Systemic Inflammation and New-Onset Atrial Fibrillation in Acute Coronary Syndromes: A Single-Center Cohort Study

Background/Objectives: New-onset atrial fibrillation (NOAF) is a common complication of acute coronary syndrome (ACS) and is associated with adverse clinical outcomes. Although systemic inflammation has been implicated in the pathogenesis of NOAF, the contribution of different inflammatory biomarkers and their incremental value beyond established clinical factors remain incompletely understood. This study aimed to examine the association between inflammatory biomarkers and NOAF in patients hospitalized with ACS and to assess their contribution beyond established clinical risk factors. Materials and Methods: This prospective single-center cohort included 100 consecutive patients hospitalized with ACS and without a documented history of atrial fibrillation. Comprehensive demographic, clinical, laboratory, echocardiographic, and angiographic data were collected. Systemic inflammatory status was assessed using C-reactive protein (CRP), the neutrophil-to-lymphocyte ratio (NLR), the monocyte-to-lymphocyte ratio (MLR), and the systemic immune-inflammation index (SII). Univariable and multivariable logistic regression analyses were performed to identify factors associated with NOAF. The incremental contribution of inflammatory biomarkers to apparent in-sample model discrimination was explored using receiver operating characteristic (ROC) curve analysis and DeLong’s test. Sensitivity analyses were performed according to the timing of NOAF occurrence. Results: NOAF occurred in 33 of 100 patients (33%) during hospitalization. Patients who developed NOAF were older and exhibited greater left atrial enlargement, more extensive coronary artery disease, and higher inflammatory biomarker levels. In univariable analyses, CRP, NLR, and SII were significantly associated with NOAF. In exploratory multivariable analyses adjusted for clinically selected covariates, CRP remained associated with NOAF (adjusted OR 1.71, 95% CI 1.08–2.91; p = 0.031), whereas NLR, SII, NT-proBNP, and troponin did not retain statistically significant associations. CRP demonstrated the highest numerical improvement in model discrimination, although the increase in AUC compared with the baseline clinical model was not statistically significant. Sensitivity analyses confirmed the consistency of the association between CRP and NOAF. Conclusions: In this exploratory single-center cohort, CRP remained associated with NOAF after adjustment for clinically selected covariates, supporting further investigation of the relationship between systemic inflammation and NOAF development. These findings require confirmation in larger cohorts with internal and external validation.