There is emerging evidence that a keen understanding of atrial myofiber
architecture is paramount to characterizing and treating atrial
arrhythmias. Heterogeneity in the three dimensional anatomic structure
of the atrium has previously been shown to create distinct endocardial
and epicardial activation patterns during tachycardia in a canine model
(1). In the clinical setting, the epicardial atrial architecture and its
contribution to arrhythmias have been less well explored until recently.
There has been a renewed interest in and appreciation of epicardial and
interatrial connections, particularly in the treatment of left atrial
arrhythmias refractory to traditional endocardial ablation.
The vein of Marshall has been postulated to harbor epicardial
connections between the coronary sinus (CS) and the left atrium (LA),
sustaining peri-mitral flutters refractory to endocardial ablation
(2,3). Conduction across the intercaval bundle, which connects the right
atrium to the right superior pulmonary vein, has been reported to render
isolation of the RSPV challenging requiring ablation at the carina or
from the RA (4,5). Similarly, the Bachmann bundle, the main pathway of
interatrial connection, has been shown to be critical for maintenance of
biatrial flutters (6,7). More recently, conduction across the
subepicardial septopulmonary bundle has been implicated in the
maintenance roof dependent flutter despite isolation of the endocardial
posterior wall (8). In contrast, the role of epicardial connections in
sustaining right atrial arrhythmias has been less well described.
In this edition of the Journal, Chaumont et al. describe five
patients who underwent electrophysiology study for typical atrial
flutter, who had persistent arrhythmia despite achieving a line of block
along the endocardial aspect of cavotricuspid isthmus (CTI) (9). Using
entrainment and activation mapping during tachycardia, they identified
atrial tissue critical to the arrhythmia circuit in the middle cardiac
vein in four patients, and in close proximity to the CS ostium in one
patient. Ablation at these locations restored sinus rhythm.
Electroanatomic mapping was not available for most of these cases.
Rather than a limitation, this absence allowed an amazing demonstration
“old school” deductive electrophysiology.
The authors should be commended for this series of cases which
demonstrate connections that sustain atrial flutter by bypassing the
endocardially blocked CTI. This study elucidates the complex, layered
physiology underpinning atrial flutter, considered among the simpler of
arrhythmias we treat in the electrophysiology laboratory. The strength
of the study is the elegant intracardiac electrograms for each case
which allowed the authors to infer the mechanism of refractory
arrhythmia and eliminate it by targeting critical areas guided by EGMs
within the coronary venous system. Prior studies of atrial fibrillation
have suggested that epicardial-endocardial breakthrough maybe an
important mechanism in maintenance of persistent AF (10). It appears
that a similar mechanism maybe responsible for maintaining typical
flutter refractory to endocardial CTI ablation.
Based on their findings, the authors propose a CS to low right atrium
(RA) epicardial connection in the first four patients, and an RA to RA
epicardial connection in one patient critical to the tachycardia
circuit. Anatomically, however, it is unclear whether discrete
connections akin to accessory pathways exist between these regions of
interest to explain the observed findings. It is more likely that the
atrial flutter circuit encompasses the entire thickness of the atrium,
and owing to fiber orientation across the two layers, there are regions
where the endocardial and epicardial surfaces communicate with each
other. At these locations we appreciate the epicardial component of
persistent flutter once the endocardium is ablated and line of block is
achieved but tachycardia continues uninterrupted. This concept is
illustrated in Figure 1, which demonstrates a case of persistent mitral
annular flutter refractory to endocardial mitral annular line.
Epicardial conduction necessary for maintaining tachycardia was observed
after endocardial ablation, and ablation from the coronary sinus slowed
and terminated the tachycardia.
The advent of high resolution 3-dimensional mapping systems has allowed
characterization of atrial activation patterns in detail during
tachycardia. Pathik et al investigated epicardial-endocardial
breakthrough in activation mapping of right atrial macro-reentry
tachycardia in 26 patients (11). They defined breakthrough as the
presence of focal endocardial activation with radial spread unaccounted
for by an endocardial wavefront, with same timing on every tachycardia
cycle. Epicardial-endocardial breakthrough was observed in over 50% of
the patients, with majority at the posterior RA, and one each at
cavotricuspid isthmus postablation, RA septum, and the inferolateral RA.
In four patients, areas of breakthrough were within the tachycardia
circuit, and in one patient the breakthrough region was critical for
arrhythmia maintenance. In all cases, breakthrough sites were adjacent
to endocardial slowing or line of block—as mentioned above this
finding is not entirely surprising, given that endocardial block is
necessary to observe epicardial breakthrough while activation mapping.
A detailed morphologic and histologic study of the inferior right atrial
isthmus by Cabrera et al may provide some anatomical insight to explain
the current study findings (12). The authors establish the isthmus to be
an anatomically heterogeneous region, with the anterior aspect being
consistently muscular, while the posterior membranous and the middle
trabeculated aspects having variable ratios of muscle fibers to
fibrofatty tissue, with myocardial bundles extending from terminal crest
toward the Eustachian ridge to cover the mouth of the coronary sinus. In
refractory atrial flutter following endocardial CT ablation, it maybe
that ablation from the CS allows the elimination of residual conduction
through these muscle fibers which is critical for maintenance of
tachycardia.
In conclusion, Chaumont et al should be congratulated for elegantly
demonstrating the multi-layer physiological architecture of typical
atrial flutter—a reflection of the anatomic complexity and
heterogeneity of the cavotricuspid isthmus and its inputs, and of the
atrial musculature in general. Appreciation of this complexity will
undoubtedly empower us to characterize and treat this arrhythmia and
others more effectively.