4.6 Article

Visualization of Fibroblast Activation After Myocardial Infarction Using 68Ga-FAPI PET

Journal

CLINICAL NUCLEAR MEDICINE
Volume 46, Issue 10, Pages 807-813

Publisher

LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/RLU.0000000000003745

Keywords

acute coronary syndrome; cardiovascular imaging; FAPI; fibroblast activation; myocardial infarction; PET

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This retrospective analysis examined cardiac Ga-68-fibroblast-activation protein-alpha inhibitor (FAPI) uptake in patients after acute myocardial infarction (AMI) using PET, correlating FAPI uptake with biomarkers of myocardial damage and left ventricular function. The study found a strong correlation between fibroblast activation volume (FAV) and peak creatine kinase level, as well as an inverse correlation of FAV with left ventricular function. The imaging modality provided important insights into structural remodeling mechanisms after AMI at an early stage.
Aims The aim of this retrospective analysis was to examine the pattern of cardiac Ga-68-fibroblast-activation protein-alpha inhibitor (FAPI) uptake in patients after acute myocardial infarction (AMI) using PET and to investigate its association with results of coronary angiography. We correlated FAPI uptake with biomarkers of myocardial damage including left ventricular function. Methods and Results A cohort of 10 patients with no history of coronary artery disease underwent PET 18 +/- 20.6 days after AMI (ST-segment elevation myocardial infarction [n = 5] and non-ST-segment elevation infarction [n = 5]), respectively. SUVmax, SUVmean, and SUVpeak of localized tracer uptake were calculated; tracer uptake volume was reported as fibroblast activation volume (FAV), with imaging data being correlated with clinical parameters. Focal FAPI uptake was observed in all patients. Average uptake at 10 minutes postinjection was 8.9 +/- 4.4 (SUVmax), 7.6 +/- 4.0 (SUVpeak), and 5.3 +/- 2.8 (SUVmean), respectively. Affected myocardium showed a partial to complete match between tracer uptake and confirmed culprit lesion by coronary angiography in 44.4% and 55.6% of patients, respectively. A strong correlation between FAV and peak creatine kinase level (r = 0.90, P < 0.01) and inverse correlation of FAV with left ventricular function (r = -0.69, P < 0.05) was observed. Conclusions This analysis demonstrates in vivo visualization of fibroblast activation after AMI. The uptake area showed a very good agreement with the affected coronary territory. A strong correlation of the de novo established parameter FAV with left ventricular function and peak creatine kinase was observed. This imaging modality may provide important insights into mechanisms of structural remodeling after AMI at an early stage.

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