Key result
Elevated Systemic Immune-Inflammation Index is linked to increased risk and burden of PVCs.
Why the study?
Systemic inflammation has emerged as a potential contributor to ventricular ectopy, but the relationship between the systemic immune-inflammation index and PVC presence and burden required investigation.
Does the Systemic Immune-Inflammation Index (SII) correlate with the presence and burden of premature ventricular contractions in patients without structural heart disease?
Observational (n=418)
No
Does the Systemic Immune-Inflammation Index (SII) correlate with the presence and burden of premature ventricular contractions in patients without structural heart disease?
Odds Ratio: 1.002 (95% CI 1.001–1.003)
p-value: p=<0.001
Higher Systemic Immune-Inflammation Index (SII) levels are independently associated with the presence and increasing burden of premature ventricular contractions in patients without structural heart disease.
SII may complement Holter data for high-burden PVC risk but should not change practice; leaves open causality in structurally normal hearts.
Background Premature ventricular contractions (PVCs) are common cardiac arrhythmias that have been associated with left ventricular dysfunction, PVC-induced cardiomyopathy, and adverse cardiovascular outcomes when present in high burden. Systemic inflammation has emerged as a potential contributor to ventricular ectopy. The Systemic Immune-Inflammation Index (SII) is an easily obtainable biomarker reflecting inflammatory status. This study aimed to investigate the association between SII and both the presence and burden of PVCs. Methods This retrospective study included 418 consecutive adult patients who underwent 24-hour Holter monitoring and complete blood count analysis. Patients were categorized according to PVC presence and further stratified by PVC burden. SII values were compared between groups and across PVC burden categories. Correlation analysis, receiver operating characteristic (ROC) analysis, and multivariable logistic regression analyses were performed to evaluate the relationship between SII and PVC burden. Results Patients with PVCs had significantly higher SII values than controls (506.69 [354.20–674.28] vs. 463.12 [349.58–573.74], p = 0.012). SII increased progressively across PVC burden categories ( p = 0.007). Spearman analysis demonstrated a weak but significant positive correlation between SII and PVC burden (rho = 0.150, p = 0.029). In multivariable analysis, SII remained independently associated with both PVC presence and high PVC burden. ROC analysis demonstrated a moderate discriminatory performance of SII for identifying high PVC burden (AUC = 0.696, 95% CI: 0.597–0.795, p < 0.001), with an optimal cut-off value of 505.6. Among the evaluated inflammatory biomarkers, SII showed the largest AUC for identifying high PVC burden, followed by NLR and PLR. Conclusion Higher SII levels were associated with both the presence and increasing burden of PVCs. These findings support a potential relationship between systemic inflammatory status and ventricular ectopy and suggest that SII may provide complementary information when interpreted together with clinical evaluation and rhythm monitoring, rather than as a standalone marker.
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Alpaslan et al. (2026) conducted an observational in Premature ventricular contractions (PVCs) (n=418). Systemic Immune-Inflammation Index (SII) vs. Lower SII levels / Control group without PVCs was evaluated on Presence of premature ventricular contractions (OR 1.002, 95% CI 1.001-1.003, p=<0.001). Higher Systemic Immune-Inflammation Index levels were independently associated with the presence of premature ventricular contractions (OR 1.002) and a high PVC burden in patients without structural heart disease.
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