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.