Abstract
Contact impedance mapping can differentiate focal atrial tachyarrhythmias from macroreentry (atrial flutter) and localized reentry (atrioventricular nodal reentry tachycardia) by detecting different patterns of regional unipolar tissue impedance distribution. Specifically, focal atrial tachycardia (AT) is characterized by the finding of a contiguous low-impedance area (CLIA) adjacent to the site of origin, surrounded by normal tissue impedance levels. However, it remains unclear whether or not this finding could distinguish different mechanisms of focal AT. In the present study, we sought to determine whether impedance and voltage maps in patients with microreentrant AT differ from those created due to triggered activity. Consecutive patients undergoing electrophysiologic study and the ablation of AT were included. All patients underwent mapping and ablation procedures in a standard manner. Contact impedance and voltage maps were collected in the background and analyzed offline for comparison. A total of 50 patients with 75 focal ATs were studied and ablated, and the mechanism of AT (ie, triggered activity versus microreentry) was determined. The 41 ATs attributed to triggered activity in 30 patients all demonstrated a CLIA containing or adjacent to the successful ablation site, while the 34 ATs in the 20 patients attributed to microreentry demonstrated uniform impedance. In contrast, microreentrant AT patients were more likely to have scar located adjacent to the site of origin (88.9% versus 18.2%). Three-dimensional mapping employing both contact impedance mapping and voltage mapping can reliably identify the mechanism of focal AT.
Highlights
Contact impedance mapping has been used to differentiate focal atrial tachyarrhythmia from macroreentry[1] and localized reentry[2] by detecting different patterns of impedance, presumably reflecting the differences in the regional patterns of perimembrane and transmembrane current flow seen with each of these arrhythmia mechanisms
There is the finding that the surface area of the contiguous low-impedance area (CLIA) in outflow tract premature ventricular complex impedance maps (5.9 ± 3.8 cm2) is larger than that in focal atrial tachycardia (AT), reflecting both the larger surface area of ventricular myocytes and the larger number of myocytes necessary to overcome the “source-sink” shunting of the ventricular syncytium
The CLIAs associated with outflow tract premature ventricular complex impedance maps have a consistent surface area (5.9 ± 3.8 cm2),[4] which correlates with the larger surface area of ventricular myocytes and the larger number of ventricular myocytes necessary to form the critical mass (n = 700,000 cells) needed to overcome the syncytial shunting
Summary
Contact impedance mapping has been used to differentiate focal atrial tachyarrhythmia from macroreentry (atrial flutter)[1] and localized reentry (atrioventricular nodal reentrant tachycardia)[2] by detecting different patterns of impedance, presumably reflecting the differences in the regional patterns of perimembrane and transmembrane current flow seen with each of these arrhythmia mechanisms. The finding of a contiguous low-impedance area (CLIA) surrounded by normal impedance, of a consistent surface area of 3.0 cm2 ± 2.0 cm[2], occurs only in focal atrial tachycardia (AT) and not in the other mechanisms.[1] We hypothesized that the existence of this CLIA may be due to a higher density of current flow in a localized region due to the afterdepolarizations that cause triggered activity and which drive the membrane to threshold in addition to the current resulting from the regenerative action potential. If the CLIA seen in focal AT results only from triggered automaticity, it should be absent in such microreentrant ATs
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