The systemic immune-inflammation index in coronary heart disease: a narrative review of thromboinflammation, phenotype-dependent utility, and clinical translation

Coronary heart disease (CHD) is essentially a thrombo-inflammatory disease, and its key pathological mechanism lies in an acute thrombotic storm driven by the interaction between platelets, neutrophils, and lymphocytes. Existing inflammatory markers, which reflect only a single dimension, struggle to accurately capture this complex network. The Systemic Immune-Inflammation Index (SII), calculated using the formula (platelets × neutrophils/Lymphocytes), integrates the three dimensions of thrombosis, inflammation, and immunity, providing a novel composite indicator for quantifying the thrombo-inflammatory burden. This article provides a review of the latest evidence regarding SII in the risk stratification of coronary heart disease. Existing studies indicate that the predictive utility of SII exhibits significant phenotype dependence: it peaks in acute coronary syndrome (ACS) and related complications, accurately reflecting the intensity of acute thromboinflammatory storms; whereas in chronic coronary syndrome (CCS), its utility is diminished, serving merely as a tool for monitoring background inflammation. This dual characteristic of “acute warning and chronic monitoring” stems from its pathological specificity-the SII molecule (P × N) directly reflects the synergistic amplification effect of platelet-neutrophil interactions and performs best in thrombus-driven events. Clinical evidence supports the establishment of a three-tiered threshold system: (1) Acute-phase high-risk threshold (>900–1400), used for predicting ACS major adverse cardiovascular events (MACE) and stratifying mortality risk; (2) Complication stratification thresholds (screening: 450–650; diagnosis: >1,000), to guide the identification and intervention of microvascular complications such as no-reperfusion phenomenon (NRP); (3) Chronic-phase monitoring thresholds (>650), indicating anatomical complexity rather than an independent prognostic factor. However, the clinical translation of SII remains limited: cut-off values show high heterogeneity (459–2,174), comparisons with the Systemic Inflammatory Response Index (SIRI) and the Pan-Inflammatory Value (PIV) remain controversial, and most existing evidence comes from observational studies. Future efforts should focus on establishing the mechanism-specificity of SII by validating its association with direct thrombotic and inflammatory markers such as neutrophil extracellular traps (NETs), developing phenotype-adaptive risk models, and conducting randomized controlled trials to verify whether SII-guided intensified anticoagulation or anti-inflammatory interventions (such as colchicine) can improve clinical outcomes. The transition from a risk stratification tool to an indicator for precision treatment decision-making represents the next critical step in the clinical application of SII.