Key result
Elevated admission SII and PIV are linked to higher stent thrombosis risk in geriatric STEMI.
Why the study?
The prognostic capacity of the systemic immune-inflammation index (SII) and pan-immune-inflammation value (PIV) to identify future stent thrombosis in geriatric STEMI patients was uncertain.
Do baseline systemic immune-inflammation index (SII) and pan-immune-inflammation value (PIV) predict the development of definite stent thrombosis in geriatric patients undergoing primary PCI for acute STEMI?
Cohort (n=1,683)
Single-blind
No
Do baseline systemic immune-inflammation index (SII) and pan-immune-inflammation value (PIV) predict the development of definite stent thrombosis in geriatric patients undergoing primary PCI for acute STEMI?
Admission-derived systemic immune-inflammation index (SII) and pan-immune-inflammation value (PIV) are easily accessible, independent predictors of subsequent definite stent thrombosis in elderly patients undergoing primary PCI for acute STEMI.
May inform thrombosis risk stratification in geriatric STEMI; leaves open prospective validation before clinical use.
Introduction: The objective of this investigation was to determine whether the systemic immune-inflammation index (SII) and pan-immune-inflammation value (PIV), which serve as comprehensive indicators of systemic inflammatory pathways, possess the prognostic capacity to identify future stent thrombosis (ST) in geriatric STEMI patients. Materials and Method: We comprehensively screened a consecutive cohort of 1,683 elderly individuals (aged 75.3 ± 6.8 years; 64.6% male) who had been treated with primary percutaneous coronary intervention (PCI) for acute ST-elevation myocardial infarction (STEMI). Stratification was performed based on the clinical manifestation of angiographically confirmed ST during follow-up. Both SII and PIV scores were computed from standard complete blood counts obtained at the time of initial clinical presentation. Results: Over an average follow-up duration of 30 ± 10 months, definite ST was documented in 104 individuals (6.2%). Patients experiencing ST exhibited distinct baseline profiles, characterized by a higher prevalence of tobacco use and hypertension, a greater frequency of early dual antiplatelet therapy (DAPT) cessation (<30 days), prolonged total stent lengths, and markedly elevated baseline high-sensitivity C-reactive protein (hs-CRP), SII, and PIV levels. In multivariable Cox proportional hazards modeling, both admission PIV and SII emerged as robust, standalone indicators of subsequent ST. Furthermore, correlation analyses demonstrated that hs-CRP levels fluctuated in tandem with both SII (r=0.342, p<0.001) and PIV (r=0.268, p<0.001) values. Conclusion: In summary, these data demonstrate that baseline immunoinflammatory indices serve as independent and highly reliable indicators of subsequent ST development within the high-risk geriatric cohort treated with primary PCI for STEMI.
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Kafes et al. (2026) conducted a cohort in ST-elevation myocardial infarction (STEMI) in geriatric patients undergoing primary PCI (n=1,683). Admission systemic immune-inflammation index (SII) and pan-immune-inflammation value (PIV) vs. Lower baseline SII and PIV levels (analyzed as continuous variables; patients without stent thrombosis) was evaluated on Definite stent thrombosis (Academic Research Consortium criteria) (HR 1.004 (for SII); HR 1.003 (for PIV), 95% CI 1.003-1.006, p=<0.001). Elevated admission SII (HR 1.004, p<0.001) and PIV (HR 1.003, p<0.001) independently predicted definite stent thrombosis in geriatric STEMI patients undergoing primary PCI.
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