Time course of myocardial fibrosis activity following ST elevation myocardial infarction using 68Ga-FAPI PET/MR

Abstract Funding Acknowledgements Type of funding sources: Private grant(s) and/or Sponsorship. Main funding source(s): British Heart Foundation - Prof Marc Dweck Senior Fellowship, and BHF Research Excellence Award 3 for Dr Anna K Barton. Background Myocardial fibrosis is a key healing response following myocardial infarction (MI). Although scar formation following MI is considered complete by 12 weeks, its exact time course is unknown. Fibroblast activation protein is a key factor in fibrogenesis that is expressed by activated fibroblasts in the myocardium following MI. Hybrid positron emission tomography and cardiovascular magnetic resonance (PET/MR) with radiolabelled fibroblast activation protein inhibitor (68Ga-FAPI) is an emerging method to measure in vivo fibrosis activity. Purpose To investigate the timing of myocardial fibrosis activity following ST-elevation MI using 68Ga-FAPI PET/MR Methods Twenty patients underwent multi-timepoint hybrid 68Ga-FAPI PET/MR <1, 2, 4, and 12 weeks following acute ST-elevation MI. They were compared to patients with prior established ST-elevation MI (>12 months) and healthy controls who underwent single-timepoint 68Ga-FAPI PET/MR to determine fibrosis activity in chronic infarcts and healthy myocardium respectively. All participants were imaged 30 min following administration of 100–200 MBq 68Ga-FAPI-04. Infarct zone 68Ga-FAPI uptake was quantified using tissue-to-background ratio (TBRmax) after correction for blood-pool activity in the left ventricle. Comparisons between timepoints for the acute MI group were assessed by ANOVA with repeated measures and post hoc Bonferroni correction, and between groups by two-tailed t-test. Results Participants were predominantly middle-aged men (Table). Focal 68Ga-FAPI uptake localised to areas of infarction within the infarct and peri-infarct zones on late gadolinium enhancement on magnetic resonance imaging (Figure). In acute MI, there was substantial uptake with consistent TBRmax values at weeks 1, 2 and 4 (Table and Figure). Though TBRmax values started to decline by week 12 they remained persistently elevated compared to prior established MI and healthy myocardium (Table). Participants with prior established MI had modestly increased 68Ga-FAPI uptake compared with the healthy myocardium of control participants (Table and Figure). Conclusions Intense myocardial fibrosis activity is observed in the infarct and peri-infarct zones throughout the first month following ST-elevation MI. Although this starts to decline by 12 weeks, it remains markedly elevated even several years after myocardial infarction, indicating that low-level chronic fibroblast activity is a feature of established MI.