Discussion
Pacing from the coronary sinus typically results in collision of
diverging wavefronts at an area remote to the site of pacing, at some
point along the lateral aspect of the tricuspid annulus. A multipolar
catheter positioned anterior to the crista terminalis, laterally within
the right atrium, reflects this collision as a ‘chevron’ pattern, and is
a classical measure in clinical EP6, 7. With the
increased use of electroanatomic mapping this site of wavefront
collision can be more accurately rendered and measured. For the purposes
of this study, we assessed the latest point of cranial and caudal
wavefront collision (Figure 1). The last point to be activated in this
area is reproducible and represents the latest collision site of the
inferior and superior wavefronts. The timing and location of this
collision point reflects the conduction properties of the atrium, which
are altered in patients with a potential atrial flutter circuit or
atrial fibrillation8, 9. This approach provides a
single, straightforward measure that incorporates the heterogenous
factors that contribute to conduction delay, whether structural or
cellular10.
We hypothesised that the collision point measure would reflect these
differences in patients with atrial flutter compared with a control
group without atrial flutter or fibrillation. In the population as a
whole we observed a large range of values, from 97 msec to 197 msec. The
vast majority of control patients had collision time of less than
120msec when pacing from the coronary sinus at 100bpm. Only 3 AFL
patients had a RACT of < 115msec, two were younger than 50
years of age, and an older male with a history of VSD repair that may
have influenced conduction time. The marked difference that was observed
between the two groups fits with the physiologic requirement of longer
conduction times to maintain a re-entrant AFL circuit with an excitable
gap11. Shorter conduction times, as observed in the
control group, would allow the wavefront to encounter the refractory
’tail’ of the circuit and extinguish conduction. Variation in RACT was
not related to sex, age or BMI. Larger atria, however, were associated
with longer RACT (Pearson 0.53, p<0.001), suggesting that RACT
may reflect an atrial myopathic process that can lead to atrial
arrhythmias, and that this can be directly measured in at-risk
individuals. Supporting this notion was the association of longer RACT
and incidence of AF during follow-up. Atrial fibrillation occurs in many
patients who initially manifest only atrial flutter and the observation
that a third of our AFL cohort developed AF is in keeping with our
previous findings2. The fact that the RACT value was
significantly longer in these patients may be helpful to guide
anticoagulation decisions during follow up, as related to risk of future
atrial fibrillation after AFL ablation.
The notion that RACT might provide a measure of atrial myopathy risk for
both atrial flutter and atrial fibrillation warrants further prospective
study in light of our compelling findings of association. In the
interim, RACT may have a role in assisting clinical decision making at
time of diagnostic study and when considering empiric cavotricuspid
isthmus ablation in the setting of ablation for atrial fibrillation.