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Analysis of novel cardiac markers sST2 and IL-33 in chronic heart failure with reduced ejection fraction

Session Poster Session 7

Speaker Peter Jirak

Congress : ESC Congress 2019

  • Topic : basic science
  • Sub-topic : Basic Science - Cardiac Diseases: Biomarkers
  • Session type : Poster Session
  • FP Number : P6287

Authors : P Jirak (Salzburg,AT), M Lichtenauer (Salzburg,AT), B Wernly (Salzburg,AT), V Paar (Salzburg,AT), C Jung (Dusseldorf,DE), A Yilmaz (Schmalkalden,DE), U Hoppe (Salzburg,AT), PC Schulze (Jena,DE), D Kretzschmar (Jena,DE), R Pistulli (Münster,DE)

P Jirak1 , M Lichtenauer1 , B Wernly1 , V Paar1 , C Jung2 , A Yilmaz3 , U Hoppe1 , PC Schulze4 , D Kretzschmar4 , R Pistulli5 , 1Universitaetsklinikum Salzburg - Salzburg - Austria , 2University Hospital Dusseldorf, Division of Cardiology, Pulmonology, and Vascular Medicine - Dusseldorf - Germany , 3Elisabeth Klinikum , Clinic of Internal Medicine II - Schmalkalden - Germany , 4University Hospital of Jena, Department of Internal Medicine I, Division of Cardiology, Angiology, Pneumology and Intensive Medic - Jena - Germany , 5University Medical Center, Coronary and Peripheral Vascular Disease, Heart Failure - Münster - Germany ,


BACKGROUND: Soluble (s) ST-2 has been recently evaluated as a monitoring parameter in heart failure (HF). Besides being a marker for cardiac strain and hemodynamic stress, studies also found an influence of ST2 on the immune system, above all mediated through its Janus-Face ligand IL-33, an alarmin released under stress conditions or by cellular death.  In contrast to sST2, the role of IL-33 in HF is yet unknown.

OBJECTIVE: In this project, we aimed for an analysis of the ST2/IL33 pathway in patients with heart failure with reduced ejection fraction (HFrEF).

METHODS: In total, 200 patients were included in the study: 59 with ischemic (ICM), 65 with dilated (DCM) cardiomyopathy (mean LVEF 38%), as well as 76 control patients without coronary artery disease or signs of heart failure. Serum samples were analyzed by use of ELISA after informed consent.

RESULTS: sST2 showed a significant elevation in all HF patients (p<0.0001) compared to the control group. No significant differences in levels of sST2 were observed between ICM and DCM patients. In contrast to sST2, no differences between HF patients and control group were observed for IL-33. Furthermore, sST2 showed a significant correlation with CRP (p<0.001, r=0.28), NT-pro-BNP (p<0.0001, r=0.40) and an inverse correlation with ejection fraction (p<0.0001, r=-0.40). Additionally, sST2 showed a significant elevation in patients in NYHA stages I-II (p=0.030) and NYHA stages III-IV (p<0.01). Again, no significant correlations were observed between IL-33 and parameters mentioned above.

CONCLUSIONS: We observed a significant increase and correlation with disease severity of sST2 in chronic HFrEF patients of both ischemic and non-ischemic origin, but contrary to our expectations, no significant changes in serum levels of IL-33. Thus, a mechanism independent of ST2/IL33 axis could be responsible of sST2 secretion in HF. Further studies including acute decompensated patients could provide a better understanding of the IL-33 role in HF.

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