Differences in inflammation biomarkers between patients with paroxysmal and persistent atrial fibrillation in the femoral vein and coronary sinus blood samples; a cohort study.

The association between inflammation and atrial fibrillation (AF) is evident, but assessing the specific inflammatory pathways involved in the pathogenesis remains complex. This study aimed to identify inflammatory biomarkers associated with paroxysmal (PAF) and persistent (PeAF) AF by evaluating blood samples from the intra- and extracardiac space. This is an observational, cross-sectional, single-centre study. A total of 92 inflammatory biomarkers were analyzed from blood samples taken from the coronary sinus (CS) and the femoral vein (FV) in 88 patients with AF who had been referred for catheter ablation at the Linköping University Hospital, Sweden. The concentrations of the biomarkers were compared between PAF and PeAF patients in the CS and FV. Significant differences in concentration were found in 36 of 92 biomarkers. Among these, 12 proteins stand out for exhibiting a higher concentration in PeAF patients: Interleukin 6 (IL-6), CUB domain-containing protein 1 (CDCP1), Interleukin 18 receptor 1 (IL-18R1) and cystatin D (CST5) in the FV, β nerve growth factor (β-NGF) and tissue growth factor α (TGF-α) at the CS level, as well as interleukin 18 (IL-18), chemokine ligand 3 (CCL-3) and tumour necrosis factor superfamily 14 (TNFSF-14) in both FV and CS. Moreover, chemokine ligand 25 (CCL-25), chemokine ligand 28 (CCL-28), and artemin (ARTN) were found at a higher concentration in the CS in the overall population. This study supports the involvement of TNFSF-14, IL-6, and IL-18 in the pathogenesis and maintenance of PeAF. Furthermore, it identifies β-NGF and TGF-α as potential participants in the pathogenesis and/or maintenance of PeAF locally in the atria. Novel inflammatory biomarkers, mainly chemokines, are also identified as possibly involved in the pathophysiology of AF.