Association of galectin-3 and soluble ST2 with in-hospital and one-year outcomes in patients with ST-segment elevation myocardial infarction treated with primary percutaneous coronary intervention

Abstract

INTRODUCTION Galectin-3 (Gal-3) and soluble interleukin-1 receptor-like 1 (sST2) have known prognostic value in already diagnosed heart failure (HF). OBJECTIVES To investigate the association of Gal-3 and sST2 with prognosis in patients with ST-segment elevation myocardial infarction (STEMI) treated with primary percutaneous coronary intervention (pPCI). PATIENTS AND METHODS The analysis was based on data collected in a prospective observational BIOSTRAT (Biomarkers for Risk Stratification After STEMI; ClinicalTrials.gov identifier, NCT03735719) study. Analysis included 117 patients with first-time STEMI treated with pPCI. Serum for Gal-3 and sST2 was sampled 72 to 96 hours after admission due to STEMI. The patients were followed for the primary endpoint (cardiovascular [CV] death or HF hospitalization at 1 year). RESULTS Both biomarkers correlated with N-terminal pro-B-type natriuretic peptide (NT-proBNP); Gal-3 correlated with older age. Data on the primary endpoint were available for 104 patients (89%). At 1-year follow-up, 9 patients (8.7%) reached the primary endpoint. In univariate Cox proportional hazards regression analysis, both Gal-3 and sST2 as continuous variables, as well as their newly-established cut offs (≥9.57 ng/ml for Gal-3 and ≥45.99 ng/ml for sST2, based on the Youden index) were predictors of the primary endpoint, and of HF hospitalizations alone. Gal-3 also predicted CV death. After adjustment for age and NT-proBNP, Gal-3 and sST2 remained predictors of the primary endpoint in multivariate models. CONCLUSIONS In patients with first-time STEMI treated with pPCI, baseline Gal-3 and sST2 predicted the composite of CV death and HF hospitalization at 1 year. Both biomarkers may play an important role in CV risk stratification after STEMI, although Gal-3 may be considered preferable.

Association of Soluble Suppression of Tumorigenicity with No-Reflow Phenomenon and Long-Term Prognosis in Patients with Non-ST-Segment Elevation Acute Coronary Syndrome after Percutaneous Coronary Intervention

“…The other subtype is soluble suppression of tumorigenicity 2 (sST2), which can bind to IL-33 and block the binding of IL-33 and ST2L, thereby weakening the cardiovascular protection of IL-33/ST2L signaling pathway 1,4) . As a mechanical stress-induced myocardial protein, sST2 is expressed from cardiac myocytes, cardiac fibroblasts, and endothelial cells in patients with acute myocardial infarction and heart failure (HF) 5,6) . A large amount of sST2 binds to free IL-33 in extracellular fluid, which effectively reduces the binding of ST2L to IL-33 and weakens the protective effect of IL-33 on the myocardium 6) .…”

Worse long-term prognosis in myocardial infarction occurring at weekends or public holidays with insight into myocardial infarction with nonobstructive coronary arteries

“…However, the higher baseline cardiac necrotic markers suggest expected longer delay during NWD. Third, we did not analyze the causes of deaths in long-term follow-up because of the registry data's limitations [44][45][46].…”

Personalized Management of Myocarditis and Inflammatory Cardiomyopathy in Clinical Practice

“…There is an increasing need for a biomarker that is specific to the inflammatory process and fibrosis, and, preferably, correlates with the severity of the disease and serves as a prognostic factor. Existing data show that elevated serum levels of soluble ST2 (an inflammatory biomarker) can predict an increased risk of HF, but the diagnostic potential of soluble ST2 in myocarditis has not been established so far [35,36].…”