Retrospective Evaluation of the Relationship Between Catheter Ablation and Systemic Immune-Inflammation Index in Cardiac Arrhythmias

Background Catheter ablation induces controlled myocardial injury and transient endothelial dysfunction, both of which may trigger a systemic inflammatory response. The systemic immune-inflammation index (SII) has emerged as a sensitive biomarker reflecting the interplay between inflammation, thrombosis, and immune regulation; however, its peri-procedural behavior after ablation remains unclear. Objective To evaluate changes in SII following catheter ablation across different arrhythmia subtypes and to determine independent predictors of ΔSII. Methods In this retrospective cohort study, 642 adult patients who underwent catheter ablation between January 2022 and December 2024 were analyzed. Pre-procedural and 1-week post-procedural SII values were compared in diagnostic EPS, supraventricular tachycardia (SVT), atrial fibrillation (AF; RF and cryoablation), atrial tachycardia (AT), atrial flutter (AFL), and ventricular ectopy (VES) groups. Multivariable linear regression assessed predictors of ΔSII. Effect sizes were calculated using Cohen’s d and Hedges’ g. Results Overall SII increased significantly after ablation (p = 0.001). AF groups demonstrated the strongest effect sizes (RF-AF: d = 0.84; Cryo-AF: d = 1.07). No significant changes were observed after diagnostic EPS or AFL ablation. Regression analysis identified EF (β = − 19.4; p = 0.045), RF-AF (β = 808; p = 0.0016), Cryo-AF (β = 710; p < 0.001), and VES ablation (β = 471; p = 0.036) as independent predictors of ΔSII. The model demonstrated adequate power (post-hoc power = 0.805). Conclusion Catheter ablation—particularly AF and VES ablation—is associated with significant early SII elevation, independent of conventional inflammatory markers such as CRP. SII may serve as a more sensitive biomarker of subclinical endothelial and inflammatory perturbations following ablation.