The Evaluation of Cardiac Sarcoidosis with ¹⁸F-FDG PET

DISCUSSION

Cardiac sarcoidosis represents the cause of death in 13%–25% of fatal cases of sarcoidosis (1). A definitive diagnosis of cardiac sarcoidosis can be made by endomyocardial biopsy, with sensitivity being less than 20% (2). For a definitive diagnosis and management, all patients will likely benefit from an echocardiogram and either cardiac MR imaging or ¹⁸F-FDG PET (1). Cardiac MR imaging is usually performed as the initial test in patients with suspected cardiac sarcoidosis. Gadolinium-enhanced cardiac MR imaging with delayed imaging has the benefit of high sensitivity and spatial resolution without radiation exposure. If the MR results are negative, ¹⁸F-FDG PET can be avoided. If the MR results suggest cardiac involvement, ¹⁸F-FDG PET imaging may be performed to establish baseline disease activity, assess the need for initiation of medical therapy, and monitor response to treatment over time. In patients with contraindications to cardiac MR imaging, ¹⁸F-FDG PET can be used as the first-line imaging method (1). Usually, cardiac MR imaging shows scarring, and thus chronic disease, whereas ¹⁸F-FDG PET identifies active involvement. Typical radionuclide protocols for imaging cardiac sarcoidosis include ¹⁸F-FDG PET for imaging inflammation combined with SPECT or PET myocardial perfusion imaging (1).

The myocardial perfusion assessment can be performed with ^99mTc, ²⁰¹Tl, ¹³N-ammonia, or ⁸²Rb-based radiotracers using standard protocols. Attenuation correction should be applied to SPECT myocardial perfusion imaging whenever possible. In the absence of coronary artery abnormalities, perfusion defects seen on PET scanning in a patient with sarcoidosis strongly suggest that the heart is involved (2). One way to describe the pattern in cardiac sarcoidosis on PET scans is to compare the degree of perfusion abnormality with the intensity of ¹⁸F-FDG uptake: normal (normal perfusion/normal ¹⁸F-FDG), early stage (mild perfusion defect/increased ¹⁸F-FDG), progressive stage (moderate perfusion defect/increased ¹⁸F-FDG), progressive myocardial impairment stage (severe perfusion defect/increased ¹⁸F-FDG), and fibrosis stage (severe perfusion defect/minimal or no ¹⁸F-FDG uptake) (1). We used this method, and the results were descriptive of the progressive myocardial impairment stage (Fig. 1). Our patient showed clinical improvement after 6 mo of treatment, and the PET findings resolved. ¹⁸F-FDG uptake was consistent with subsided inflammation, although clinical improvement (Fig. 2) is ultimately limited by the previous damage.