Impact of adenosine on wavefront propagation in persistent atrial fibrillation: Insights from global noncontact charge density mapping of the left atrium
Impact of adenosine on wavefront propagation in persistent atrial fibrillation: Insights from global noncontact charge density mapping of the left atrium
Background: adenosine shortens action potential duration and refractoriness and provokes atrial fibrillation. This study aimed to evaluate the effect of adenosine on mechanisms of wavefront propagation during atrial fibrillation.
Methods and results: the study included 22 patients undergoing catheter ablation for persistent atrial fibrillation. Left atrial mapping was performed using the AcQMap charge density system before and after administration of intravenous adenosine at 1 or more of 3 time points during the procedure (before pulmonary vein isolation, after pulmonary vein isolation, and after nonpulmonary vein isolation ablation). Wave-front propagation patterns were evaluated allowing identification and quantification of localized rotational activation (LRA), localized irregular activation, and focal firing. Additional signal processing was performed to identify phase singularities and calculate global atrial fibrillation cycle length and dominant frequency. A total of 35 paired maps were analyzed. Adenosine shortened mean atrial fibrillation cycle length from 181.7±14.3 to 165.1±16.3, (mean difference 16.6 ms; 95% CI, 11.3–21.9, P<0.0005) and increased dominant frequency from 6.0±0.7 Hz to 6.6±0.8 Hz (95% CI, 0.4–0.9, P<0.0005). This was associated with a 50% increase in the number of LRA occurrences (16.1±7.6–24.2±8.1; mean difference 8.1, 95% CI, 4.1–12, P<0.0005) as well as a 20% increase in the number of phase singularities detected (30.1±7.8– 36.6±9.3; mean difference 6.5; 95% CI, 2.6–10.0, P=0.002). The percentage of left atrial surface area with LRA increased with adenosine and 42 of 70 zones (60%) with highest density of LRA coincided with high density LRA zones at baseline with only 28% stable across multiple maps.
Conclusions: adenosine accelerates atrial fibrillation and promotes rotational activation patterns with no impact on focal activation. There is little evidence that rotational activation seen with adenosine represents promising targets for ablation aimed at sites of stable arrhythmogenic sources in the left atrium.
AcQMap, adenosine, atrial fibrillation, localized rotational activation
Pope, Michael T.B.
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Kuklik, Pawel
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Briosa e Gala, Andre
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Leo, Milena
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Mahmoudi, Michael
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Paisey, John
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Betts, Timothy R.
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7 June 2022
Pope, Michael T.B.
4e7343b7-a8c4-4ce4-a813-ff0d894b0f92
Kuklik, Pawel
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Briosa e Gala, Andre
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Leo, Milena
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Mahmoudi, Michael
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Paisey, John
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Betts, Timothy R.
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Pope, Michael T.B., Kuklik, Pawel, Briosa e Gala, Andre, Leo, Milena, Mahmoudi, Michael, Paisey, John and Betts, Timothy R.
(2022)
Impact of adenosine on wavefront propagation in persistent atrial fibrillation: Insights from global noncontact charge density mapping of the left atrium.
Journal of the American Heart Association, 11 (11), [e021166].
(doi:10.1161/JAHA.121.021166).
Abstract
Background: adenosine shortens action potential duration and refractoriness and provokes atrial fibrillation. This study aimed to evaluate the effect of adenosine on mechanisms of wavefront propagation during atrial fibrillation.
Methods and results: the study included 22 patients undergoing catheter ablation for persistent atrial fibrillation. Left atrial mapping was performed using the AcQMap charge density system before and after administration of intravenous adenosine at 1 or more of 3 time points during the procedure (before pulmonary vein isolation, after pulmonary vein isolation, and after nonpulmonary vein isolation ablation). Wave-front propagation patterns were evaluated allowing identification and quantification of localized rotational activation (LRA), localized irregular activation, and focal firing. Additional signal processing was performed to identify phase singularities and calculate global atrial fibrillation cycle length and dominant frequency. A total of 35 paired maps were analyzed. Adenosine shortened mean atrial fibrillation cycle length from 181.7±14.3 to 165.1±16.3, (mean difference 16.6 ms; 95% CI, 11.3–21.9, P<0.0005) and increased dominant frequency from 6.0±0.7 Hz to 6.6±0.8 Hz (95% CI, 0.4–0.9, P<0.0005). This was associated with a 50% increase in the number of LRA occurrences (16.1±7.6–24.2±8.1; mean difference 8.1, 95% CI, 4.1–12, P<0.0005) as well as a 20% increase in the number of phase singularities detected (30.1±7.8– 36.6±9.3; mean difference 6.5; 95% CI, 2.6–10.0, P=0.002). The percentage of left atrial surface area with LRA increased with adenosine and 42 of 70 zones (60%) with highest density of LRA coincided with high density LRA zones at baseline with only 28% stable across multiple maps.
Conclusions: adenosine accelerates atrial fibrillation and promotes rotational activation patterns with no impact on focal activation. There is little evidence that rotational activation seen with adenosine represents promising targets for ablation aimed at sites of stable arrhythmogenic sources in the left atrium.
Text
JAHA.121.021166
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Accepted/In Press date: 18 March 2022
e-pub ahead of print date: 27 May 2022
Published date: 7 June 2022
Keywords:
AcQMap, adenosine, atrial fibrillation, localized rotational activation
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Local EPrints ID: 474962
URI: http://eprints.soton.ac.uk/id/eprint/474962
PURE UUID: 0cbc583d-3db2-41b4-aaf0-dbcaffc91227
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Date deposited: 07 Mar 2023 17:47
Last modified: 17 Sep 2025 02:08
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Author:
Michael T.B. Pope
Author:
Pawel Kuklik
Author:
Andre Briosa e Gala
Author:
Milena Leo
Author:
John Paisey
Author:
Timothy R. Betts
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