Sensitivity and specificity of soluble interleukin-2 receptor combined with cardiac imaging for diagnosing inflammatory cardiac sarcoidosis

T. Kling (München)1, M. Ulbrich (München)1, C. Reithmann (München)1
1Helios Klinikum München West Medizinische Klinik I, Kardiologie München, Deutschland
Background: At present, serum biomarkers such as soluble interleukin-2 receptor (sIL-2 R) and angiotensin converting enzyme (ACE) are not ready for clinical use in diagnosing cardiac sarcoidosis. Ventricular arrhythmias and higher degree atrioventricular (AV) block are clinical manifestations of cardiac sarcoidosis.
Aims: The purpose of the study was to evaluate the role of sIL-2 R and ACE in the process of diagnosing cardiac sarcoidosis in patients with ventricular arrhythmias and/or AV block who are suspected for cardiac sarcoidosis among other diseases.
Patients and methods: 66 patients (45 male, 49+-14 years) with unexplained ventricular arrhythmias and/or AV block suspected for cardiac sarcoidosis or other inflammatory cardiac diseases were included in the study. All patients underwent cardiac imaging using cardiac magnetic resonance imaging (cMRI) (n=56) and/or fluorodeoxy glucose positron emisson tomography (FDG-PET) (n=16). Serum sIL2-R and ACE were determined in all patients. If cMRI or FDG-PET suggested a high probability of cardiac sarcoidosis, other cardiac storage disease or inflammatory cardiomyopathy, myocardial biopsy was performed. Active inflammatory cardiac sarcoidosis was defined as a signal enhancement in T2-weighted cMRI or an enhanced myocardial FDG uptake in FDG-PET.
Results: Findings from cMRI and/or FDG-PET were consistent with the differential diagnosis of cardiac sarcoidosis in 43 patients. Increased levels of sIL-2 R (>623 U/ml) were detected in 23 patients and increased levels of ACE (> 70 U/l) in 6 patients. 33 patients were diagnosed with biopsy-proven cardiac sarcoidosis. Among the 33 patients with cardiac sarcoidosis, active inflammatory cardiac sarcoidosis was found in 18 patients and chronic fibrotic state of cardiac sarcoidosis in 15 patients. Increased levels of sIL-2 R were found in 14 patients with active inflammatory cardiac sarcoidosis, no patient with chronic fibrotic state of cardiac sarcoidosis and in 9 patients with non-sarcoidosis diseases (myocarditis, n=4; giant cell myocarditis, n=1; inflammatory cardiomyopathy, n=2; other infectious diseases, n = 2).  Increased levels of ACE were found in 6 patients with cardiac sarcoidosis. The sensitivity and specificity of sIL-2 R combined with cardiac imaging to detect inflammatory cardiac sarcoidosis in patients with ventricular arrhythmias or AV block was 82,4 and 81,2 %, respectively. The sensitivity of ACE was low (< 30 %).
Conclusions: Serum sIL-2 R can be a useful tool in the process of diagnosing inflammatory cardiac sarcoidosis when combined with cardiac imaging in patients with ventricular arrhythmias and higher degree AV block.