Clin Res Cardiol (2023). https://doi.org/10.1007/s00392-023-02180-w

Serum soluble interleukin 2-receptor to monitor inflammatory activity in patients with cardiac sarcoidosis and ventricular arrhythmias

S. Min1, M. Ulbrich1, T. Kling1, C. Reithmann1

1Medizinische Klinik I, Kardiologie, Helios Klinikum München West, München;

Introduction: Advanced cardiac imaging with cardiac magnetic resonance imaging (cMRI) and flourodeoxyglucose (FDG) positron-emission tomography (PET) are standard of care to monitor the progress of myocardial inflammation in patients with cardiac sarcoidosis. However, the utility of cMRI may be limited even in patients with MRI-compatible pacemakers and defibrillators by artifacts. FDG-PET may be limited by adequate dietary preparation before PET and availability. Recently, the serum biomarker soluble interleukin  2-receptor (sIL2-R) has been shown to be superior to serum angiotensin converting enzyme (ACE) in the detection of inflammatory activity in patients with cardiac sarcoidosis presenting with ventricular arrhythmias (VA). Aims: The purpose of this study was to examine whether close monitoring of serum sIL2-R may be helpful during the follow-up in the prevention of recurrences of VA in patients with cardiac sarcoidosis. Patients and methods: 21 patients with biopsy-proven cardiac sarcoidosis presented with ventricular fibrillation (VF) (n=3), sustained ventricular tachycardia (VT) (n=9), non-sustained VT (n=4), and frequent ventricular extrasystoles (n=5) between 2009 and 2022. All patients underwent cMRI and determination of serum biomarkers. Active inflammation was defined as signal enhancement in T2-weighted cMRI in combination with the typical pattern of delayed enhancement cMRI. Patients had close follow-up in our outpatient clinic after initiation or enhancement of immunosuppressive therapy, catheter ablation of VT or initiation of antiarrhythmic drug therapy. Results: At initial presentation in our institution, active inflammation was detected in 12 patients and chronic fibrotic stage in 9 patients. Serum sIL2-R levels were higher in the active inflammatory stage (855+-399 U/ml) compared to the chronic fibrotic stage (377+-146 U/ml) (normal range 158-623 U/ml) whereas serum ACE levels were not significantly different. Upon initiation or enhancement of immunosuppressive therapy with corticosteroids and methotrexate or azathioprine, sIL2-R decreased from 791+-305 U/ml to 350+-115 U/ml. Close monitoring of serum biomarkers contributed to guidance and titration of immunosuppressive therapy in 10 patients. During the follow-up of 53+-46 months, 8 of the 21 patients had at least one recurrence of symptomatic sustained VT or VF, and 2 patients had to undergo heart transplantation. Findings from cMRI and/or FDG-PET, in correlation with changes in sIL2-R levels, suggested that recurrences of VA were due to progression or relapse of inflammation in 2 patients and were associated with chronic fibrotic stage in 6 patients. Conclusions: Serum sIL2-R seems to correlate with active inflammation in cardiac sarcoidosis. Close monitoring of sIL2-R can possibly predict progression or relapse of inflammation after discontinuation of immunosuppressive therapy. Thus, monitoring of sIL2-R can help to prevent recurrences of VA associated with active inflammation but most recurrences of VA are apparently associated with scarring in chronic fibrotic stage.

https://dgk.org/kongress_programme/jt2023/aV247.html