Coronary disease & ACSCohort study
Myocardial Fibroblast Activation After Acute Myocardial Infarction
- Prospective observational imaging study
- hybrid PET-CMR
- matched controls
Authors' conclusion
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.
Study context
- Population
- Patients with acute MI
- Participants
- 40 / 19 / 20
- Exposure
- Acute MI vs chronic MI vs matched controls
- Acute MIn = 40
- Controln = 19reference
- Chronic MIn = 20
- Outcome
- Intensity, distribution and time-course of fibroblast activation ([68Ga]FAPI-46 TBRmax; burden as % myocardial involvement)
Main finding
As reported in the abstract
[68Ga]FAPI-46 burden vs late gadolinium enhancement burden (acute MI)
27.8% ± 12.4% vs 15.2% ± 10.6%; P < 0.001
Right ventricular involvement
One-third of patients
TBRmax at 1, 2, 4 and 12 weeks
4.0 ± 1.1, 3.7 ± 1.0, 3.1 ± 0.8, and 2.7 ± 0.7; P < 0.001
TBRmax Controls vs Chronic MI vs Acute MI
1.2 ± 0.1 vs 1.7 ± 0.5 vs 4.0 ± 1.1; P < 0.001
Observational data: associations, not effects.
Further findings
Baseline [68Ga]FAPI-46 burden vs remodelling · 1 year
- Correlation with lower LVEF
- r = −0.606
- Correlation with higher indexed LV end-diastolic volume
- r = 0.572
- Correlation with higher scar burden
- r = 0.871
- P < 0.001 for all
Remote myocardial [68Ga]FAPI-46 uptake
- Increased remote uptake associated with LV dilatation and systolic dysfunction
Original publication
Summarised from the published abstract; every number is checked against it