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Relapse in cardiac sarcoidosis: Patterns and predictors on serial 18F-fluorodeoxyglucose positron emission tomography
Ferdinand Jr Gerodias1, Lucas C Godoy2, Karl Magtibay3
1Robert J. Burns Nuclear Cardiology Laboratory, University Health Network, Toronto Western Hospital, 399 Bathurst Street, Toronto, ON, M5T 2S8, Canada; Division of Cardiology, Peter Munk Cardiac Centre and Ted Rogers Centre for Heart Research, University Health Network, Toronto, ON, M5G 2N2, Canada; Stephenson Cardiac Imaging Centre, Libin Cardiovascular Institute, University of Calgary, Foothills Medical Centre, Calgary, AB, T2N 2T9, Canada.
Background:
Cardiac sarcoidosis follows a relapsing-remitting course, but imaging patterns and predictors of relapse remain poorly defined. The aim of this study was to characterize spatial and metabolic features of relapse in cardiac sarcoidosis and identify predictors using serial 18F-fluorodeoxyglucose positron emission tomography (FDG-PET).
Methods:
Patients with cardiac sarcoidosis who underwent three serial FDG-PET-baseline (PET 1), response (PET 2), and follow-up (PET 3)-at a tertiary center in Toronto, Canada (2011-2024), were included in the study. Eligibility required abnormal myocardial FDG uptake at PET 1 and metabolic response at PET 2, defined as ≥20% reduction in total cardiac metabolic activity (tCMA) relative to PET 1. Left ventricular segmental FDG analysis assessed spatial patterns. Candidate predictors included baseline inflammatory burden and response-phase imaging features. Imaging-defined relapse was defined as a ≥20% increase in tCMA from PET 2 to PET 3. Logistic regression identified predictors.
Results:
Among 50 patients (median age: 54 years; 60% male), 23 (46%) had relapse. Most relapses (91%) occurred in previously affected myocardial segments, with 70% showing lower FDG intensity and extent. Relapsed patients had higher baseline tCMA (564.0 vs 120.1; P = 0.006) and more extracardiac involvement (2.61 vs 1.19 organs; P = 0.01). Higher odds of relapse were observed among patients with residual myocardial FDG uptake (adjusted odds ratio: 5.30; 95% confidence interval: 1.14-29.13; P = 0.039).
Conclusions:
Relapse occurred in nearly half of patients after an initial response, typically involving previously affected myocardial regions with lower inflammatory burden. Residual FDG uptake on response-phase imaging was associated with relapse, supporting the role of serial FDG-PET for surveillance in cardiac sarcoidosis.
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