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Background: Left atrial (LA) fibrosis is thought to be a substrate for atrial fibrillation (AF) and can be quantified by late gadolinium enhancement magnetic resonance imaging (LGE‐MRI). Fibrosis formation in LA is a dynamic process and may either progress or regress following AF ablation. We examined the impact of postablation progression in LA fibrosis on AF recurrence. Methods: LA enhancement in LGE‐MRI was quantified in 127 consecutive patients who underwent first time AF ablation. Serial LGE‐MRIs were done prior to AF ablation, 3 months postablation and at least 12 months after second LGE‐MRI. Transient postablation lesion (TL) was defined as atrial enhancement caused by ablation lesions that was detected on the first (3 month) but not on the second postablation LGE‐MRI. New fibrosis (NF) was defined as atrial enhancement detected on the most recent LGE‐MRI, at least 15 months after the ablation procedure. AF recurrence and its correlation with TL and NF was assessed in all patients during the follow‐up period. Results: An increase of 1% NF increased the chance of postablation AF recurrence by 3% (hazard ratio [HR] 1.03, 95% CI 1‐1.06, P =.05). TL had no significant impact on recurrence (P =.057). After adjusting for cardiovascular risk factors, HR increased as NF became greater. Greater volume of NF (≥21%) corresponded with lower arrhythmia‐free survival (37% vs 62%, P =.01). Conclusion: NF formation postablation of AF is a novel marker of long‐term procedural outcome. Extensive NF is associated with significantly higher risk of atrial arrhythmia recurrence. [ABSTRACT FROM AUTHOR]

Introduction: Besides the traditional concept of atrial fibrillation (AF) perpetuating atrial structural remodeling, there is increasing evidence that atrial fibrosis might precede AF, highlighting the need for better characterization of the fibrotic substrate. We aimed to assess atrial fibrosis by use of late gadolinium enhancement magnetic resonance imaging (LGE‐MRI) in non‐AF individuals and to identify predisposing risk factors. A second aim was to establish a risk score for the prevalence of AF using atrial fibrosis in addition to established clinical variables. Methods and Results: Non‐AF individuals without structural heart disease (n = 91) and matched AF controls (n = 91) underwent MRI for assessment of LGE. According to the established UTAH classification, atrial LGE ≥20% was considered extensive. Mean left atrial (LA) fibrosis in non‐AF and AF individuals were 8.8 ± 6.5% and 12.5 ± 5.8%, respectively. Body mass index (BMI) >30 kg/m 2 and LA volume were predictors of atrial fibrosis. Diastolic function was not significantly different with respect to atrial fibrosis. A novel scoring system for the prevalence of AF (2 points for arterial hypertension and/or left ventricular ejection fraction <55%; 3 points for atrial fibrosis >6%) was derived demonstrating that patients in the intermediate/high‐risk group had a significantly increased risk of AF. Conclusion: This study reports unexpectedly high atrial fibrosis in non‐AF patients without apparent heart disease, highlighting the concept that structural fibrotic alterations may precede AF onset in a significant proportion of individuals. BMI as a predictor of atrial fibrosis suggests that lifestyle and drug intervention, that is, weight reduction, could positively influence fibrosis development. The derived risk score for AF prevalence provides the basis for prospective studies on AF incidence. [ABSTRACT FROM AUTHOR]

Introduction: Left atrial (LA) fibrosis is thought to be a substrate for Atrial Fibrillation (AF) and its ablation emerges as a complementary method for AF management. However, LA fibrosis often continues to increase after ablation and likely affects maintenance of sinus rhythm. Hypothesis: We examined how regression and progression of LA fibrosis affected AF recurrent. Methods: LA enhancement was quantified with Late Gadolinium Enhancement MRI (LGE-MRI) for 127 consecutive AF patients who underwent first time AF ablation. Quantification was done before ablation, 3 months post-ablation and then at least 12 months later. Regressed Fibrosis (RF) was defined as enhancement seen on the first (3-months) post-ablation scan but not on the 1-year post-ablation scan and New Fibrosis (NF) as the enhancement detected only on the 1-year post ablation scan. Results: NF and RF showed no correlation with pre-ablation LA fibrosis. An increase of 1% NF increased the chance of AF recurrence by 3%. (HR 1.03, CI 95% 1 - 1.06, p = 0.05). RF alone showed no impact on future AF recurrence. Hazard ratio for AF recurrence increased when NF become greater (Figure 1-A). Additionally, patients with greater volume of NF (>21%, obtained from ROC analysis) experience significantly more recurrence post-ablation (AF freedom 37% vs 61%, p = 0.01, adjusted for cardiovascular risk factors) than those with less than 21% NF (Figure 1-B). Conclusions: Atrial fibrosis formation is an ongoing process and continues to evolve even after targeted ablation. This data suggests that new fibrosis formation after AF ablation (regardless of pre-ablation enhancement) is a novel marker of long-term procedural outcome and is an independent predictor of AF recurrence. It remains unclear whether contemporary AF management aimed at containing fibrotic structures, can help prolong the arrhythmia free period. [ABSTRACT FROM AUTHOR]