Cardiac Sarcoidosis (FDG PET)
FDG PET detects active myocardial inflammation in cardiac sarcoidosis, typically paired with a rest perfusion study: focal (or focal-on-diffuse) FDG uptake — especially with a resting perfusion defect in the same segment (the highest-risk pattern) — indicates active disease and guides immunosuppression. Pooled sensitivity is ≈89% and specificity ≈78%. Rigorous dietary preparation to suppress physiological myocardial uptake is essential. (See also the Infection & inflammation chapter.)
Sarcoid granulomas are metabolically active and take up FDG. Because normal myocardium also uses glucose, a high-fat/very-low-carbohydrate diet with prolonged fasting (± heparin) is required to suppress physiological uptake so that inflammation stands out.
When to image
- Suspected cardiac sarcoidosis (conduction disease, arrhythmia, unexplained cardiomyopathy in known sarcoid).
- Assessing disease activity to start or adjust immunosuppression.
- Monitoring response to therapy.
How to read it
- Focal or focal-on-diffuse FDG uptake indicates active inflammation.
- Focal FDG uptake in a segment with a resting perfusion defect indicates active inflammation with myocardial damage and predicts death/VT; a defect without FDG suggests scar.
- Interpret against the adequacy of dietary suppression.
Protocol
- Strict high-fat, very-low-carbohydrate diet then prolonged fast (± IV heparin).
- Rest perfusion imaging plus whole-heart FDG PET; whole-body coverage assesses extracardiac disease.
- Confirm suppression before interpreting.
Pitfalls
- Inadequate preparation → physiological uptake mimicking disease (the dominant pitfall).
- Lateral-wall physiological uptake can persist.
- Correlate with MRI, ECG and clinical context.
Evidence & guidelines
- Youssef et al. meta-analysis (J Nucl Med 2012; 7 studies, 164 patients, against Japanese MHLW criteria): sensitivity ≈89%, specificity ≈78%.
- Joint SNMMI/ASNC expert consensus on FDG PET for cardiac sarcoidosis (Chareonthaitawee et al., 2017).
- FDG PET assesses activity; MRI shows scar/oedema — often complementary.
In depth
- SNMMI/ASNC preparation: at least two high-fat (>35 g), low-carbohydrate (<3 g) meals the day before followed by a 4–12 h fast, or a fast of more than 18 h; a 50 IU/kg IV bolus of unfractionated heparin about 15 min before FDG is an optional adjunct. Non-specific myocardial uptake still occurs in up to 20% of patients.
- Pair FDG with rest perfusion imaging (¹³N-ammonia, ⁸²Rb or SPECT) to separate inflammation (FDG uptake with normal perfusion or a mismatch), fibrosis (perfusion defect without FDG), and mixed patterns.
- Focal or focal-on-diffuse FDG uptake matched to a perfusion defect (mismatch pattern) strongly suggests active cardiac sarcoidosis; FDG is described as absent, diffuse, focal or focal-on-diffuse, and diffuse homogeneous uptake usually reflects inadequate preparation.
- For follow-up, quantify intensity with SUVmax and extent with the volume of FDG-positive myocardium above an SUV threshold (or cardiac metabolic activity); a change is more likely to be real when both intensity and extent change in the same direction by at least 20%.
- A meta-analysis of FDG PET against Japanese MHLW criteria gave pooled sensitivity of 89% and specificity of 78%; the imperfect reference standard probably underestimates specificity.
- Isolated, homogeneous lateral-wall uptake without a perfusion defect is often non-specific, and non-attenuation-corrected images should be reviewed to avoid mistaking uptake around device leads on attenuation-corrected images for sarcoid.
- A perfusion defect plus abnormal FDG uptake carried about a four-fold risk of death or ventricular tachycardia (hazard ratio 3.9), and focal right ventricular FDG uptake identified a very high event rate.
Sources: Joint SNMMI–ASNC expert consensus 2017 (PMID 28770463 · J Nucl Med 2017, PMC6944184) · Joint SNMMI–ASNC expert consensus 2017 (PMID 28770463) · PMID 22228794 (Youssef, J Nucl Med 2012) · PMID 24140661 (Blankstein, JACC 2014)
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