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Published on: May 26, 2015
Left atrial myopathy development and progression in atrial fibrillation patients with recurrent left atrial ablation
Karan Saraf1, Michael Malaty2, David Ferreira3
1Department of Cardiac Sciences, Libin Cardiovascular Institute, University of Calgary, Calgary, Alberta, Canada.
Background:
Pulmonary vein isolation remains central to atrial fibrillation (AF) ablation; however, recurrence can occur despite durable isolation, and is associated with low voltage areas (LVAs), a surrogate for atrial fibrosis.
Objective:
This study characterized longitudinal LVA changes in repeat ablation patients and identified predictors of substrate progression.
Methods:
Consecutive adults undergoing de novo left atrial (LA) ablation for AF were enrolled, with repeat ablation cases analyzed. LVAs were quantified, with progression defined as >10% LVA increase. Conduction velocity (CV) and electrogram complexity were measured, with regression analysis assessing predictors and association with AF recurrence.
Results:
In 90 patients, total LVA increased from 9.5 ± 16.8% to 19.0 ± 24.7% (P < .001); 33% of patients had >10% progression, mainly in septal (42%), anterior (37%), and posterior (34%) segments. Patients with progression had higher CHA2DS2-VASc (2.75 vs 2.05, P = .021), larger LA volumes (152 vs 122 mL, P = .008), and slower baseline CV (0.86 vs 1.02 m/s, P = .013). Multivariable analysis confirmed baseline LA volume (P = .002) and CV (P = .043) as predictors of progression (R2= 0.206). LVA burden predicted 12-month AF recurrence (odds ratio 3.65 per 1%, P = .049 baseline; odds ratio 2.54, P = .012 at second procedure).
Conclusion:
LA myopathy advances in one-third of repeat AF ablation patients without chamber enlargement, exhibiting heterogeneous progression favoring septal, anterior, and posterior segments while sparing the lateral wall. Baseline CV and LA volume robustly predict LVA progression, indicating functional electrical remodeling precedes structural fibrosis, highlighting the importance of integrating functional markers when characterizing atrial substrate progression.
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