Adenosine-insensitive focal atrial tachycardia: evidence for de novo micro-re-entry in the human atrium.
OBJECTIVE
The purpose of this work was to describe the entity and mechanism of adenosine-insensitive focal atrial tachycardia (AT).


BACKGROUND
The majority of regular focal ATs demonstrate properties consistent with triggered activity, including termination by adenosine. Less commonly, AT may be due to enhanced automaticity, which is transiently suppressed by adenosine. Small re-entrant circuits may also give rise to focal AT, but limited data exist regarding this entity as a de novo arrhythmia in the human atrium.


METHODS
Eighty cases of focal AT were mapped in the electrophysiology laboratory and challenged with adenosine. Adenosine-sensitive and -insensitive groups were compared with regard to demographics, anatomical distribution, and electrogram characteristics at the tachycardia origin.


RESULTS
In response to adenosine, termination occurred in 67 cases (84%), transient suppression in 5 (6%), 6 were insensitive (8%), and 2 exhibited nonspecific responses. Adenosine-insensitive AT arose near the pulmonary vein ostia (4) and from the right atrium (2), whereas adenosine-sensitive AT arose from a wide distribution in both atria. Electrograms at the site of origin for adenosine-insensitive AT were highly fractionated, with longer durations and lower amplitudes compared with AT that terminated or was transiently suppressed. The electrograms at the origin of adenosine-insensitive ATs comprised 22% to 69% of the tachycardia cycle length, compared with 4% to 21% for adenosine-sensitive ATs. In 3 adenosine-insensitive ATs, entrainment was demonstrated with post-pacing intervals equivalent to the tachycardia cycle length.


CONCLUSIONS
The characteristics of adenosine-insensitive focal AT differ from adenosine-sensitive AT and are consistent with small re-entrant circuits. These data provide evidence that focal re-entry is a mechanism of AT and has an electropharmacologic profile that differs from AT due to automaticity and triggered activity.
Markowitz
Steven M
SM
Department of Medicine, Division of Cardiology, Cornell University Medical Center, New York, New York, USA. smarkow@med.cornell.edu
Nemirovksy
Dmitry
D
Stein
Kenneth M
KM
Mittal
Suneet
S
Iwai
Sei
S
Shah
Bindi K
BK
Dobesh
David P
DP
Lerman
Bruce B
BB
D000241:Adenosine / Q000494:pharmacology / Q000627:therapeutic use*; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D018780:Body Surface Potential Mapping / Q000187:drug effects / Q000379:methods; D005260:Female; D006325:Heart Atria / Q000187:drug effects; D006801:Humans; D008297:Male; D008875:Middle Aged; D013611:Tachycardia, Atrioventricular Nodal Reentry / Q000188:drug therapy / Q000503:physiopathology; D013612:Tachycardia, Ectopic Atrial / Q000188:drug therapy* / Q000503:physiopathology*
D000241:Adenosine