BACKGROUND: A biomarker that is of great interest in relation to adverse cardiovascular events is soluble ST2 (sST2), a member of the interleukin family. Considering that metabolic syndrome (MetS) is accompanied by a proinflammatory state, we aimed to assess the relationship between sST2 and left ventricular (LV) structure and function in patients with MetS. METHODS: A multicentric, cross-sectional study was conducted on180 MetS subjects with normal LV ejection fraction as determined by echocardiography. LV hypertrophy (LVH) was defined as an LV mass index greater than the gender-specific upper limit of normal as determined by echocardiography. LV diastolic dysfunction (DD) was assessed by pulse-wave and tissue Doppler imaging. sST2 was measured by using a quantitative monoclonal ELISA assay. RESULTS: LV mass index (β=0.337, P<0.001, linear regression) was independently associated with sST2 concentrations. Increased sST2 was associated with an increased likelihood of LVH [Exp (B)=2.20, P=0.048, logistic regression] and increased systolic blood pressure [Exp (B)=1.02, P=0.05, logistic regression]. Comparing mean sST2 concentrations (adjusted for age, body mass index, gender) between different LV remodeling patterns, we found the greatest sST2 level in the group with concentric hypertrophy. There were no differences in sST2 concentration between groups with and without LV DD. CONCLUSIONS: Increased sST2 concentration in patients with MetS was associated with a greater likelihood of exhibiting LVH. Our results suggest that inflammation could be one of the principal triggering mechanisms for LV remodeling in MetS.
Adult ; Age Factors ; Aged ; Area Under Curve ; Blood Pressure ; Body Mass Index ; Cross-Sectional Studies ; Echocardiography, Doppler ; Enzyme-Linked Immunosorbent Assay ; Female ; Humans ; Hypertrophy, Left Ventricular/diagnostic imaging ; Interleukin-1 Receptor-Like 1 Protein/*analysis ; Linear Models ; Logistic Models ; Male ; Metabolic Syndrome X/metabolism/*physiopathology ; Middle Aged ; ROC Curve ; Sex Factors ; Ventricular Function, Left/*physiology ; Ventricular Remodeling/physiology