What question did this study set out to answer?

To evaluate the independent prognostic utility of soluble suppression of tumorigenesis-2 (sST2) when added to NT-proBNP and high-sensitivity troponin T in chronic heart failure.

April 27, 2026Journal of the American College of CardiologyOpen Access

sST2 Predicts Outcome in Chronic Heart Failure Beyond NT−proBNP and High-Sensitivity Troponin T

Q: What are the key findings of this study?

In chronic heart failure, each doubling of sST2 independently increased the risk of all-cause death, cardiovascular death, and HF hospitalization by 26%, 25%, and 30%, respectively (all p<0.001).

Q: What is the clinical evidence from this study?

Study design: Meta-Analysis. Population: Chronic heart failure (n=4268). Intervention: sST2 biomarker assessment. Primary outcome: All-cause death, cardiovascular death, and HF hospitalization (HR 1.26, HR 1.25, and HR 1.30 per doubling of sST2, p=<0.001).

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Key result

Each doubling of sST2 in chronic HF is linked to ~26% greater all-cause mortality risk.

HR 1.26, HR 1.25, and HR 1.30 per doubling of sST2
P<0.001
n=4,268

Why the study?

This study evaluated the independent prognostic value of sST2, a biomarker of inflammation and fibrosis, in chronic heart failure.

Key Points

To evaluate the independent prognostic utility of soluble suppression of tumorigenesis-2 (sST2) when added to NT-proBNP and high-sensitivity troponin T in chronic heart failure.
Retrieved individual patient data from studies evaluating sST2 alongside NT-proBNP and hs-TnT in chronic heart failure (N=4,268; median age 68 years; 75% male; 87% with LVEF <40%).
Assessed outcomes including all-cause mortality, cardiovascular mortality, and heart failure hospitalization over a median follow-up of 2.4 years (2.2 years for hospitalization).
Over follow-up, 1,319 patients (31%) died from all causes, 932 (22%) died from cardiovascular causes, and 1,029 of 4,118 patients (24%) were hospitalized for heart failure.
An sST2 cutoff of 28 ng/ml identified patients at elevated risk for all-cause death, cardiovascular death, and hospitalization (all log-rank p < 0.001).
In multivariable models adjusting for clinical risk factors, NT-proBNP, and hs-TnT, each doubling of sST2 increased the risk of all-cause death by 26%, cardiovascular death by 25%, and heart failure hospitalization by 30%.

Study Design

Type

Meta-Analysis (n=4,268)

Multicenter

Yes

PICO

Population

Chronic heart failure (n=4,268)

Intervention / Comparator

sST2 biomarker assessment

Primary Outcome

All-cause death, cardiovascular death, and HF hospitalization — HR 1.26, HR 1.25, and HR 1.30 per doubling of sST2, p=<0.001

Main Result

Effect estimate: HR 1.26, HR 1.25, and HR 1.30 per doubling of sST2

p-value: p=<0.001

Discussion

No takes yet. Share an insight, caveat, or question.

Implication

Supports sST2 for risk stratification in chronic HF; leaves open whether guided management improves outcomes.

Cite This Study

Emdin et al. (2018) conducted a meta-analysis in Chronic heart failure (n=4,268). sST2 biomarker assessment was evaluated on All-cause death, cardiovascular death, and HF hospitalization (HR 1.26, HR 1.25, and HR 1.30 per doubling of sST2, p=<0.001). In chronic heart failure, each doubling of sST2 independently increased the risk of all-cause death, cardiovascular death, and HF hospitalization by 26%, 25%, and 30%, respectively (all p<0.001).

synapsesocial.com/papers/69efd2c1b8a53e2a171bc98a https://doi.org/10.1016/j.jacc.2018.08.2165

Topics

Heart failure HFrEF treatment

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sST2 Predicts Outcome in Chronic Heart Failure Beyond NT−proBNP and High-Sensitivity Troponin T

Key Points

Study Design

PICO

Main Result

Discussion

Implication

Cite This Study

Topics

sST2 Predicts Outcome in Chronic Heart Failure Beyond NT−proBNP and High-Sensitivity Troponin T

Key Points

Study Design

PICO

Main Result

Discussion

Implication

Cite This Study

Also Consider

Topics

Also Consider