Mechanism of adenosine-induced termination of focal atrial tachycardia

Satoshi Higa, Ching Tai Tai, Yenn Jiang Lin, Tu Ying Liu, Pi Chang Lee, Jin Long Huang, Yoga Yuniadi, Bien Hsien Huang, Ming Hsiung Hsieh, Shih Huang Lee, Jen Yuan Kuo, Kun Tai Lee, Shih Ann Chen

Research output: Contribution to journalArticle

9 Citations (Scopus)

Abstract

Focal Atrial Tachycardia. Introduction: Adenosine can terminate most focal atrial tachycardias (ATs). However, information about the termination mechanism is limited. This study investigated the effects and mechanism of adenosine on terminating focal AT using a three-dimensional noncontact mapping system. Methods and Results: The study consisted of 7 patients (4 men and 3 women; age 44 ± 29 years) with focal AT. Cycle length variation and atrial activation pattern at baseline and just before AT termination by adenosine (3-12mg) were analyzed. Noncontact mapping demonstrated focal AT propagated from the origin (O) with preferential conduction and spread away from the breakout sites to the whole atrium. Compared to baseline AT, termination episodes revealed higher mean beat-to-beat variation of AT cycle length (11.7 ± 11.7 msec vs 4.7 ± 4.5 msec, P <0.001) and standard deviation of normalized AT cycle length (0.033 ± 0.014 vs 0.011 ± 0.005, P <0.001). In termination episodes, adenosine significantly decreased the peak negative voltage of AT-O (-27.2 ± 15.3%, P <0.01), preferential conduction (proximal: -32.1 ± 18.7, mid: -28.4 ± 22.8, distal portion: -29.6 ± 21.4%, P <0.01), and breakout (-31.4 ± 12.5%, P <0.01). However, adenosine did not affect voltage in nontermination episodes. Adenosine shifted the locations of AT-O in 5 of 10 AT episodes with termination. Mean number of shifting AT-O was 2.4 ± 1.5 (range 1-4), with maximum shifting distance of 15.0 ± 3.1 (range 10-19) mm. Focal activation at AT-O simply disappeared in all termination episodes and therefore was not due to conduction block within preferential conduction or breakout site. Catheter ablation lesions covered 50% of total shifting origins, without late recurrence. Conclusion: Adenosine-induced AT termination was associated with significantly decreased electrogram voltage, shifting AT-O locations, and disappearance of focal activation.

Original languageEnglish
Pages (from-to)1387-1393
Number of pages7
JournalJournal of Cardiovascular Electrophysiology
Volume15
Issue number12
DOIs
Publication statusPublished - Dec 2004

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Tachycardia
Adenosine
Catheter Ablation

Keywords

  • Ablation
  • Adenosine
  • Atrial
  • Mapping
  • Tachycardia

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Physiology

Cite this

Higa, S., Tai, C. T., Lin, Y. J., Liu, T. Y., Lee, P. C., Huang, J. L., ... Chen, S. A. (2004). Mechanism of adenosine-induced termination of focal atrial tachycardia. Journal of Cardiovascular Electrophysiology, 15(12), 1387-1393. https://doi.org/10.1046/j.1540-8167.2004.04346.x

Mechanism of adenosine-induced termination of focal atrial tachycardia. / Higa, Satoshi; Tai, Ching Tai; Lin, Yenn Jiang; Liu, Tu Ying; Lee, Pi Chang; Huang, Jin Long; Yuniadi, Yoga; Huang, Bien Hsien; Hsieh, Ming Hsiung; Lee, Shih Huang; Kuo, Jen Yuan; Lee, Kun Tai; Chen, Shih Ann.

In: Journal of Cardiovascular Electrophysiology, Vol. 15, No. 12, 12.2004, p. 1387-1393.

Research output: Contribution to journalArticle

Higa, S, Tai, CT, Lin, YJ, Liu, TY, Lee, PC, Huang, JL, Yuniadi, Y, Huang, BH, Hsieh, MH, Lee, SH, Kuo, JY, Lee, KT & Chen, SA 2004, 'Mechanism of adenosine-induced termination of focal atrial tachycardia', Journal of Cardiovascular Electrophysiology, vol. 15, no. 12, pp. 1387-1393. https://doi.org/10.1046/j.1540-8167.2004.04346.x
Higa, Satoshi ; Tai, Ching Tai ; Lin, Yenn Jiang ; Liu, Tu Ying ; Lee, Pi Chang ; Huang, Jin Long ; Yuniadi, Yoga ; Huang, Bien Hsien ; Hsieh, Ming Hsiung ; Lee, Shih Huang ; Kuo, Jen Yuan ; Lee, Kun Tai ; Chen, Shih Ann. / Mechanism of adenosine-induced termination of focal atrial tachycardia. In: Journal of Cardiovascular Electrophysiology. 2004 ; Vol. 15, No. 12. pp. 1387-1393.
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abstract = "Focal Atrial Tachycardia. Introduction: Adenosine can terminate most focal atrial tachycardias (ATs). However, information about the termination mechanism is limited. This study investigated the effects and mechanism of adenosine on terminating focal AT using a three-dimensional noncontact mapping system. Methods and Results: The study consisted of 7 patients (4 men and 3 women; age 44 ± 29 years) with focal AT. Cycle length variation and atrial activation pattern at baseline and just before AT termination by adenosine (3-12mg) were analyzed. Noncontact mapping demonstrated focal AT propagated from the origin (O) with preferential conduction and spread away from the breakout sites to the whole atrium. Compared to baseline AT, termination episodes revealed higher mean beat-to-beat variation of AT cycle length (11.7 ± 11.7 msec vs 4.7 ± 4.5 msec, P <0.001) and standard deviation of normalized AT cycle length (0.033 ± 0.014 vs 0.011 ± 0.005, P <0.001). In termination episodes, adenosine significantly decreased the peak negative voltage of AT-O (-27.2 ± 15.3{\%}, P <0.01), preferential conduction (proximal: -32.1 ± 18.7, mid: -28.4 ± 22.8, distal portion: -29.6 ± 21.4{\%}, P <0.01), and breakout (-31.4 ± 12.5{\%}, P <0.01). However, adenosine did not affect voltage in nontermination episodes. Adenosine shifted the locations of AT-O in 5 of 10 AT episodes with termination. Mean number of shifting AT-O was 2.4 ± 1.5 (range 1-4), with maximum shifting distance of 15.0 ± 3.1 (range 10-19) mm. Focal activation at AT-O simply disappeared in all termination episodes and therefore was not due to conduction block within preferential conduction or breakout site. Catheter ablation lesions covered 50{\%} of total shifting origins, without late recurrence. Conclusion: Adenosine-induced AT termination was associated with significantly decreased electrogram voltage, shifting AT-O locations, and disappearance of focal activation.",
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AU - Yuniadi, Yoga

