What is the clinical evidence from this study?

Study design: Cohort. Population: Heart failure (n=1084). Intervention: Systemic immune-inflammation index (SII) highest quartile vs. Lowest quartile of SII. Primary outcome: All-cause mortality (HR 1.59, 95% CI 1.03-2.46, p=0.036).

What question did this study set out to answer?

This research examines how the systemic immune-inflammatory index (SII) relates to mortality rates in heart failure patients.

April 28, 2026Open Access

Association between systemic immune-inflammation index(SII) and all-cause and cardiovascular mortality in heart failure patients: a single-center retrospective analysis

Key Result

Elevated systemic immune-inflammation index (highest vs lowest quartile) was independently associated with an increased risk of all-cause mortality (HR 1.59) in patients with heart failure.

Key Points

This research examines how the systemic immune-inflammatory index (SII) relates to mortality rates in heart failure patients.
Conducted a retrospective cohort study with 1,084 heart failure patients
Follow-up was done through telephone and outpatient visits until death or July 22, 2025
Cox models and restricted cubic splines were used to assess the association between log-transformed SII and mortality.
Higher LnSII is linked to increased all-cause mortality (fully adjusted HR = 1.59, 95% CI: 1.03–2.46)
No significant relationship with cardiovascular mortality was found due to a limited number of cases (n = 60)
Smoking status showed a significant interaction, with smokers having a higher risk (HR = 2.41, 95% CI: 1.57–3.68).

Study Design

Type

Cohort (n=1,084)

Multicenter

Structured PICO

Does an elevated systemic immune-inflammation index (SII) predict increased all-cause and cardiovascular mortality in patients with heart failure?

Population

1,084 adults (age 18-90) hospitalized for heart failure (HFmrEF or HFrEF, LVEF ≤ 49% at admission), mean age 62, 78.7% male, in China. Exclusions: malignant tumors, severe infectious diseases, active tuberculosis, autoimmune diseases, pregnancy, severe hepatic or renal insufficiency, in-hospital death, acute myocardial infarction.

Intervention

Higher Systemic Immune-Inflammation Index (SII), analyzed as log-transformed SII (LnSII) in the highest quartile (Q4: 6.66-8.78)

Comparator

Lower Systemic Immune-Inflammation Index (SII), specifically the lowest quartile (Q1: 2.36-5.84)

Outcome

All-cause mortality and cardiovascular mortality at mean 29.3 months follow-uphard clinical

Elevated systemic immune-inflammation index (SII) is an independent predictor of all-cause mortality in patients with heart failure, suggesting its potential utility as a prognostic biomarker.

Main Result

Effect estimate: HR 1.59 (95% CI 1.03-2.46)

p-value: p=0.036

Limitations

Retrospective single-center design limits causal inference and generalizability
Residual confounding is possible
Limited number of cardiovascular deaths reduced statistical power
Exclusion of patients who died in-hospital or had acute myocardial infarction may introduce selection bias
LVEF and SII were only assessed at baseline without capturing dynamic changes

Abstract

Objective This study aimed to investigate the association between the systemic immune-inflammatory index (SII) and mortality in patients with heart failure (HF). Method We conducted a retrospective cohort study of 1,084 HF patients. In this retrospective cohort study, we enrolled patients hospitalized for heart failure between January 2022 and June 2023. Follow-up was conducted via telephone and outpatient visits until death or July 22, 2025, with all-cause and cardiovascular mortality as primary endpoints. Patients were categorized by log-transformed SII (LnSII). Cox models assessed associations between LnSII and mortality, while restricted cubic splines evaluated nonlinearity. Subgroup, mediation (NT-proBNP, LVEF), and sensitivity analyses were performed. Results A higher LnSII was significantly associated with an increased risk of all-cause mortality (fully adjusted HR = 1.59, 95% CI: 1.03–2.46), No statistically significant association was detected with cardiovascular mortality, which may be attributable to the limited number of cardiovascular deaths ( n = 60) and consequent reduced statistical power. Subgroup analysis revealed a significant interaction with smoking status ( P for interaction=0.023), showing a stronger association between LnSII and all-cause mortality among smokers (HR = 2.41, 95% CI: 1.57–3.68). Mediation analysis indicated that NT-proBNP and LVEF mediated 35.8% and 15.0% of this association, respectively. Conclusion Elevated SII is independently associated with an increased risk of all-cause mortality in HF patients, particularly among smokers, and may serve as a useful prognostic biomarker.

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