Key result
Higher Systemic Immune-Inflammation Index linked to ~5.4-fold higher odds of post-PCI MACE per quartile.
Why the study?
MACE continue after PCI despite advances in revascularisation, and systemic inflammation contributes to atherosclerosis and plaque instability. This study evaluated the prognostic value of the Systemic Immune-Inflammation Index (SII), a biomarker derived from routine blood counts, for MACE after PCI.
Does the pre-procedural Systemic Immune-Inflammation Index (SII) predict in-hospital major adverse cardiovascular events (MACE) in adult patients undergoing percutaneous coronary intervention (PCI)?
Cohort (n=400)
No
Does the pre-procedural Systemic Immune-Inflammation Index (SII) predict in-hospital major adverse cardiovascular events (MACE) in adult patients undergoing percutaneous coronary intervention (PCI)?
Answers are grounded in this paper and cite their sources.
Pre-procedural Systemic Immune-Inflammation Index (SII) is an inexpensive, routine blood count-derived biomarker that strongly and independently predicts in-hospital MACE, greater coronary complexity (SYNTAX score > 27), and lower discharge LVEF in patients undergoing PCI.
Background Major adverse cardiovascular events (MACE) continue after percutaneous coronary intervention (PCI) despite advances in revascularisation. Systemic inflammation contributes to atherosclerosis and plaque instability. The Systemic Immune-Inflammation Index (SII) is an inexpensive, easily calculated biomarker derived from routine blood counts that integrates inflammatory and immune pathways. This study evaluated its prognostic value for MACE after PCI. Methods This single-center retrospective observational study included 400 consecutive adults undergoing PCI for stable angina or acute coronary syndromes over 1 year. Pre-procedural complete blood counts were used to calculate SII [(platelet × neutrophil)/lymphocyte]. The primary outcome was in-hospital MACE, comprising all-cause mortality, non-fatal myocardial infarction, and ischemic stroke. Patients were stratified by SII quartiles. ROC analysis and multivariable logistic regression assessed predictive performance and independent associations. Results MACE occurred in 6.8% (n = 27). SII was significantly higher in patients with MACE than without (1127.19 ± 335.99 vs. 599.92 ± 324.55 ×10⁹/L; p < 0.001). High SYNTAX scores (> 27) occurred in 72% of the highest versus 1% of the lowest SII quartile (p < 0.001). Increasing SII was associated with higher troponin positivity and lower discharge left ventricular ejection fraction (p < 0.01). ROC analysis showed excellent predictive ability (AUC 0.886; 95% CI 0.827–0.945), with an optimal cut-off ≥ 776 ×10⁹/L. Multivariable analysis identified SII (adjusted OR 5.36 per quartile increase; p = 0.001) and diabetes mellitus (adjusted OR 4.41; p = 0.024) as independent predictors of MACE. Conclusion Elevated SII independently predicts MACE after PCI and may serve as a simple, cost-effective risk-stratification tool in routine clinical practice.
No takes yet. Share an insight, caveat, or question.
Gambhire et al. (2026) conducted a cohort in Stable angina or acute coronary syndromes undergoing percutaneous coronary intervention (PCI) (n=400). Systemic Immune-Inflammation Index (SII) per 1-quartile increase vs. Lower SII quartiles was evaluated on In-hospital major adverse cardiovascular events (MACE: composite of all-cause mortality, non-fatal myocardial infarction, and ischemic stroke) (OR 5.36, 95% CI 2.06-13.98, p=0.001). Each one-quartile increase in the Systemic Immune-Inflammation Index independently increased the odds of in-hospital MACE after PCI (adjusted OR 5.36, 95% CI 2.06–13.98; p=0.001).
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: