Abstract
Background: The pathogenesis of atrial fibrillation (AF) consists of an interaction between focal triggers and substrate abnormalities. Increased chamber size, reduced conduction velocity and decreased refractoriness (AERP) are considered to be part of that arrhythmogenic substrate. Pulmonary vein isolation (PVI) carries a significant failure rate and we hypothesise that patients with greater degrees of substrate remodelling are less likely to benefit from ablation strategies targeting focal triggers.
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