Abstract 18847: Visualization of Inflammation and Characterization of Lesions in Viral Myocarditis Mouse Model by Combined 19F-MR Cell Tracking and 1H Cardiac MRI
Introduction Myocarditis is a challenging disease for diagnosis and treatment. Recently, we have established a non-invasive cellular 19F-MR method to visualize inflammation of myocarditis in mice . In this study, we correlated detection of inflammation by 19F-MR and tissue characterization by 1H-MR in viral myocarditis mouse model.
Methods Viral myocarditis was induced by infecting ABY mice (n=5 infected+3 control) with CVB3. 19F-perfluorocarbon emulsion (PFC) (150μl) was injected i.v. 13 days post-infection to label monocytes and macrophages in blood. The labeling efficiency was examined by FACS in blood samples. 19F/1H-images were acquired at a 7T MR. 19F-MRI was superimposed on 1H-Cine to localize inflammation in myocardium. Lesions were characterized by T2WI, T2*WI and Gd-DTPA enhancement. MR findings were examined by Histology and immunohistochemistry (IHC).
Results Blood FACS and confocal microscopy on IHC revealed that the 19F-MR signal in myocardium was due to internalized PFC in macrophages. 19F-MR detected macrophage infiltrating myocarditis lesions. Edema and Gd enhancement could be found in some lesions. Interestingly, most patchy 19F signal co-localized with T2* hypo-intense signal in lesions, which has been reported in various mouse strains post CVB3 infection . Necrosis, T cells, fibrosis, and mineral deposition were found in lesions by histology and IHC.
Conclusion 19F-MRI unambiguously detected active recruitment of macrophages to myocarditis lesions. On T2*WI signal voids in lesions were closely related to 19F signal in location and volume, which indicates its association to inflammation. Caution should be taken to apply iron oxide particles to visualizing inflammation in viral myocarditis, while the significance and mechanism of this contrast, especially its existence in human, need further investigation. 1. Ye et al ISMRM proceeding 2012. 2. Helluy et al. ISMRM proceeding 2011. This work was supported partly by BMBF 01EZ0816.
- © 2012 by American Heart Association, Inc.