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Myocardial Fibroblast Activation in Ischemic and Nonischemic Cardiomyopathy
Shruti S Joshi1,2, Anna K Barton1,2, Krithika Loganath1
1British Heart Foundation Centre of Research Excellence, University of Edinburgh, Edinburgh, United Kingdom.
JAMA Cardiology
|April 15, 2026
Summary
Heart failure patients show persistent myocardial fibroblast activation, detectable noninvasively. This imaging may guide risk stratification and antifibrotic therapy development for heart failure.
Area of Science:
- Cardiology
- Nuclear Medicine
- Radiology
Background:
- Myocardial remodeling and fibrosis, driven by activated fibroblasts, worsen heart failure.
- Noninvasive assessment of fibroblast activation could improve heart failure phenotyping and risk stratification.
Purpose of the Study:
- To evaluate myocardial fibroblast activation in heart failure with reduced ejection fraction (HFrEF) patients.
- Utilized gallium 68-labeled fibroblast activation protein inhibitor 46 ([68Ga]FAPI-46) positron emission tomography (PET) and magnetic resonance imaging (MRI).
Main Methods:
- Prospective case-control study involving HFrEF patients, patients with prior myocardial infarction (MI) without heart failure, and healthy volunteers.
- All participants underwent [68Ga]FAPI-46 PET/MRI.
- Myocardial fibroblast activation quantified using maximum standardized uptake values (SUVmax) of [68Ga]FAPI-46.
Main Results:
- HFrEF patients exhibited increased myocardial [68Ga]FAPI-46 uptake compared to controls (SUVmax 2.7 vs 1.5).
- Uptake was highest in ischemic cardiomyopathy, localizing to MI regions (SUVmax 3.2). Non-ischemic cardiomyopathy showed diffuse uptake (SUVmax 2.3).
- Higher baseline [68Ga]FAPI-46 uptake correlated with less ejection fraction improvement in HFrEF patients on optimal medical therapy.
Conclusions:
- Heart failure patients demonstrate persistent myocardial fibroblast activation with distinct patterns based on etiology.
- Noninvasive [68Ga]FAPI-46 PET/MRI offers mechanistic insights into heart failure.
- This imaging approach may aid risk stratification and the development of targeted antifibrotic therapies.
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