Journal of nuclear cardiology : official publication of the American Society of Nuclear Cardiology · 2017
Effect of prolonged fasting and low molecular weight heparin or warfarin therapies on 2-deoxy-2-[18F]-fluoro-D-glucose PET cardiac uptake.
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Giorgetti Assuero, Marras Gavino, Genovesi Dario, Filidei Elena, Bottoni Antonio, Mangione Maurizio, Emdin Michele, Marzullo Paolo
Аннотация
BACKGROUND: Whether anticoagulants other than unfractionated heparin are able to suppress cardiac PET uptake of 2-deoxy-2-[18F]-fluoro-D-glucose (18F-FDG) is unknown.
METHODS: One-hundred-seventy-four patients without history and clinical evidence of cardiac dysfunction and/or coronary heart disease underwent a 18F-FDG PET/CT study. All patients were studied with a >12-hours fasting and divided into 2 groups: group-1 without anticoagulant therapy (n:75); group-2 patients on low molecular weight heparin (n:60) or warfarin therapy (n:39). Cardiac 18F-FDG uptake was estimated qualitatively using a 4-point scale and semiquantitatively as total LV glycolysis (LVG) and metabolic volume (MV), drawing isocontour volume of interest (VOI) including the whole LV.
RESULTS: Qualitatively, LV 18-FDG uptake was scored 0 or 1, indicating a good suppression, in 10/75 (13%) patients of group-1 and 77/99 (78%) of group-2 (p < .001). Semiquantitatively, patients of group-1 showed higher values of 18-FDG uptake than patients of group-2, assessed as LVG (802,649 ± 468,442 vs 198,989 ± 261,439, p < .0001) or MV (219 ± 77 vs 57 ± 48 cm3, p < .0001). Subanalysis for anticoagulant drugs showed similar results.
CONCLUSIONS: Prolonged fasting combined to anticoagulants other than unfractionated heparin is able to minimize glucose cardiac metabolism. Our data confirm previous observation on the possibility to influence the metabolic pattern of the heart before the PET scan and broadens the spectrum of pharmacological options.
METHODS: One-hundred-seventy-four patients without history and clinical evidence of cardiac dysfunction and/or coronary heart disease underwent a 18F-FDG PET/CT study. All patients were studied with a >12-hours fasting and divided into 2 groups: group-1 without anticoagulant therapy (n:75); group-2 patients on low molecular weight heparin (n:60) or warfarin therapy (n:39). Cardiac 18F-FDG uptake was estimated qualitatively using a 4-point scale and semiquantitatively as total LV glycolysis (LVG) and metabolic volume (MV), drawing isocontour volume of interest (VOI) including the whole LV.
RESULTS: Qualitatively, LV 18-FDG uptake was scored 0 or 1, indicating a good suppression, in 10/75 (13%) patients of group-1 and 77/99 (78%) of group-2 (p < .001). Semiquantitatively, patients of group-1 showed higher values of 18-FDG uptake than patients of group-2, assessed as LVG (802,649 ± 468,442 vs 198,989 ± 261,439, p < .0001) or MV (219 ± 77 vs 57 ± 48 cm3, p < .0001). Subanalysis for anticoagulant drugs showed similar results.
CONCLUSIONS: Prolonged fasting combined to anticoagulants other than unfractionated heparin is able to minimize glucose cardiac metabolism. Our data confirm previous observation on the possibility to influence the metabolic pattern of the heart before the PET scan and broadens the spectrum of pharmacological options.