Role of the coronary sinus ostium musculature in reentrant formation.

Background: Radiofrequency ablation of focal atrial tachycardias (AT) is a validated technique with high success rates. However, electrophysiological (EP) characteristics and ablation strategy of localized reentrant AT originating from the coronary sinus ostium (CSo) have not been reported in detail so far.

Methods: From January 2009 to July 2010, 1,453 patients underwent clinically motivated EP studies. Four patients were diagnosed with localized reentrant AT originating from the CSo. P wave morphology and consistency of tachycardia cycle length were studied. Subsequently, if reentry was suggested as an underlying mechanism for AT, color-coded 3-dimensional (3D) entrainment mapping was performed to localize the reentrant circuit or differentiate a localized reentrant AT from macroreentant AT, and also confirm reentry as an underlying mechanism of AT by evaluating consistency of return cycles after entrainment at multiple sites in both atria. Finally, activation mapping was performed to localize the earliest activation site.

Results: The P wave morphologies and isoelectric line between the P waves suggested most likely an AT originating from the CSo with a centrifugal activation pattern, which was confirmed by activation mapping. Consistency of return cycles and continuously fragmented local electrograms at successful ablation sites suggested reentry as an underlying AT mechanism. Color-coded 3D entrainment mapping in all 4 patients located the reentrant circuit in the CSo. There were also two specific features observed. One was fragmented and/or double potentials recorded in the CSo with prominent prolonged electrogram duration compared to those during sinus rhythm. The other is a significant conduction delay within the CS. The myocardium of the CSo was suggested as a part of the critical isthmus within the reentrant circuit, while the rest of atria distal to the CSo and myocardial coat of the distal CS were not involved in the tachycardia circuit, which was confirmed by entrainment mapping.

Conclusion: Although CSo myocardium has been implicated to be a part of atrioventricular nodal reentrant tachycardia, to the best of our knowledge, this is the first report showing the localized reentrant AT confined to the CSo. Three of our patients (75%) had concomitant atrial fibrillation (AF). Further studies should be warranted to clarify the role of AT from the CS in triggering AF.