroblast Activation in Patients Early After Acute Myocardial Infarction: Integration with MR Tissue Characterization and Subsequent Functional Outcome. J Nucl Med 2022; 63: 1415-23
• 27 Diekmann J, Koenig T, Zwadlo C. et al. Molecular Imaging Identifies Fibroblast Activation Beyond the Infarct Region After Acute Myocardial Infarction. J Am Coll Cardiol 2021; 77: 1835-7
• 28 Barton AK, Craig NJ, Loganath K. et al. Myocardial Fibroblast Activation After Acute Myocardial Infarction: A Positron Emission Tomography and Magnetic Resonance Study. J Am Coll Cardiol 2025; 85: 578-91
• 29 Aghajanian H, Kimura T, Rurik JG. et al. Targeting cardiac fibrosis with engineered T cells. Nature 2019; 573: 430-3
• 30 Rurik JG, Tombacz I, Yadegari A. et al. CAR T cells produced in vivo to treat cardiac injury. Science 2022; 375: 91-6