Complete suppression of physiological FDG uptake achieved by means of more than 18 hr fasting with low carbohydrate diet in patients with cardiac sarcoidosis

2019 
380 Purpose: The physiological uptake of F-18 fluorodeoxyglucose (FDG) in the myocardium interferes with the diagnosis of cardiac sarcoidosis (CS). However, complete suppression of it in all the patients has not been reported (1-5). The initial aim of the study is to compare the suppression effects between a more than 18-h long fasting (LF) with low-carbohydrate diet (LCD) the day before PET and that with an additional unfractionated heparin (UFH) injection in healthy volunteers. The second aim is to apply the better method in a clinical setting. Methods: Thirty healthy, non-diabetic volunteers (16 males, range 45-71 y.o.) were participated in the randomized-control study. They were divided into 2 groups: 15 subjects with a >18-h overnight fast with LCD (less than 4 g) preparation (group A) and the other 15 subjects with an additional injection of UFH (50 IU/kg) 15 minutes prior to FDG injection (group B). At the 4 time points of 3 hours before, just before, 15 min after, and 1 hour after UFH injection, blood samples were obtained to measure free fatty acid (FFA), immunoreactive insulin (IRI), and fasting plasma glucose (FPG) level. Cardiac spot and whole body PET/CT imaging were performed 60 minutes after FDG injection. Then, PET images were visually assessed using a 4-point scale (grade 1, myocardial FDG uptake lower than hepatic uptake; grade 2, It is similar to that; grade 3, somewhat higher than that; and grade 4, evidently higher than that, and quantitatively assessed using myocardial maximum standard uptake value (SUVmax). Subsequently, 66 consecutive patients who were suspected of having CS according to the SNMMI/ASNC Expert Consensus Document (6) prospectively underwent FDG PET/CT after LF with LCD protocol. Final diagnosis of CS was determined by the updated Japanese Circulation Society Guidelines 2017 (7). Results: All subjects were well tolerated and completed the LF with LCD protocol. Fasting durations of group A and B were 1160±48 and 1160±66 min (n.s.), respectively. There were also no significant differences in serum levels of FPG and IRI between the two groups. Although the FFA levels of 15 min after heparin injection significantly increased in group B as compared to group A (1.55 ± 0.49 vs. 1.97 ± 0.58 mEq/L, p =0.039), there was no difference in SUVmax between the two groups (1.57±0.27 vs. 1.61±0.24, P=0.84). In addition, all participants showed grade 1 uptake in the myocardium, whose SUVmax was lower than those of the liver (1.58±0.26 vs. 1.91±0.33, P 7.0. An inverse correlation between the SUVmax and FFA levels before heparin injection were found in the group of non-diabetic subjects with glycohemoglobin < 6.5 (P=0.011, R=0.39), while no correlation was found between the SUVmax and IRI or FPG levels. Finally, it is obviously higher in active CS patients than those in non-CS (4.99 ± 2.24 vs.1.95 ± 0.55, p<0.0001, Figure). Thus, the suppression of physiological uptake in the myocardium was achieved in all patients without severe diabetes mellitus. Conclusions: The complete suppression of physiological FDG uptake in the myocardium is visually and quantitatively achieved by means of more than 18-h LF with LCD preparation protocol. Under the circumstances, UFH administration could not bring added value to the suppression. Nonetheless, attention needs to be paid to severe diabetic patients with insulin therapy or glycohemoglobin value exceeding 7.0.
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