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ToolsBarton, Anna K., Craig, Neil J., Loganath, Krithika, Joshi, Shruti, Tsampasian, Vasiliki, Mahendran, Menaka, Lenell, Joel, Tzolos, Evangelos, Singh, Trisha, Whittington, Beth, Nash, Jennifer, Williams, Michelle C., van Beek, Edwin J. R., MacAskill, Mark G., Berkeley, Bronwyn, Vezaides, Stefan, Brittan, Mairi, Baker, Andrew H., Sellers, Stephanie, Fletcher, Alison, Clark, Tim, Waight, Clint, Slart, Riemer H. J. A., Berman, Daniel, Dey, Damini, Slomka, Piotr, Newby, David E. and Dweck, Marc R. (2025) Myocardial fibroblast activation after acute myocardial infarction: A positron emission tomography and magnetic resonance study. Journal of the American College of Cardiology. ISSN 0735-1097
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Abstract
Background: Myocardial fibrosis is a key healing response after myocardial infarction driven by activated fibroblasts. Gallium-68-labeled fibroblast activation protein inhibitor ([68Ga]-FAPI) is a novel positron-emitting radiotracer that binds activated fibroblasts. Objectives: The aim of this study was to investigate the intensity, distribution, and time-course of fibroblast activation after acute myocardial infarction. Methods: A total of 40 patients with acute myocardial infarction underwent hybrid [68Ga]FAPI-46 positron emission tomography and cardiac magnetic resonance and were compared with matched control subjects (n = 19) and those with chronic (>2 years) myocardial infarction (n = 20). Intensity of [68Ga]FAPI-46 uptake was quantified by maximum target-to-background ratio (TBRmax). Burdens of fibroblast activation and scar were assessed by percent myocardial involvement of [68Ga]FAPI-46 uptake and late gadolinium enhancement, respectively. Results: Myocardial [68Ga]FAPI-46 uptake was observed in the acute infarct and peri-infarct regions that exceeded the extent of late gadolinium enhancement (burden 27.8% ± 12.4% vs 15.2% ± 10.6%; P < 0.001). One-third of patients also demonstrated right ventricular involvement. Myocardial [68Ga]FAPI-46 uptake was most intense at 1 and 2 weeks before declining at 4 and 12 weeks (TBRmax 4.0 ± 1.1, 3.7 ± 1.0, 3.1 ± 0.8, and 2.7 ± 0.7; P < 0.001). In comparison with control subjects, increased [68Ga]FAPI-46 uptake was observed in chronic (7 ± 6 years ago) infarcts at lower intensity than acute infarction (TBRmax 1.2 ± 0.1 vs 1.7 ± 0.5 vs 4.0 ± 1.1; P < 0.001). Baseline [68Ga]FAPI-46 burden correlated with lower left ventricular ejection fraction (r = −0.606), higher indexed left ventricular end-diastolic volume (r = 0.572), and higher scar burden (r = 0.871) at 1 year (P < 0.001 for all). Increased remote myocardial [68Ga]FAPI-46 uptake was associated with left ventricular dilatation and systolic dysfunction. Conclusions: Myocardial fibroblast activation peaks within a week of acute myocardial infarction and extends beyond the infarct region. It declines slowly with time, persists for years, and is associated with subsequent left ventricular remodeling. (PROFILE-MI–The FAPI Fibrosis Study; NCT05356923)
| Item Type: | Article |
|---|---|
| Faculty \ School: | Faculty of Medicine and Health Sciences > Norwich Medical School |
| UEA Research Groups: | Faculty of Medicine and Health Sciences > Research Centres > Metabolic Health |
| Depositing User: | LivePure Connector |
| Date Deposited: | 18 Jan 2025 01:09 |
| Last Modified: | 22 Jan 2025 01:04 |
| URI: | https://ueaeprints.uea.ac.uk/id/eprint/98264 |
| DOI: | 10.1016/j.jacc.2024.10.103 |
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