ABSTRACT
ObjectiveCOVID-19 primarily causes pneumonitis but can also cause myocarditis. Injury may be due to a generalised inflammatory immune process or by direct viral infection. Using 18F-fluorodeoxyglucose positron emission tomography/computed tomography (18F-FDG-PET/CT) and cardiac magnetic resonance (CMR) imaging we correlated the metabolic activity/injury between the reticuloendothelial system (bone marrow [BM] and spleen) and myocardial/pulmonary tissue.Methods18F-FDG-PET/CT (n=29, fasted n=27) and CMR (n=23) were performed on hospitalised patients with acute COVID-19. 18F-FDG PET/CT standardised uptake values (SUV) were measured in the spleen, spinal BM, myocardial and pulmonary tissue. Cardiac target-to-background ratio (TBR) was calculated by indexing to blood-pool SUV. Myocarditis was assessed using the sensitive 2018 Lake Louise criteria (LLC), and viral load (by cycle threshold).Results13 patients had myocarditis on CMR (57%), 8 (30%) visually on 18F-FDG-PET/CT. There was no statistical difference comparing LLC positive and negative patients for BM (4.21±0.30, 4.98±0.56, P=0.23), spleen (4.40±0.40, 5.15±0.08, P=0.38) and lung (4.08±0.72, 4.16±0.91, P=0.94) SUV. Lung SUV was significantly associated with BM (r=0.61, P<0.001) and spleen (r=0.48, P<0.05) SUV. Cardiac TBR, T1 and T2 mapping showed no significant association with BM and spleen SUV (P>0.05 for all). Cycle threshold did not correlate with either cardiac TBR and T1 or T2 (p>0.05 for all).ConclusionReticuloendothelial system activation strongly correlated with lung activity, suggesting pulmonary injury is part of a systemic inflammatory process. Cardiac inflammation was not associated with either spleen, BM or viral load, suggesting injury is multifactorial.