Key result
Acute 18F-FAPI uptake mirrors 18F-FDG inflammatory extent in reperfused STEMI.
Why the study?
Does the spatial distribution and functional significance of myocardial fibroblast activation differ from inflammation in post-PCI STEMI patients?
Cross-Sectional (n=20)
No
Does the spatial distribution and functional significance of myocardial fibroblast activation differ from inflammation in post-PCI STEMI patients?
Fibroblast activation and inflammation demonstrate similar spatial extension beyond the infarct zone in early STEMI, but their distinct correlations with biomarkers suggest they reflect divergent mechanisms in post-infarction remodeling.
Background: Myocardial inflammation and fibroblast activation are key processes in post-infarction remodeling after ST-elevation myocardial infarction (STEMI). However, their relative contributions and functional implications remain incompletely understood, particularly in patients undergoing successful primary percutaneous coronary intervention (PCI). This study aimed to compare the extent and functional significance of myocardial fibroblast activation and inflammation using positron emission tomography/computed tomography (PET/CT) in patients with STEMI after successful PCI. Methods: Two groups of STEMI patients (n=10 per group) after primary PCI were retrospectively selected from two prospective studies at our institution. The two groups were matched for infarct size, age, and gender. They underwent fibroblast activation imaging with 18F-fibroblast activation protein inhibitor (18F-FAPI) or inflammation imaging with 18F-fluorodeoxyglucose (18F-FDG) using a physiological uptake suppression protocol. Imaging was performed 5±2 days after STEMI. The extent of tracer uptake (% of left ventricle) was obtained from the polar maps. Resting 99mTc-sestamibi myocardial perfusion imaging (MPI) was performed in all patients just before PET/CT to identify the infarct size. The mismatch ratio was calculated as the PET extent minus infarct size and divided by the infarct size. Left ventricular ejection fraction (LVEF), left ventricular end-diastolic volume (LVEDV), and left ventricular end-systolic volume (LVESV) were assessed by gated MPI. Results: The extent and mismatch ratio of 18F-FAPI were similar to those of 18F-FDG [extent: 37.5% (IQR, 25.8%, 45.3%) vs. 36.2% (IQR, 29.4%, 51.5%), P>0.99; mismatch ratio: 3.9% (IQR, 1.2%, 4.9%) vs. 1.5% (IQR, 0.9%, 6.2%), P=0.739]. 18F-FAPI extent positively correlated with circulating monocyte counts (r=0.763, P=0.010), B-type natriuretic peptide (BNP; r=0.717, P=0.019), and lactate dehydrogenase (LDH; r=0.672, P=0.033), whereas 18F-FDG extent correlated with creatine kinase (CK; r=0.874, P<0.001) and creatine kinase-MB (CK-MB; r=0.876, P<0.001). Additionally, 18F-FDG extent correlated positively with LVEDV (r=0.662, P=0.037) and LVESV (r=0.723, P=0.018). Notably, both the mismatch ratios of 18F-FDG and 18F-FAPI were negatively correlated with LVEDV (r=−0.638, P=0.047; r=−0.742, P=0.014, respectively), and the mismatch ratio of 18F-FAPI was negatively correlated with LVESV (r=−0.773, P=0.009). Conclusions: Fibroblast activation and inflammation exhibit similar spatial distribution beyond the infarct zone at the acute stage following STEMI. However, their associations with circulating biomarkers differ, implying divergent pathophysiological mechanisms and clinical implications. Although both processes are associated with global cardiac function, their regional impacts differ substantially, particularly between infarct and peri-infarct zones.
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Xi et al. (2026) conducted a cross-sectional in ST-elevation myocardial infarction (STEMI) (n=20). 18F-FAPI PET/CT imaging vs. 18F-FDG PET/CT imaging was evaluated on Extent of tracer uptake (% of left ventricle) (p=>0.99). The spatial extent of fibroblast activation assessed by 18F-FAPI (37.5%) was similar to inflammation assessed by 18F-FDG (36.2%) at the acute stage in reperfused STEMI patients (P>0.99).
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