Optimizing radionuclide imaging in the assessment of cardiac sarcoidosis.

Sarcoidosis is a disease of unknown etiology and is characterized by the development of non-caseating granulomas with a predilection for the pulmonary system. Involvement of the cardiovascular system ranges from 20% in the United States to over 75% in Japan. Up to 85% of sarcoid-related mortality results from cardiac sarcoidosis (CS). Observational studies suggest that early initiation of glucocorticoids may inhibit the inflammatory response to CS, thereby limiting fibrotic formation within the heart and ultimately improving long-term survival. Consequently, prompt and accurate diagnosis of CS is critical given its prognostic and therapeutic ramifications. Unfortunately, the diagnosis of CS has proven challenging since approximately half the of patients with CS are initially asymptomatic and, due to heterogenous myocardial involvement, CS detection by endomyocardial biopsy (EMB) has a sensitivity of only 20% to 30%. Gallium (Ga) singlephoton emission tomography (SPECT) is specific for CS but has a sensitivity of less than 40%. Non-radionuclide techniques for the diagnosis of CS include echocardiography which has a poor sensitivity (25%) and cardiac MRI which has substantially greater sensitivity for CS detection at 75% but may be contraindicated in some patients with suspected CS such as those with cardiac devices. Cardiac imaging with fluorine-18 fluorodeoxyglucose (FDG) positron emission tomography (PET) appears to have high diagnostic accuracy for CS as demonstrated in several observational studies. Consequently, experts have recently included cardiacFDGPET imaging in the standard diagnostic algorithm for CS. The gradual adoption of cardiacFDG-PET imaging as a standard of care in the assessment and treatment of CS underscores the need for studies focusing on standardization of patient preparation, imaging protocols, and interpretation of cardiacFDGPET imaging for CS. An important component of cardiac imaging with FDG-PET is patient preparation. The objective of patient preparation for an FDG-PET CS imaging protocol is to suppress physiologic myocardial FDG uptake in order to enhance detection of pathologic FDG uptake in inflamed tissues. Under postprandial conditions, increased serum insulin levels upregulate glucose transporter 1 and 2 (GLUT-1 and GLUT-2) which in turn facilitate myocyte glucose uptake. Therefore, diffuse myocardial FDG uptake in the nonfasting state may be a normal physiologic finding. In some healthy individuals, FDG uptake may be more heterogeneous, and may be present even in the fasting state. At the same time, inflamed tissue, such as that seen in CS, can also increase glucose utilization and result in elevated intramyocardial levels of FDG. The appearance of FDG uptake in inflamed tissues may be indistinguishable from heterogeneous or focal FDG uptake in healthy myocardium, underscoring the importance of suppression of normal physiologic myocardial FDG uptake. Current means of suppressing physiologic myocardial FDG uptake for CS PET imaging include (1) prolonged fasting, (2) low-carbohydrate diet (LCD) with or without high fat, and/or (3) use of intravenous unfractionated heparin (UFH) to stimulate lipolytic activity and increase free fatty acid (FFA) levels. Limited studies suggest varying degrees of efficacy of these protocols. Similarly, prior studies using other means of physiologic suppression such as shorter fasting protocols have noted varying degrees of myocardial FDG uptake in a majority of patients, Reprint requests: Panithaya Chareonthaitawee, MD, Division of Cardiovascular Diseases, Mayo Clinic, 200 First Street SW, Rochester, MN 55905; chareonthaitawee.panithaya@mayo.edu J Nucl Cardiol 2016;23:253–5. 1071-3581/$34.00 Copyright 2015 American Society of Nuclear Cardiology.