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    • Myocardial Fibroblast Activation after Acute Myocardial Infarction: A Positron Emission Tomography and Magnetic Resonance Study

    Anna K. Barton,Neil J. Craig， Stephanie Sellers,Alison Fletcher

    Journal of the American College of Cardiology（2025）

    Norwich Medical School | Uppsala Clinical Research Center | Edinburgh Imaging Facility

    Cited 0|Views0
    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)
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    fibroblast activation protein inhibitor,molecular PET,myocardial Infarction
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