Myocardial Fibroblast Activation After Acute Myocardial Infarction: A Positron Emission Tomography and Magnetic Resonance Study.
Summary
Using [68Ga]-FAPI PET/MR in 40 MI patients, fibroblast activation peaked within one week, extended beyond infarct territories, and persisted for years with gradual decline. Activity levels correlated with subsequent LV remodeling, highlighting a therapeutic window and a candidate biomarker for anti-fibrotic strategies.
Key Findings
- Fibroblast activation peaked within 1 week post-MI and extended beyond the infarct region.
- Activation declined slowly but persisted for years, indicating prolonged remodeling biology.
- Higher FAPI signal was associated with subsequent LV remodeling, suggesting prognostic utility and a therapeutic window.
Clinical Implications
FAPI PET/MR may guide risk stratification and the initiation/monitoring of anti-fibrotic interventions in the subacute phase of MI to mitigate adverse remodeling.
Why It Matters
First-in-human serial mapping of fibroblast activation dynamics after MI provides a mechanistic imaging biomarker linked to remodeling, enabling precision timing for anti-fibrotic therapies.
Limitations
- Single-center, modest sample size (n=40) limits generalizability and outcome power.
- Radiotracer availability and standardization may constrain widespread clinical adoption.
Future Directions
Multicenter studies to validate prognostic thresholds, test anti-fibrotic therapies timed to peak activation, and evaluate cost-effectiveness and clinical utility.
Study Information
- Study Type
- Cohort
- Research Domain
- Pathophysiology
- Evidence Level
- II - Prospective imaging cohort using [68Ga]-FAPI PET/MR with serial assessments post-MI.
- Study Design
- OTHER