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


Journal

Clinical nuclear medicine
ISSN: 1536-0229
Titre abrégé: Clin Nucl Med
Pays: United States
ID NLM: 7611109

Informations de publication

Date de publication:
01 Oct 2021
Historique:
entrez: 3 9 2021
pubmed: 4 9 2021
medline: 16 10 2021
Statut: ppublish

Résumé

The aim of this retrospective analysis was to examine the pattern of cardiac 68Ga-fibroblast-activation protein-α 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. 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. 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.

Identifiants

pubmed: 34477601
doi: 10.1097/RLU.0000000000003745
pii: 00003072-202110000-00004
doi:

Substances chimiques

68Ga-FAPI 0
Quinolines 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

807-813

Informations de copyright

Copyright © 2021 Wolters Kluwer Health, Inc. All rights reserved.

Déclaration de conflit d'intérêts

Conflicts of interest and sources of funding: none declared.

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Auteurs

Lukas Kessler (L)

From the Department of Nuclear Medicine, University Hospital Essen.

Jana Kupusovic (J)

Department of Cardiology and Vascular Medicine, West German Heart and Vascular Center Essen.

Justin Ferdinandus (J)

From the Department of Nuclear Medicine, University Hospital Essen.

Nader Hirmas (N)

From the Department of Nuclear Medicine, University Hospital Essen.

Lale Umutlu (L)

Department of Diagnostic and Interventional Radiology, University Hospital Essen, University of Duisburg-Essen, Essen, Germany.

Fadi Zarrad (F)

From the Department of Nuclear Medicine, University Hospital Essen.

Michael Nader (M)

From the Department of Nuclear Medicine, University Hospital Essen.

Wolfgang P Fendler (WP)

From the Department of Nuclear Medicine, University Hospital Essen.

Matthias Totzeck (M)

Department of Cardiology and Vascular Medicine, West German Heart and Vascular Center Essen.

Reza Wakili (R)

Department of Cardiology and Vascular Medicine, West German Heart and Vascular Center Essen.

Thomas Schlosser (T)

Department of Diagnostic and Interventional Radiology, University Hospital Essen, University of Duisburg-Essen, Essen, Germany.

Tienush Rassaf (T)

Department of Cardiology and Vascular Medicine, West German Heart and Vascular Center Essen.

Christoph Rischpler (C)

From the Department of Nuclear Medicine, University Hospital Essen.

Johannes Siebermair (J)

Department of Cardiology and Vascular Medicine, West German Heart and Vascular Center Essen.

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