Key result
18F-FOL PET shows ~5-fold higher uptake in inflamed myocardium compared to non-inflamed controls.
Why the study?
Currently available imaging techniques have limited specificity for detecting active myocardial inflammation, motivating evaluation of 18F-FOL PET targeting FR-β on activated macrophages.
Does 18F-FOL PET imaging detect active myocardial inflammation in a rat model of autoimmune myocarditis?
Does 18F-FOL PET imaging detect active myocardial inflammation in a rat model of autoimmune myocarditis?
Absolute Event Rate: 2.1% vs 0.4%
p-value: p=<0.01
18F-FOL PET imaging specifically targets FR-β expressing macrophages, offering a potential novel approach for detecting active myocardial inflammation.
Hypothesis-generating for FR-β–targeted PET in myocarditis; human studies required before clinical consideration.
Currently available imaging techniques have limited specificity for the detection of active myocardial inflammation. Aluminum 18F-labeled 1,4,7-triazacyclononane-N,N′,N″-triacetic acid conjugated folate (18F-FOL) is a PET tracer targeting folate receptor β (FR-β), which is expressed on activated macrophages at sites of inflammation. We evaluated 18F-FOL PET for the detection of myocardial inflammation in rats with autoimmune myocarditis and studied the expression of FR-β in human cardiac sarcoidosis specimens. Methods: Myocarditis was induced by immunizing rats (n = 18) with porcine cardiac myosin in complete Freund adjuvant. Control rats (n = 6) were injected with Freund adjuvant alone. 18F-FOL was intravenously injected, followed by imaging with a small-animal PET/CT scanner and autoradiography. Contrast-enhanced high-resolution CT or 18F-FDG PET images were used for coregistration. Rat tissue sections and myocardial autopsy samples from 6 patients with cardiac sarcoidosis were studied for macrophages and FR-β. Results: The myocardium of 10 of 18 immunized rats showed focal macrophage-rich inflammatory lesions, with FR-β expression occurring mainly in M1-polarized macrophages. PET images showed focal myocardial 18F-FOL uptake colocalizing with inflammatory lesions (SUVmean, 2.1 ± 1.1), whereas uptake in the remote myocardium of immunized rats and controls was low (SUVmean, 0.4 ± 0.2 and 0.4 ± 0.1, respectively; P < 0.01). Ex vivo autoradiography of tissue sections confirmed uptake of 18F-FOL in myocardial inflammatory lesions. Uptake of 18F-FOL in inflamed myocardium was efficiently blocked by a nonlabeled FR-β ligand folate glucosamine in vivo. The myocardium of patients with cardiac sarcoidosis showed many FR-β–positive macrophages in inflammatory lesions. Conclusion: In a rat model of autoimmune myocarditis, 18F-FOL shows specific uptake in inflamed myocardium containing macrophages expressing FR-β, which were also present in human cardiac sarcoid lesions. Imaging of FR-β expression is a potential approach for the detection of active myocardial inflammation.
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Jahandideh et al. (2020) studied Autoimmune myocarditis and cardiac sarcoidosis (n=30). 18F-FOL PET imaging vs. Remote myocardium and control rats was evaluated on Myocardial 18F-FOL uptake (SUVmean) (p=<0.01). 18F-FOL PET imaging demonstrated significantly higher uptake in focal myocardial inflammatory lesions compared to remote myocardium and controls (SUVmean 2.1 vs 0.4; P<0.01).
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