Systemic Immune–Inflammation Index Predicting Acute Cardiovascular Outcomes

Background/Objectives: Acute coronary syndrome (ACS) and acute decompensated heart failure (ADHF) are associated with substantial short-term morbidity and mortality. The systemic immune–inflammation index (SII) reflects inflammatory and thrombotic activity, but its prognostic value beyond conventional biomarkers and clinical risk scores remains uncertain. This study aimed to evaluate the prognostic value of SII for short-term major adverse cardiovascular events (MACEs) and assess its incremental value beyond established biomarkers and clinical risk scores. Methods: In this prospective observational study, 555 adults with ACS or ADHF were enrolled. Admission SII was calculated from the complete blood count. The primary outcome was 30-day MACE. Multivariable logistic regression evaluated the independent association between log-transformed SII (lnSII) and outcomes. Receiver operating characteristic analyses compared SII with cardiac troponin, BNP, and CRP in the overall cohort. GRACE and TIMI risk scores, and their incremental performance after the addition of SII, were evaluated specifically in the ACS subgroup. Results: Among the 555 patients (mean age 55.9 ± 9.8 years; 54.6% women), 59.5% experienced the primary outcome of 30-day MACE. Elevated lnSII independently predicted 30-day MACE (adjusted OR 2.31, 95% CI 1.61–3.32; p < 0.001). Lower LVEF, lower eGFR, and higher ln-troponin I and ln-BNP levels were also independent predictors of 30-day MACE. SII showed moderate discrimination (AUC 0.72), comparable to BNP and superior to CRP. Among patients with ACS, incorporation of SII significantly improved discrimination of the GRACE score (AUC 0.82 to 0.86) and TIMI score (AUC 0.76 to 0.81). Conclusions: SII independently predicts short-term adverse cardiovascular outcomes in patients with ACS and ADHF. In the ACS subgroup, SII provided incremental prognostic information beyond established GRACE and TIMI risk scores, supporting its potential role as a complementary biomarker for early risk stratification.