Key result
Persistent FDG-PET uptake after cardiac sarcoidosis treatment linked to ~3.2-fold higher MACE risk.
Why the study?
18F-FDG-PET imaging identifies inflammatory burden in cardiac sarcoidosis, but its utility in guiding immunosuppressive therapy intensity and predicting long-term outcomes remains incompletely characterized.
Does persistent myocardial glucose uptake (12-month SUVmax >4.5) on serial 18F-FDG-PET imaging predict major adverse cardiac events, mortality, and ventricular arrhythmias in patients with cardiac sarcoidosis undergoing immunosuppressive therapy?
Meta-Analysis (n=487)
Does persistent myocardial glucose uptake (12-month SUVmax >4.5) on serial 18F-FDG-PET imaging predict major adverse cardiac events, mortality, and ventricular arrhythmias in patients with cardiac sarcoidosis undergoing immunosuppressive therapy?
In patients with cardiac sarcoidosis on immunosuppressive therapy, persistent myocardial inflammation on 18F-FDG-PET at 12 months (SUVmax >4.5) strongly predicts MACE and ventricular arrhythmias, whereas complete metabolic normalization is associated with 94% 5-year arrhythmia-free survival.
Supports serial FDG-PET at 12 months for MACE/VT risk stratification in treated cardiac sarcoidosis; confirms metabolic response as a key prognostic marker.
Background Cardiac sarcoidosis (CS) causes 5% of sudden cardiac death in young patients but remains underdiagnosed. 18F-FDG-PET imaging identifies inflammatory burden; however, utility in guiding immunosuppressive therapy intensity and predicting long-term outcomes remains incompletely characterized. Recent evidence suggests FDG-PET-derived SUVmax at 12 months predicts mortality and arrhythmia risk superior to traditional markers. Objective To systematically evaluate FDG-PET quantitative parameters (SUVmax, TBR) for predicting major adverse cardiac events and fatal ventricular arrhythmias in CS patients undergoing immunosuppressive therapy via meta-analysis of prospective imaging studies. Methods MEDLINE, Embase, Cochrane CENTRAL (2015–January 2026) searched for prospective cohort studies in CS patients with serial FDG-PET imaging (baseline, 6-month, 12-month post-therapy). Inclusion: N≥20, documented immunosuppressive therapy (prednisolone-based ± steroid-sparing agents), reported quantitative FDG uptake (SUVmax, TBR), outcomes (MACE, ventricular tachycardia, sudden cardiac death). Primary outcomes: association of FDG-PET parameters with mortality and ventricular arrhythmia risk. Random-effects meta-analysis; I² heterogeneity assessment; subgroup analyses by therapy intensity (PSL dose), baseline LVEF, presence of late gadolinium enhancement on MRI. Results Eighteen studies (n=487 CS patients; 189 MACE events; median 3.8-year follow-up) included. Pooled analysis: 12-month SUVmax >4.5 independently predicted MACE (HR 3.2, 95% CI 2.1–4.9, p<0.001) and ventricular tachycardia (HR 2.8, 95% CI 1.6–4.8, p<0.001). Six-month SUVmax >3.5 also showed prognostic value (HR 2.1, 95% CI 1.4–3.2). Patients with complete metabolic response (SUVmax normalization at 12 months) demonstrated 5-year arrhythmia-free survival 94% versus 48% in persistent FDG uptake (p<0.001). LVEF <40% at baseline conferred additional mortality risk (HR 1.9). Prednisolone dose ≥10 mg daily associated with treatment failure and persistent FDG uptake. Conclusions FDG-PET SUVmax at 12 months is a critical prognostic biomarker in CS with superior predictive value for arrhythmia and mortality risk. Persistent FDG uptake predicts poor prognosis and may guide escalation to steroid-sparing immunosuppression. Integration of serial FDG-PET into CS management protocols is supported.
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Gohri et al. (2026) conducted a meta-analysis in Cardiac sarcoidosis (n=487). 12-month FDG-PET SUVmax >4.5 (persistent FDG uptake) vs. SUVmax ≤4.5 or complete metabolic response (SUVmax normalization at 12 months) was evaluated on Major adverse cardiac events (MACE) and ventricular tachycardia (HR 3.2, 95% CI 2.1-4.9, p=<0.001). 12-month FDG-PET SUVmax >4.5 in treated cardiac sarcoidosis independently predicted MACE (HR 3.2; 95% CI 2.1-4.9; p<0.001) and ventricular tachycardia (HR 2.8; 95% CI 1.6-4.8; p<0.001).
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