AU - Huang, Bien Hsien

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AU - Lee, Kun Tai

AU - Chen, Shih Ann

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N2 - Focal Atrial Tachycardia. Introduction: Adenosine can terminate most focal atrial tachycardias (ATs). However, information about the termination mechanism is limited. This study investigated the effects and mechanism of adenosine on terminating focal AT using a three-dimensional noncontact mapping system. Methods and Results: The study consisted of 7 patients (4 men and 3 women; age 44 ± 29 years) with focal AT. Cycle length variation and atrial activation pattern at baseline and just before AT termination by adenosine (3-12mg) were analyzed. Noncontact mapping demonstrated focal AT propagated from the origin (O) with preferential conduction and spread away from the breakout sites to the whole atrium. Compared to baseline AT, termination episodes revealed higher mean beat-to-beat variation of AT cycle length (11.7 ± 11.7 msec vs 4.7 ± 4.5 msec, P <0.001) and standard deviation of normalized AT cycle length (0.033 ± 0.014 vs 0.011 ± 0.005, P <0.001). In termination episodes, adenosine significantly decreased the peak negative voltage of AT-O (-27.2 ± 15.3%, P <0.01), preferential conduction (proximal: -32.1 ± 18.7, mid: -28.4 ± 22.8, distal portion: -29.6 ± 21.4%, P <0.01), and breakout (-31.4 ± 12.5%, P <0.01). However, adenosine did not affect voltage in nontermination episodes. Adenosine shifted the locations of AT-O in 5 of 10 AT episodes with termination. Mean number of shifting AT-O was 2.4 ± 1.5 (range 1-4), with maximum shifting distance of 15.0 ± 3.1 (range 10-19) mm. Focal activation at AT-O simply disappeared in all termination episodes and therefore was not due to conduction block within preferential conduction or breakout site. Catheter ablation lesions covered 50% of total shifting origins, without late recurrence. Conclusion: Adenosine-induced AT termination was associated with significantly decreased electrogram voltage, shifting AT-O locations, and disappearance of focal activation.

AB - Focal Atrial Tachycardia. Introduction: Adenosine can terminate most focal atrial tachycardias (ATs). However, information about the termination mechanism is limited. This study investigated the effects and mechanism of adenosine on terminating focal AT using a three-dimensional noncontact mapping system. Methods and Results: The study consisted of 7 patients (4 men and 3 women; age 44 ± 29 years) with focal AT. Cycle length variation and atrial activation pattern at baseline and just before AT termination by adenosine (3-12mg) were analyzed. Noncontact mapping demonstrated focal AT propagated from the origin (O) with preferential conduction and spread away from the breakout sites to the whole atrium. Compared to baseline AT, termination episodes revealed higher mean beat-to-beat variation of AT cycle length (11.7 ± 11.7 msec vs 4.7 ± 4.5 msec, P <0.001) and standard deviation of normalized AT cycle length (0.033 ± 0.014 vs 0.011 ± 0.005, P <0.001). In termination episodes, adenosine significantly decreased the peak negative voltage of AT-O (-27.2 ± 15.3%, P <0.01), preferential conduction (proximal: -32.1 ± 18.7, mid: -28.4 ± 22.8, distal portion: -29.6 ± 21.4%, P <0.01), and breakout (-31.4 ± 12.5%, P <0.01). However, adenosine did not affect voltage in nontermination episodes. Adenosine shifted the locations of AT-O in 5 of 10 AT episodes with termination. Mean number of shifting AT-O was 2.4 ± 1.5 (range 1-4), with maximum shifting distance of 15.0 ± 3.1 (range 10-19) mm. Focal activation at AT-O simply disappeared in all termination episodes and therefore was not due to conduction block within preferential conduction or breakout site. Catheter ablation lesions covered 50% of total shifting origins, without late recurrence. Conclusion: Adenosine-induced AT termination was associated with significantly decreased electrogram voltage, shifting AT-O locations, and disappearance of focal activation.

KW - Ablation

KW - Adenosine

KW - Atrial

KW - Mapping

KW - Tachycardia

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