Serum sST2 emerged as an independent risk factor for hypertensive left ventricular hypertrophy and major cardiovascular events, though it did not substantially improve existing predictive models.
Cohort (n=140)
Does serum sST2 level predict major cardiovascular events and cardiac remodeling in patients with essential hypertension?
While sST2 is an independent risk factor for hypertensive left ventricular hypertrophy and is associated with cardiovascular events, it does not significantly improve risk prediction beyond established clinical variables.
Objective: Hypertension induces chronic pressure overload on the myocardium, leading to maladaptive structural and functional changes. The interleukin-33 (IL-33)/suppression of tumorigenicity-2 (ST2) signaling pathway plays a cardioprotective role under mechanical stress; however, this pathway is disrupted by increased release of soluble ST2 (sST2), binds IL-33 and inhibits its protective effects, thereby promoting myocardial fibrosis, wall thickening, and increased ventricular stiffness. Consequently, early identification and intervention of left ventricular remodeling, particularly left ventricular hypertrophy (LVH), are critical for preventing major cardiovascular events in patients with essential hypertension (EH). Nevertheless, reliable biomarkers for detecting hypertensive cardiac remodeling remain limited. Design and method: This study aimed to investigate the association between serum sST2 levels and cardiac remodeling in EH patients and to evaluate the potential of sST2 as a biomarker for hypertensive heart disease. A total of 140 EH patients were enrolled, including 60 men aged and 80 women aged more 50 years. Participants were stratified into four groups according to LVH status and sST2 levels: LVH with high sST2 (n = 45), non-LVH with high sST2 (n = 20), non-LVH with low sST2 (n = 60), and LVH with low sST2 (n = 15). Results: The primary endpoint was the first occurrence of a composite major cardiovascular events, including nonfatal myocardial infarction, nonfatal stroke, hospitalization for acute decompensated heart failure, arterial revascularization, or confirmed cardiovascular death. Follow-up visits were conducted at 1, 12, and 18 months, during which MACEs, left ventricular mass index (LVMI), and sST2 levels were assessed. Conclusions: A non-linear relationship was observed between sST2 concentrations and the risk of major cardiovascular events. After adjustment for clinical variables, including LVH, sST2 levels below a specific threshold remained significantly associated with clinical outcomes. sST2 emerged as an independent risk factor for hypertensive LVH and may serve as a biomarker for cardiac remodeling. However, the addition of sST2 did not substantially improve the predictive performance of models already incorporating established clinical variables. Further studies are warranted to determine whether longitudinal monitoring of sST2 can meaningfully enhance risk stratification and improve clinical outcomes in hypertensive heart disease.
Shengelia et al. (2026) conducted a cohort in Essential hypertension (n=140). Serum sST2 levels was evaluated on First occurrence of a composite of major cardiovascular events, including nonfatal myocardial infarction, nonfatal stroke, hospitalization for acute decompensated heart failure, arterial revascularization, or confirmed cardiovascular death. Serum sST2 emerged as an independent risk factor for hypertensive left ventricular hypertrophy and major cardiovascular events, though it did not substantially improve existing predictive models.