Correlation between late gadolinium enhancement mri and high-definition electroanatomical voltage mapping for atrial fibrosis assessment across multiple thresholds

Background/Introduction Atrial fibrosis represents a pathological substrate associated with increased risk of arrhythmia recurrence and thromboembolic complications in patients with atrial fibrillation (AF). Cardiac magnetic resonance imaging (CMR) offers a non-invasive alternative for the assessment of atrial fibrosis; however, the supporting evidence are still inconclusive. Purpose This study investigated the association between atrial fibrosis observed as low-voltage areas on electroanatomical mapping (LVS-EAM) and fibrosis identified by CMR using late gadolinium enhancement (LA-LGE) across different thresholds. Method The study included patients with AF scheduled for first time catheter ablation (CA). Prior to electroanatomical mapping (EAM), patients underwent CMR imaging for the assessment of LA-LGE. The presence and amount of fibrosis was calculated using four different image intensity ratio (IIR) thresholds (0.97, 1.2, 1.32, 1.61 times mean blood pool signal intensity). High density EAM with a multipolar catheter followed and low-voltage areas (LVS-EAM) were calculated using three thresholds for the definition of scar (0.5 mV, 0.25 mV, 0.1 mV). Data were summarized using appropriate descriptive statistics, missing values were handled through multiple imputation (mice package), and associations between CMR- and EAM-derived fibrosis measures were evaluated using Spearman’s correlation and Gwet’s AC1 coefficient, with significance set at p < 0.05. Result A total of 54 ablation-naïve patients with AF were included (80% men, 65% paroxysmal AF, 74% with heart failure). LVS-EAM areas were present in 96%, 93%, and 47% of patients at voltage thresholds of 0.5 mV, 0.25 mV, and 0.1 mV, respectively. Atrial fibrosis detected on CMR was observed in 100%, 96%, 63%, and 21% of patients at IIR thresholds of 0.97, 1.20, 1.32, and 1.61, respectively. The correlation between CMR- and EAM-derived fibrosis was generally weak, with the strongest associations noted between CMR 0.97 and EAM 0.5 mV (ρ = 0.23), 0.25 mV (ρ = 0.20), and 0.1 mV (ρ = 0.16). When fibrosis was analyzed dichotomously (present vs. absent), the highest agreement was observed between EAM 0.5 mV and CMR thresholds of 0.97 (AC1 = 0.96) and 1.2 (AC1 = 1.0), as well as between EAM 0.25 mV and CMR thresholds of 0.97 (AC1 = 0.92) and 1.2 (AC1 = 0.97). Conclusions Among ablation-naïve patients with AF, quantitative correlation between CMR- and EAM-derived atrial fibrosis was weak across tested thresholds, though dichotomous analysis demonstrated better concordance. These results emphasize the importance of developing standardized and reproducible CMR methodologies for reliable, non-invasive characterization of atrial fibrosis.