BACKGROUND:Cardiac 18F-fluorodeoxyglucose (18F-FDG) positron emission tomography preceded by extended fasting is used to demonstrate active cardiac sarcoidosis. However, physiological insulin-dependent myocardial 18F-FDG uptake often obscures 18F-FDG uptake in sarcoid lesions. We therefore aimed to completely suppress physiological myocardial 18F-FDG uptake by pharmaceutically blocking endogenous insulin secretion while elevating free fatty acids (FFAs). METHODS AND RESULTS:Six patients with suspected cardiac sarcoidosis were studied in a randomized cross-over design: (1) 12 hours fasting followed by 2 hours saline infusion (SALINE), and (2) 12 hours fasting followed by 2 hour infusions of somatostatin (300 μg/hour) and heparin (70 mIE/kg/minutes) (SOMA). 18F-FDG PET scans were performed post-infusion. Glucose, insulin, and FFA levels were measured and left ventricle SUV-values were recorded. During the SALINE infusion, insulin, glucose, and FFAs remained stable. By design, the SOMA infusions rapidly (<60 minutes) suppressed insulin completely, while FFA levels peaked at 1.13 ± 0.23 mM. However, SOMA infusions only suppressed cardiac 18F-FDG uptake insignificantly globally [SUVmean (g/mL): 4.0 ± 3.3 (SALINE) vs 2.4 ± 1.2 (SOMA), P = .15] and regionally. CONCLUSIONS: Complete insulin suppression combined with markedly increased circulating FFAs does not completely suppress physiological myocardial 18F-FDG uptake and thus conveys no extra diagnostic value compared with extended fasting.
RCT Entities:
BACKGROUND:Cardiac 18F-fluorodeoxyglucose (18F-FDG) positron emission tomography preceded by extended fasting is used to demonstrate active cardiac sarcoidosis. However, physiological insulin-dependent myocardial 18F-FDG uptake often obscures 18F-FDG uptake in sarcoid lesions. We therefore aimed to completely suppress physiological myocardial 18F-FDG uptake by pharmaceutically blocking endogenous insulin secretion while elevating free fatty acids (FFAs). METHODS AND RESULTS: Six patients with suspected cardiac sarcoidosis were studied in a randomized cross-over design: (1) 12 hours fasting followed by 2 hours saline infusion (SALINE), and (2) 12 hours fasting followed by 2 hour infusions of somatostatin (300 μg/hour) and heparin (70 mIE/kg/minutes) (SOMA). 18F-FDG PET scans were performed post-infusion. Glucose, insulin, and FFA levels were measured and left ventricle SUV-values were recorded. During the SALINE infusion, insulin, glucose, and FFAs remained stable. By design, the SOMA infusions rapidly (<60 minutes) suppressed insulin completely, while FFA levels peaked at 1.13 ± 0.23 mM. However, SOMA infusions only suppressed cardiac 18F-FDG uptake insignificantly globally [SUVmean (g/mL): 4.0 ± 3.3 (SALINE) vs 2.4 ± 1.2 (SOMA), P = .15] and regionally. CONCLUSIONS: Complete insulin suppression combined with markedly increased circulating FFAs does not completely suppress physiological myocardial 18F-FDG uptake and thus conveys no extra diagnostic value compared with extended fasting.
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