Evaluation of myocardial fibrosis and wall motion abnormality with 68Ga-FAPI PET/MR in coronary heart disease

Figures

• 

  Fig. 1. Flowchart Flow diagram showing participant selection details. FAPI = fibroblast activation protein inhibitor

• 

  Fig. 2. Representative images from a 58-year-old man with CHD. (A–L) Myocardial strain analysis. A–C: Curves of global radial strain, global circumferential strain, and global longitudinal strain were constructed automatically by software. D, H, I–L: Endocardial and epicardial borders drawn on 2-, 3-, and 4-chamber long-axis and short-axis images in the same end-diastolic phase. E–G: Regional radial strain, regional circumferential strain, and regional longitudinal strain; M–P: Short axis and 2-chamber view of fused 68 Ga–labeled fibroblast activation protein inhibitor (FAPI) PET/MR. Q–T: Short axis and 2-chamber view of late gadolinium enhancement (LGE) cardiac MRI. i–iv: Segmental FAPI uptake and LGE analyzed according to the AHA17-segment model

• 

  Fig. 3. Images illustrating different combinations of FAPI uptake and LGE. First column: FAPI (standardized uptake value [SUV]max < 1.5)/no significant LGE (FAPI inactive/MRI viable); second column: FAPI (SUVmax ≥ 1.5)/LGE transmural or subendocardial (FAPI active/MRI non-viable); third column: FAPI (SUVmax ≥ 1.5)/no significant LGE (FAPI active/MRI viable); fourth column: FAPI (SUVmax < 1.5)/LGE transmural or subendocardial (FAPI inactive/MRI non-viable)

• 

  Fig. 4. Scatter-box plots for PET parameters and wall motion abnormality evaluation. (A–C): PET parameters for overall study cohort. All participants exhibited regional moderate-to-intense fibroblast activation protein inhibitor (FAPI) uptake, standardized uptake value (SUV) parameters differed significantly between the focal myocardium and remote normal myocardium. SUVmax and SUVmean, but not SUVpeak, differed significantly between remote normal myocardium and adjacent skeletal muscle. (D–F): Regional wall motion assessment. FAPI active and MRI non-viable segments had higher wall motion abnormality scores than negative regions. In integrated analysis, the highest abnormal wall motion score was observed in the FAPI active/MRI non-viable group, with no obvious disparities in scores across the remaining groups

• 

  Fig. 5. Correlation matrix heatmap of FAPI uptake and clinical parameters. Regarding laboratory hematological data, SUVpeak of FAPI uptake was positively correlated with K time (R = 0.48; p = .046) and negatively correlated with Angle (R = − 0.52; p = .026). In addition, K time (R = 0.57; p = .014) was positively correlated with SUVmean and negatively correlated with Angle (R = − 0.56; p = .026)

• 

  Fig. 6. Corresponding photomicrograph for a 54-year-old man with ventricular aneurysm resection. A Mild-to-moderate interstitial fibrosis on hematoxylin and eosin-stained slides (magnification, 200 × ; scale, 0.5 mm). B FAP-positive fibroblasts were observed in the infarct area and border zone, but infrequently in the distal myocardium (magnification, 400 × ; scale, 0.5 mm). C Alpha-smooth muscle actin (α-SMA) and vimentin were highly expressed in FAP-positive cells (magnification, 200 × ; scale, 0.5 mm)