# Prognostic Value of SII for Prediction of Pharmacological Cardioversion Success in Newly Diagnosed Atrial Fibrillation

**Authors:** Çetin Mirzaoğlu, Barış Karaca, Mehdi Karasu, Yücel Karaca, Özkan Yavçin, Mehmet Ali Gelen

PMC · DOI: 10.3390/jcm15041407 · 2026-02-11

## TL;DR

This study shows that a blood-based inflammation marker called SII can predict whether patients with new-onset atrial fibrillation will successfully respond to a common drug treatment for restoring normal heart rhythm.

## Contribution

The study demonstrates that SII is a novel independent predictor of pharmacological cardioversion success in new-onset atrial fibrillation.

## Key findings

- Higher SII levels were independently associated with lower success rates of pharmacological cardioversion.
- An SII cutoff of 645.16 predicted successful rhythm restoration with 75% sensitivity and 75% specificity.
- SII and left atrial volume index were both identified as independent predictors of cardioversion success.

## Abstract

Background: Pharmacological cardioversion (PC) with antiarrhythmic agents is a common initial rhythm control strategy in patients with new-onset atrial fibrillation (AF). However, predictive tools for estimating the likelihood of successful PC remain limited. The systemic immune-inflammation index (SII), a novel composite marker derived from neutrophil, lymphocyte, and platelet counts, may reflect atrial inflammatory burden and structural remodeling. This study aimed to investigate the prognostic value of SII in predicting pharmacological cardioversion success in patients with acute-onset symptomatic AF. Methods: This prospective observational study included patients with hemodynamically stable, new-onset symptomatic AF admitted since October 2025. All patients received intravenous amiodarone for pharmacological cardioversion. Baseline clinical, echocardiographic, and laboratory parameters were recorded. Patients were classified into cardioversion-success and non-response groups based on ECG-confirmed restoration of sinus rhythm. Logistic regression analyses were performed to identify independent predictors of rhythm control, and ROC curves were generated to determine predictive performance. Results: Among 95 patients (mean age 54.2 ± 9.8 years, 48.4% female), successful pharmacological cardioversion was achieved in 74.7%. Compared to the non-response group, the cardioversion-success group had significantly lower SII levels (p < 0.001) and left atrial volume index (LAVI, p < 0.001). Multivariate analysis identified both SII and LAVI as independent predictors of cardioversion success. Inverse correlations were observed between both SII (r = −0.419, p < 0.01) and LAVI (r = −0.567, p < 0.01) and rhythm control. The optimal SII cutoff of 645.16 predicted successful rhythm restoration with 75% sensitivity and 75% specificity (AUC: 0.803, 95% CI: 0.710–0.895). Conclusions: Higher SII levels were independently associated with lower rates of successful pharmacological cardioversion in patients with new-onset atrial fibrillation. Incorporating SII into routine assessment may enhance clinical decision-making and patient stratification for rhythm control strategies.

## Linked entities

- **Diseases:** atrial fibrillation (MONDO:0004981)

## Full-text entities

- **Genes:** CRP (C-reactive protein) [NCBI Gene 1401] {aka PTX1}, IL6 (interleukin 6) [NCBI Gene 3569] {aka BSF-2, BSF2, CDF, HGF, HSF, IFN-beta-2}, TCEA1 (transcription elongation factor A1) [NCBI Gene 6917] {aka GTF2S, SII, TCEA, TF2S, TFIIS}
- **Diseases:** neutrophilia (MESH:C563010), atrial remodeling (MESH:D064752), hypertension (MESH:D006973), atrial fibrosis (MESH:D005355), overload (MESH:D019190), shock (MESH:D012769), injury to (MESH:D014947), Inflammation (MESH:D007249), chest discomfort (MESH:D013898), myocardial ischemia (MESH:D017202), immune (MESH:D007154), AF (MESH:D001281), diabetes mellitus (MESH:D003920), lymphopenia (MESH:D008231), malignant diseases (MESH:D009369), myocardial infarction (MESH:D009203), cardiovascular diseases (MESH:D002318), dyspnea (MESH:D004417), infections (MESH:D007239), Stroke (MESH:D020521), coronary artery disease (MESH:D003324), cardiac damage (MESH:D006331), AADs (MESH:D000069279), myocardial injury (MESH:D009202), thromboembolism (MESH:D013923), fatigue (MESH:D005221), cardiac remodeling (MESH:D020257), arrhythmia (MESH:D001145), heart failure (MESH:D006333), bleeding (MESH:D006470), thyroid dysfunction (MESH:D013959), hypotension (MESH:D007022), abnormal thyroid function (MESH:D013966), fibrilation (MESH:D014693)
- **Chemicals:** oxygen (MESH:D010100), potassium (MESH:D011188), AAD (-), digoxin (MESH:D004077), amiodarone (MESH:D000638), creatinine (MESH:D003404), Glucose (MESH:D005947), magnesium (MESH:D008274), colchicine (MESH:D003078)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Figures

4 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12941650/full.md

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Source: https://tomesphere.com/paper/PMC12941650