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.