Quantifying myocardial inflammation using F18-fluorodeoxyglucose positron emission tomography in cardiac sarcoidosis

Abstract

Sarcoidosis is a disease of unknown etiology which is characterized by the formation of non-caseating granulomas in multiple organs. Cardiac involvement in sarcoidosis, which occurs in at least one in four patients, is associated with a worse prognosis and significant morbidity from conduction abnormalities, arrhythmias, and congestive heart failure. Nevertheless, the diagnosis of cardiac sarcoidosis (CS) is often challenging, and relies on integrating both clinical and imaging findings. In addition to diagnosis, advanced imaging techniques such as cardiac magnetic resonance imaging (CMR) and cardiac positron emission tomography (PET) are now also being used to determine the risk of future adverse events, to identify which patients are most likely to benefit from immunosuppressive therapy, and to monitor response to therapy. Cardiac PET imaging for CS includes a rest myocardial perfusion imaging scan (using either NAmmonia or Rubidium) and an F-fluorodeoxyglucose (FDG) scan to identify areas of myocardial inflammation. Interpretation of the cardiac PET study is performed using a qualitative assessment with the perfusion and FDG images being simultaneously displayed (see Figure 1 for example). Rest myocardial perfusion defects may represent areas of scar related to fibrosis or areas of decreased perfusion from inflammation causing compression of the microvasculature. Following suppression of glucose uptake from the normal myocardium, and in the absence of coronary heart disease, which can be associated with hibernating myocardium, focal areas of FDG uptake represent active myocardial inflammation. Importantly, such abnormalities are not only useful for establishing the diagnosis of CS, but provide important prognostic information regarding a patient’s future risk of death or ventricular tachycardia. However, a limitation of FDG PET scans is that diffuse uptake of FDG may be visualized which is non-specific and due to either incomplete suppression of FDG from normal areas of myocardium vs diffuse inflammation. Such results—which despite ideal patient preparation occur *10%-15% of the time—may lead to inconclusive study results. However, there are no established quantitative methods that can reliably distinguish patients with diffuse FDG from inflammation related to CS from those who have benign uptake. Tahara et al have shown that heterogeneous myocardial FDG uptake is more common in CS patients and further data are needed regarding the discriminatory performance of this parameter among patients who have inconclusive FDG scans. To date, there is relatively little data on quantitative assessment of CS by PET imaging—with some studies evaluating the intensity of FDG uptake and only one prior study evaluating the extent of myocardial inflammation. The intensity of FDG uptake on PET can be measured by standardized uptake value (SUV), where a reader identifies voxels with FDG uptake, and the voxel with the highest intensity of FDG is used to define the SUVmax. The extent of FDG (e.g., SUV volume or volume of inflammation) can be measured by identifying voxels with an SUV intensity above a pre-defined threshold value. In this issue of the Journal of Nuclear Cardiology, Ahmadian et al propose a new method to quantify the Reprint requests: Ron Blankstein, MD, Non-Invasive Cardiovascular Imaging Program, Departments of Medicine (Cardiovascular Division) and Radiology, Brigham and Women’s Hospital, 75 Francis Street – Room Shapiro 5096, Boston, MA 02115; rblankstein@mgh. harvard.edu; rblankstein@partners.org J Nucl Cardiol 2014;21:940–3. 1071-3581/$34.00 Copyright 2014 American Society of Nuclear Cardiology.