Response to adenosine differentiates focal from macroreentrant atrial tachycardia: Validation using three-dimensional electroanatomic mapping

Sei Iwai, Steven M. Markowitz, Kenneth M. Stein, Suneet Mittal, David J. Slotwiner, Mithilesh K. Das, Jennifer D. Cohen, Steven C. Hao, Bruce B. Lerman

Research output: Contribution to journalArticle

67 Citations (Scopus)

Abstract

Background - We previously proposed that adenosine has mechanism-specific effects on atrial tachycardia (AT), such that adenosine terminates AT attributable to triggered activity, transiently suppresses automatic rhythms, and has no effect on macroreentrant AT. This, however, remains controversial, because other studies have reported that adenosine terminates reentrant AT. To clarify this issue, we used 3D electroanatomic mapping to delineate the tachycardia circuit and thereby determine whether the response to adenosine differentiates focal from macroreentrant AT. Methods and Results - We examined the effect of adenosine on 43 ATs in 42 consecutive patients (59±15 years of age; 26 female) who received adenosine during tachycardia and whose mechanism of AT was characterized by pharmacological perturbation, entrainment, 3D electroanatomic mapping, and results of radiofrequency ablation. Eight tachycardias were macroreentrant (noncavotricuspid isthmus-dependent), and 35 ATs were focal (either triggered or automatic). Adenosine administered during AT (at doses sufficient to result in AV block) terminated or transiently suppressed focal AT in 33 of 35 cases, whereas 8 of 8 macroreentrant ATs were adenosine insensitive (P<0.001). Twenty-eight of 35 focal ATs were located along the crista terminalis or tricuspid annulus. Conclusions - The response of AT to adenosine can immediately differentiate atrial tachycardia arising from a focal source from that attributable to macroreentry. This finding can be exploited to facilitate developing a focused, strategic ablative approach at the onset of a procedure.

Original languageEnglish (US)
Pages (from-to)2793-2799
Number of pages7
JournalCirculation
Volume106
Issue number22
DOIs
StatePublished - Nov 26 2002
Externally publishedYes

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Tachycardia
Adenosine
Atrioventricular Block
Pharmacology

Keywords

  • Ablation
  • Adenosine
  • Mapping
  • Tachycardia

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

Cite this

Response to adenosine differentiates focal from macroreentrant atrial tachycardia : Validation using three-dimensional electroanatomic mapping. / Iwai, Sei; Markowitz, Steven M.; Stein, Kenneth M.; Mittal, Suneet; Slotwiner, David J.; Das, Mithilesh K.; Cohen, Jennifer D.; Hao, Steven C.; Lerman, Bruce B.

In: Circulation, Vol. 106, No. 22, 26.11.2002, p. 2793-2799.

Research output: Contribution to journalArticle

Iwai, Sei ; Markowitz, Steven M. ; Stein, Kenneth M. ; Mittal, Suneet ; Slotwiner, David J. ; Das, Mithilesh K. ; Cohen, Jennifer D. ; Hao, Steven C. ; Lerman, Bruce B. / Response to adenosine differentiates focal from macroreentrant atrial tachycardia : Validation using three-dimensional electroanatomic mapping. In: Circulation. 2002 ; Vol. 106, No. 22. pp. 2793-2799.
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T1 - Response to adenosine differentiates focal from macroreentrant atrial tachycardia

T2 - Validation using three-dimensional electroanatomic mapping

AU - Iwai, Sei

AU - Markowitz, Steven M.

AU - Stein, Kenneth M.

AU - Mittal, Suneet

AU - Slotwiner, David J.

AU - Das, Mithilesh K.

AU - Cohen, Jennifer D.

AU - Hao, Steven C.

AU - Lerman, Bruce B.

PY - 2002/11/26

Y1 - 2002/11/26

N2 - Background - We previously proposed that adenosine has mechanism-specific effects on atrial tachycardia (AT), such that adenosine terminates AT attributable to triggered activity, transiently suppresses automatic rhythms, and has no effect on macroreentrant AT. This, however, remains controversial, because other studies have reported that adenosine terminates reentrant AT. To clarify this issue, we used 3D electroanatomic mapping to delineate the tachycardia circuit and thereby determine whether the response to adenosine differentiates focal from macroreentrant AT. Methods and Results - We examined the effect of adenosine on 43 ATs in 42 consecutive patients (59±15 years of age; 26 female) who received adenosine during tachycardia and whose mechanism of AT was characterized by pharmacological perturbation, entrainment, 3D electroanatomic mapping, and results of radiofrequency ablation. Eight tachycardias were macroreentrant (noncavotricuspid isthmus-dependent), and 35 ATs were focal (either triggered or automatic). Adenosine administered during AT (at doses sufficient to result in AV block) terminated or transiently suppressed focal AT in 33 of 35 cases, whereas 8 of 8 macroreentrant ATs were adenosine insensitive (P<0.001). Twenty-eight of 35 focal ATs were located along the crista terminalis or tricuspid annulus. Conclusions - The response of AT to adenosine can immediately differentiate atrial tachycardia arising from a focal source from that attributable to macroreentry. This finding can be exploited to facilitate developing a focused, strategic ablative approach at the onset of a procedure.

AB - Background - We previously proposed that adenosine has mechanism-specific effects on atrial tachycardia (AT), such that adenosine terminates AT attributable to triggered activity, transiently suppresses automatic rhythms, and has no effect on macroreentrant AT. This, however, remains controversial, because other studies have reported that adenosine terminates reentrant AT. To clarify this issue, we used 3D electroanatomic mapping to delineate the tachycardia circuit and thereby determine whether the response to adenosine differentiates focal from macroreentrant AT. Methods and Results - We examined the effect of adenosine on 43 ATs in 42 consecutive patients (59±15 years of age; 26 female) who received adenosine during tachycardia and whose mechanism of AT was characterized by pharmacological perturbation, entrainment, 3D electroanatomic mapping, and results of radiofrequency ablation. Eight tachycardias were macroreentrant (noncavotricuspid isthmus-dependent), and 35 ATs were focal (either triggered or automatic). Adenosine administered during AT (at doses sufficient to result in AV block) terminated or transiently suppressed focal AT in 33 of 35 cases, whereas 8 of 8 macroreentrant ATs were adenosine insensitive (P<0.001). Twenty-eight of 35 focal ATs were located along the crista terminalis or tricuspid annulus. Conclusions - The response of AT to adenosine can immediately differentiate atrial tachycardia arising from a focal source from that attributable to macroreentry. This finding can be exploited to facilitate developing a focused, strategic ablative approach at the onset of a procedure.

KW - Ablation

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KW - Mapping

KW - Tachycardia

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