sST2 and Heart Failure—Clinical Utility and Prognosis

Abstract

New parameters and markers are constantly being sought to help better assess patients with heart failure (HF). ST2 protein has gained interest as a potential biomarker in cardiovascular disease. It is known that the IL-33/ST2L system belongs to the cardioprotective pathway, which prevents the fibrosis, hypertrophy, and apoptosis of cardiomyocytes and also inhibits the inflammatory response. Soluble ST2 (sST2) is involved in the immune response and secreted in response to the mechanical overload of the myocardium, thus providing information on the processes of myocardial remodeling and fibrosis. A total of 110 hospitalized patients diagnosed with heart failure with reduced ejection fraction (HFrEF) were included in the study. Clinical and biochemical parameters were studied. During the follow-up, 30.9% patients died and 57.3% patients reached the composite endpoint. Using ROC curves, the reference cut-off point for sST2 was determined to be 45.818 pg/mL for all-cause deaths. Significantly higher concentrations of inflammatory parameters and natriuretic peptides were found in the group of patients with higher sST2 concentrations. sST2 protein is an independent risk factor for all-cause deaths of patients with HFrEF.

Soluble ST2 in Heart Failure: A Clinical Role beyond B-Type Natriuretic Peptide

“…Some of these have been more convincing and are used in some clinics today. Of particular prominence is soluble ST2 (sST2) [1], which was first classified as an indicator of ventricular myocyte stress [6], but is mainly produced in extracardiac tissues [7] in response to inflammatory and fibrotic stimuli [8], representing an indicator of the myocardial fibrotic process and a predictor of cardiac remodeling [9][10][11].…”

Correlations between soluble ST2 concentration and the nutritional status in patients with heart failure with reduced ejection fraction — cross-sectional study

“…Soluble ST2 (sST2) acts as a decoy receptor, directly bound to IL-33, and suppresses activation of JNK (c-Jun N-terminal kinase), NF-κB (nuclear factor kappa-light-chain-enhancer of activated B cells) and ERK (extracellular signalregulated kinases), reversing the beneficial effects of the IL-33/ST2 system, thus destabilizing the defense mechanism. The association between sST2 and mortality rates was confirmed in patients with acute [10][11][12][13], chronic decompensated [14] and chronic HF [3,15,16]. Moreover, the association was observed regardless of the left ventricular ejection fraction (LVEF) values, as well as in patients with reduced ejection fraction (HFrEF) [3,17,18].…”

Mechanisms of myocardial reverse remodelling and its clinical significance: A scientific statement of the ESC Working Group on Myocardial Function

“…Indeed, elevated sST2 levels are a strong indicator of AR and predict a lower likelihood of RR and clinical recovery. 207,208 Conversely, in stable ischaemic heart disease patients, invasive therapy needs to be cautiously considered in the setting of angina burden and background medical therapy. 132 Indeed, in patients with stable coronary disease and severe or moderate ischaemia, an initial invasive strategy did not reduce the risk of ischaemic cardiovascular events or death from any cause, compared with a conservative approach.…”