DOI: 10.1093/ejhf/xuag193.419 ISSN: 1388-9842

Association between soluble ST2 levels and pulmonary congestion in heart failure

M Kobayashi, A Kuwahara, R Takagi

Abstract

Background

Soluble ST2 (sST2) is released from lung tissue in response to hemodynamic stress and is generally elevated in patients with acute heart failure (HF) compared with those with stable HF. However, its association with the severity of pulmonary congestion has not been fully elucidated.

Methods

In this prospective study, we enrolled patients with HF, including those hospitalized for acute HF and ambulatory patients with stable HF. Associations between circulating congestion-related biomarkers, including sST2, B-type natriuretic peptide (BNP), cancer antigen-125 (CA125), growth differentiation factor-15 (GDF-15), and CD146, and pulmonary congestion severity assessed by an 8-zone lung ultrasound B-line method were examined.

Results

Among 33 patients with HF (median age 78 [66 to 84] years; 58% male), the median left ventricular ejection fraction (LVEF) was 41% (20 to 55%), and 52% presented with acute HF. Median sST2 concentration was 27.4 (18.0 to 66.0) ng/mL, and median number of B-lines was 15 (3 to 35), showing a moderate correlation (Pearson’s r = 0.33; P< 0.05). Higher sST2 levels were observed in patients with acute HF versus stable HF, consistent with more severe signs and symptoms of congestion (all-P<0.05). sST2 levels were significantly associated with a greater number of B-lines (β, 95% CI=0.21, 0.02 to 0.40; P=0.033), and this association remained persistent after covariate adjustment (i.e., LVEF and renal function) (P<0.05). These associations were consistent across acute and stable HF (P for interaction> 0.10). In contrast, other congestion-related biomarkers, i.e. BNP, CA125, GDF-15, and CD146, were not significantly associated with B-line number (all-P>0.05).

Conclusion

Circulating sST2 levels are independently associated with lung ultrasound-assessed pulmonary congestion in patients with HF, suggesting that sST2 may serve as a key biomarker reflecting the severity of pulmonary congestion. Larger, adequately powered studies are warranted to confirm these findings.

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