Variant Forms of Adenosine-Sensitive Atrial Tachycardia Due to Focal Reentry: Electrophysiological Characteristics, Anatomical Distribution, and Consideration to Embryological Substrates

Abstract

Backgrounds: Adenosine-sensitive reentrant AT (ASRAT) was originally reported due to focal reentry involving AV nodal transitional tissues close to the His bundle. However, ASRAT sometimes arises from other regions and its precise anatomical distribution is unclear. Recent histological studies demonstrated the presence of the embryological remnants of node-like tissues around the AV annuli in adult hearts. The roles of those remnants in the arrhythmogenesis are poorly understood. Methods & Results: The electrophysiological and ablation data were reviewed in 62 ASRAT cases. All of the ASRATs (cycle length: 394±82 msec) were reproducibly induced by atrial extrastimulation with an inverse relationship between the coupling interval of the extrastimulus and post-extrastimulation interval to the first tachycardia beat, and they were terminated by an atrial extrastimulus and a bolus of very small amount of adenosine triphosphate (3.7±3.9 mg). The earliest atrial activation during the tachycardia was found in the septal resions [n=37; right superoseptum (20)/midseptum (1)/inferoseptum (14) and left superoseptum (1)/inferoseptum (1)], tricuspid annulus [n=11; superior (2)/lateral (3)/inferior aspect (6)], mitral annulus [n=6; aorto-mitral continuity (5)/lateral aspect (1)], aortic sinuses [n=6; non-coronary (4)/left-coronary sinuses (3)],and proximal CS (n=2). Sixty (97%) of the 62 ASRATs were rendered non-inducible by ablations to the earliest atrial activation site during the tachycardia where the fragmented atrial potentials were recorded. Conclusions: ASRAT arose not only from the AV node vicinity, but also from the AV annuli, aortic sinuses and proximal CS. It was speculated that microreentry involving the embryological remnants of nodal tissues would be the mechanism of ASRAT.