INTRODUCTION: Left atrial (LA) fibrosis is strongly associatedwitha worse prognosis foratrial fibrillation (AF) and recurrence after pulmonary vein isolation (PVI). There is also strong evidence ofthe pivotal role of inflammation in the pathogenesis of LA fibrosis. Proinflammatory forms of immunoglobulin G (IgG) and plasma N-glycans are associated with hypertension, atherosclerosis, cardiovascular mortality, left ventricular hypertrophy and aortic stenosis. This study is the first to investigate IgG and plasma N-glycansin AF patients.OBJECTIVES: To determine whether there is an association between specific glycosylation traits of IgG and plasma N-glycans, LA fibrosis and AF recurrence after PVI. STUDY DESIGN: Patients with paroxysmal or persistent AF undergoing PVI were consecutively included in this prospective non-randomized study. PATIENTS AND METHODS: Patients with structural heart disease, acute or chronic inflammatory disease or cancer history were excluded from the study. After blood sampling for IgG and plasma N-glycan ultraperformance liquid chromatography analysis, PVI was performed with radio-frequent ablation using the Carto 3D system,contact-force catheter, CLOSE protocol and ablation index. Immediately before ablation, electro-anatomical voltage mapping of the left atrium was performed in sinus rhythm. Patients were followed for 6 months. AF recurrence was detected by symptom reporting, 24-hour Holter ECG or trans-telephonic ECG. RESULTS: 114 patients (65 % male and 35 % female) were included, with a mean age of 61 and standard deviation 9 years. Persistent AF was found in 30 (27 %) patients and paroxysmal in 83 (73 %) patients.Significant LA fibrosis (≥ 5 % surface) was found in 62 patients (54 %). AF recurred in 34 patients (30 %) and was verified by trans-telephonic ECG in 31 patients and by Holter ECG in only 12 patients. Patients with persistent AF had a higher recurrence rate (46 %) in comparison to paroxysmal AF patients (23 %). 19 patients (36 %) with and 14 patients (23 %) without LA fibrosis had AF recurrence. There was no statistically significant difference in IgG N-glycans between patients with and without AF recurrence after PVI. Plasma GP15 was nominally decreased in patients with AF recurrence, but the difference did not remain statistically significant.IgG GP8 was increased in patients with LA fibrosis (P < 0.01). IgG GP6 as well as G1 and B were also only nominally different, but without a statistical difference. There was also onlya nominal increase in plasma GP4 and LB and a decrease in GP26 and GP32 in patients with LA fibrosis without any statistical significance. CONCLUSION: There is no association between the specific glycosylation of both IgG and plasma N-glycans and AF recurrence after PVI. IgG GP8 is significantly increased in patients with LA fibrosis. The preliminary results have shown for the first time that there is an association between pro-inflammatory IgG glycosylation and the pathological substrate in AF patients, but further studies are needed to confirm this theory.