Atrial fibrillation requires a
trigger that initiates the arrhythmia and substrate that favors perpetuation. Cardiac mapping is
necessary to locate triggers and substrate so that an ablation strategy can be
optimized. The most commonly used
cardiac mapping approach is isochronal or activation mapping, which aims to
create a spatial model of electrical wavefront propagation. Historically, activation mapping has been
successful for mapping point source and single or double wave reentrant
arrhythmias, while mapping multiple wavelets or driving sources that underlie
most episodes of atrial fibrillation remains
challenging. In the multiple wavelet model
of AF there is no particular area critical to sustain atrial fibrillation, and a
“critical mass” of atrium is required to maintain AF. Recent studies suggest endocardial and
epicardial dissociation may play an important role. Investigation of driving sources that
sustain AF has focused on the presence of rotors. Rotors in human AF have now been observed
using multiple imaging modalities, however ablation strategies targeting rotors
remain of unproven benefit. In addition,
substrate mapping of AF is now feasible. Increasing degrees of atrial fibrosis on delayed enhancement magnetic
resonance imaging (DE-MRI) has been shown to correlate with poor procedural
outcomes for AF ablation, which suggests the increased burden of scar promotes
more complex and extensive arrhythmia substrate. Atrial fibrosis is also
identifiable using electrogram voltage tagging in an electro-anatomic mapping
system. Patient-specific ablation
strategies targeting areas of fibrosis are currently under investigation. Recent technological advances have
facilitated greater understanding of the potential role for AF mapping and has
allowed initiation of clinical studies to evaluate the effectiveness of
mapping-based intervention. Multi-modality mapping is likely to play an increasingly important role
in AF ablation, but is currently limited by the inability to simultaneously
record and interpret electrical signals from both atria and from both the
epicardium and endocardium.
Credits: Chirag R. Barbhayia; Saurabh Kumar; Gregory F. Michaud