T2 mapping is a valuable tool for monitoring inflammation in cardiac sarcoidosis during immunosuppressive therapy

Julia-Mareen Treiber (Bad Nauheim)1, J. S. Wolter (Bad Nauheim)1, A. Rieth (Bad Nauheim)1, S. Kriechbaum (Bad Nauheim)1, M. Weferling (Bad Nauheim)1, C. W. Hamm (Gießen)2, S. T. Sossalla (Gießen)2, A. Rolf (Bad Nauheim)1

1Kerckhoff Klinik GmbH Abteilung für Kardiologie Bad Nauheim, Deutschland; 2Universitätsklinikum Gießen und Marburg GmbH Medizinische Klinik I - Kardiologie und Angiologie Gießen, Deutschland


Background: Cardiac sarcoidosis (CS) is a potentially life-threatening inflammatory disease that requires high-dose immunosuppressive therapy. Monitoring the effectiveness of immunosuppression in CS is of utmost importance. T2 mapping has been shown to be ideally suited to monitoring convalescence in viral myocarditis and autoimmune disease; however, T2 mapping data for CS are lacking.

Objective: The aim is to assess the suitability of cardiac magnetic resonance (CMR) T2 mapping for evaluating myocardial inflammation during therapy in CS. 

Methods: Between 2017 and 2023 we retrospectively enrolled patients diagnosed with active CS based on the Japanese Circulation Society consensus statement who underwent CMR and 18FDG-PET-CT and who received standard heart failure therapy and high-dose immunosuppressive therapy. Follow-up CMR was performed after at least 6 months of therapy. Patients were evaluated for changes in morphological parameters including end-diastolic (EDVi) and end-systolic volume index (ESVi), functional parameters including ejection fraction (EF) and global longitudinal strain (GLS), and tissue characteristics including global and regional native T1 and T2 mapping, global and regional extracellular volume (ECV), and relative late gadolinium enhancement mass (rLGEmass) at baseline and during therapy. 

Results: Since 2017 we found 48 with active CS confirmed by CMR and FDG-PET-CT and 26 who underwent follow-up CMR. Only global (39 ± 2.3 ms vs. 36.6 ± 2.5 ms, p = 0.002) and regional T2 mapping (44.2 ± 5.7 ms vs. 40.7 ± 5.0 ms, p = 0.004) as well as rLGEmass (24 ± 15 % vs. 20 ± 14 %; p = 0.03) showed significant improvements during therapy. No significant difference was found for the functional parameters EF (45 ± 8 % vs. 45 ± 13 %, p =0.87) and GLS (-12.8 ± 3.8 % vs. -11.4 ± 7.6 %, p = 0.42), the morphological parameters EDVi (103 ± 23 ml/m2 vs. 100 ± 22 ml/m2, p = 0.41) and ESVi (63 ± 23 ml/m2 vs. 57 ± 26 ml/m2, p = 0.25), or the structural changes measured by native T1 mapping (1152 ± 48 ms vs. 1130 ± 37 ms, p = 0.13) and rLGE­mass­ (0.28 ± 0.07 % vs. 0.26 ± 0.02 %, p = 0.012).


Conclusion: CMR T2 mapping is a valuable tool for monitoring myocardial inflammation during therapy for CS. The primary impact of immunosuppressive treatment appears to be to reduce cardiac inflammation rather than improve remodelling.   



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