Fluorine-18 fluorodeoxyglucose (18F-FDG) positron emission tomography/computer tomo-graphy (PET/CT) plays a critical role in the diagnosis and treatment assessment of indivi duals with suspected or known cardiac sarcoidosis (CS) and is included in diagnostic algorithms of multisociety guidelines
Diagnosis of active inflammation and assessment of response to treatment are the two primary indications for 18F-FDG PET/CT in CS.
Cardiac PET/CT imaging of perfusion and metabolism with 18F-FDG has the potential to risk stratify patients with CS for future cardiac events.
Several studies have shown the usefulness of 18F-FDG PET/CT as an additional tool in detecting infections associated with devices and grafts, now incorporated into guidelines for the management of infective endocarditis.
18F-FDG PET/CT has high sensitivity to detect infection in challenging causes of cardiac device infections and prosthetic valves, although the specificity may be low, particularly in the early postoperative period.
Molecular imaging with hybrid positron emission tomography/computer tomography (PET/CT) using fluorine-18 fluorodeoxyglucose (18F-FDG) is essential in oncology for the diagnosis and prognosis of malignancy. In cardiovascular medicine, 18F-FDG has historically been used for the assessment of myocardial hibernation/viability. More recently, the usefulness of 18F-FDG PET/CT has been investigated for the diagnosis of cardiac infections, such as cardiac implantable electronic device (CIED) infections, infective endocarditis (both native valve and prosthetic valve), and myocardial inflammatory conditions, such as sarcoidosis. This chapter will describe the role of 18F-FDG imaging for cardiac sarcoidosis (CS), which includes indications, patient preparation, imaging and reporting, as well as potential value in the assessment of treatment success. In addition, the role of 18F-FDG in assessing potential cardiovascular infections such as prosthetic cardiac valves, devices, and leads will also be discussed.
18F-FDG is a cyclotron-produced glucose analog with a half-life of 110 minutes. 18F-FDG undergoes facilitated diffusion across the cardiomyocyte sarcolemma (primarily through GLUT1 and GLUT4 channels),1 where it is phosphorylated by hexokinase to 18F-FDG-6-phosphate and is not metabolized further. The trapped 18F-FDG-6-phosphate within the cell provides the imaging signal, acting as a surrogate marker for cellular glucose metabolism, representing the integrated process of uptake and phosphorylation. GLUT1 and GLUT3 synthesis and cell membrane expression are upregulated in activated macrophages, which facilitate increased glucose utilization. In addition, circulating cytokines and growth factors are thought to increase the affinity of glucose transporters for 18F-FDG. This high glycolytic activity from infiltrates of active inflammatory cells is the rationale for utilizing 18F-FDG for imaging inflammation and infection. However, increased glucose uptake is not specific for inflammation. Myocardial ischemia, for example, is a potent stimulus for increased glucose utilization by increased cell surface mobilization of GLUT4 in cardiomyocytes through insulin-independent pathways. Therefore, the suppression of endogenous myocardial glucose utilization for the purpose of imaging inflammation is key to the technique and is discussed later in this chapter.
18F-FDG PET/CT IMAGING OF ...