Association of the Systemic Immune-Inflammation Index with Ascending Aortic Diameter and Dilatation: A Retrospective Cross-Sectional Study

Background and Objectives: Complete blood count-derived inflammatory indices are inexpensive and widely available, but data on their relationship with ascending aortic size are limited. This study examined the association between the systemic immune-inflammation index (SII) and ascending aortic diameter, and compared these indices according to the presence of ascending aortic dilatation (AAD) defined by a 40 mm threshold. Materials and Methods: In this single-centre retrospective cross-sectional study, 251 patients aged 18 years or older (mean age, 53.1 ± 16.7 years; range, 18–95 years; 160 men) who underwent thoracic computed tomography angiography were grouped by maximum tubular ascending aortic diameter (<40 mm, n = 158; ≥40 mm, n = 93). Inference for the primary linear model was based on heteroscedasticity-consistent (HC3) standard errors. Height and weight were not recorded, so the models could not be adjusted for body size. Results: In unadjusted comparisons, platelet and neutrophil counts, creatinine and all five inflammatory indices were nominally higher in the dilated group (all p < 0.05), whereas C-reactive protein did not differ. In the primary adjusted model, each 100-unit increase in SII was associated with a 0.59 mm greater ascending aortic diameter (HC3 95% CI 0.28 to 0.90; β = 0.197; p < 0.001), approximately 1.6 mm across the interquartile range of SII; the model explained 26.9% of the variance. Higher SII was also associated with AAD in the secondary logistic model (odds ratio per 100 units, 1.34; 95% CI 1.17 to 1.53; p < 0.001). Discrimination was weak (area under the curve for SII, 0.658; 95% CI 0.590 to 0.726); the sample-derived cut-off gave a positive likelihood ratio of 1.38, and its 2.5–97.5th percentile interval on bootstrap internal validation was 305 to 579. None of the 75 correlations survived false discovery rate adjustment, and the SII-by-sex interaction was not significant (p = 0.621). Conclusions: Higher SII was associated with a greater ascending aortic diameter and with the presence of AAD after adjustment for the measured covariates; because body size could not be accounted for, residual confounding cannot be excluded. The adjusted difference was modest and discrimination was weak. These findings do not support the use of SII as a standalone diagnostic marker for ascending aortic dilatation.