Acute atrial stretch results in conduction slowing and complex signals at the pulmonary vein to left atrial junction: Insights into the mechanism of pulmonary vein arrhythmogenesis

Tomos E. Walters, Geoffrey Lee, Steven Spence, Marco Larobina, Victoria Atkinson, Phillip Antippa, John Goldblatt, Michael O'Keefe, Prashanthan Sanders, Peter M. Kistler, Jonathan M. Kalman

Research output: Contribution to journalArticle

23 Citations (Scopus)

Abstract

Background: The pulmonary vein-left atrial (PV-LA) junction is key in pathogenesis of AF, and acute stretch is an important stimulus to AF. We aimed to characterize the response of the junction to acute stretch, hypothesizing that stretch would result in electrophysiological changes predisposing to re-entry. Methods and Results: Fifteen participants undergoing cardiac surgery underwent evaluation of the right superior PV-LA junction using an epicardial mapping plaque. In 10, this was performed before and after atrial stretch imposed by rapid volume expansion, and in 5, it was performed with an intervening observation period. Activation was characterized by conduction slowing and electrogram fractionation transversely across the PV-LA junction, with lines of block also demonstrated perpendicular to the junction. Conduction was decremental (plaque activation time 135.8±46.8 ms with programmed extra stimuli at 10 ms above effective refractory period versus 66.1±22.9 ms with pacing at 400 ms; P<0.001) and percentage fractionation was greater with programmed extra stimuli at 10 ms above (33.5%±15.3% versus 20.7%±14.0%, P=0.001). Right atrial pressure increased by 2.5±1.8 mm Hg (P=0.002) with volume expansion. Stretch resulted in conduction slowing across the PV-LA junction (increase in activation time 10.9±14.6 ms in acute stretch group versus -0.1±4.5 ms in control group; P=0.002). Conduction slowing was more marked with programmed extra stimuli at 10 ms above effective refractory period than with stable pacing (13.4±16.5 ms versus 1.7±5.4 ms; P=0.003). Stretch resulted in a significant increase in fractionated electrograms (7.9%±7.0% versus -0.4±3.3; P=0.004). Conclusions: Acute stretch results in conduction slowing across the PV-LA junction, with a greater degree of signal complexity. This substrate may be important in AF initiation and maintenance by promoting re-entry.

LanguageEnglish
Pages1189-1197
Number of pages9
JournalCirculation: Arrhythmia and Electrophysiology
Volume7
Issue number6
DOIs
Publication statusPublished - 1 Dec 2014

Keywords

  • Atrial fibrillation
  • Electrophysiology
  • Pulmonary vein
  • Stretch

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

Cite this

Walters, Tomos E. ; Lee, Geoffrey ; Spence, Steven ; Larobina, Marco ; Atkinson, Victoria ; Antippa, Phillip ; Goldblatt, John ; O'Keefe, Michael ; Sanders, Prashanthan ; Kistler, Peter M. ; Kalman, Jonathan M. / Acute atrial stretch results in conduction slowing and complex signals at the pulmonary vein to left atrial junction : Insights into the mechanism of pulmonary vein arrhythmogenesis. In: Circulation: Arrhythmia and Electrophysiology. 2014 ; Vol. 7, No. 6. pp. 1189-1197.
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abstract = "Background: The pulmonary vein-left atrial (PV-LA) junction is key in pathogenesis of AF, and acute stretch is an important stimulus to AF. We aimed to characterize the response of the junction to acute stretch, hypothesizing that stretch would result in electrophysiological changes predisposing to re-entry. Methods and Results: Fifteen participants undergoing cardiac surgery underwent evaluation of the right superior PV-LA junction using an epicardial mapping plaque. In 10, this was performed before and after atrial stretch imposed by rapid volume expansion, and in 5, it was performed with an intervening observation period. Activation was characterized by conduction slowing and electrogram fractionation transversely across the PV-LA junction, with lines of block also demonstrated perpendicular to the junction. Conduction was decremental (plaque activation time 135.8±46.8 ms with programmed extra stimuli at 10 ms above effective refractory period versus 66.1±22.9 ms with pacing at 400 ms; P<0.001) and percentage fractionation was greater with programmed extra stimuli at 10 ms above (33.5{\%}±15.3{\%} versus 20.7{\%}±14.0{\%}, P=0.001). Right atrial pressure increased by 2.5±1.8 mm Hg (P=0.002) with volume expansion. Stretch resulted in conduction slowing across the PV-LA junction (increase in activation time 10.9±14.6 ms in acute stretch group versus -0.1±4.5 ms in control group; P=0.002). Conduction slowing was more marked with programmed extra stimuli at 10 ms above effective refractory period than with stable pacing (13.4±16.5 ms versus 1.7±5.4 ms; P=0.003). Stretch resulted in a significant increase in fractionated electrograms (7.9{\%}±7.0{\%} versus -0.4±3.3; P=0.004). Conclusions: Acute stretch results in conduction slowing across the PV-LA junction, with a greater degree of signal complexity. This substrate may be important in AF initiation and maintenance by promoting re-entry.",
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Acute atrial stretch results in conduction slowing and complex signals at the pulmonary vein to left atrial junction : Insights into the mechanism of pulmonary vein arrhythmogenesis. / Walters, Tomos E.; Lee, Geoffrey; Spence, Steven; Larobina, Marco; Atkinson, Victoria; Antippa, Phillip; Goldblatt, John; O'Keefe, Michael; Sanders, Prashanthan; Kistler, Peter M.; Kalman, Jonathan M.

In: Circulation: Arrhythmia and Electrophysiology, Vol. 7, No. 6, 01.12.2014, p. 1189-1197.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Acute atrial stretch results in conduction slowing and complex signals at the pulmonary vein to left atrial junction

T2 - Circulation: Arrhythmia and Electrophysiology

AU - Walters, Tomos E.

AU - Lee, Geoffrey

AU - Spence, Steven

AU - Larobina, Marco

AU - Atkinson, Victoria

AU - Antippa, Phillip

AU - Goldblatt, John

AU - O'Keefe, Michael

AU - Sanders, Prashanthan

AU - Kistler, Peter M.

AU - Kalman, Jonathan M.

PY - 2014/12/1

Y1 - 2014/12/1

N2 - Background: The pulmonary vein-left atrial (PV-LA) junction is key in pathogenesis of AF, and acute stretch is an important stimulus to AF. We aimed to characterize the response of the junction to acute stretch, hypothesizing that stretch would result in electrophysiological changes predisposing to re-entry. Methods and Results: Fifteen participants undergoing cardiac surgery underwent evaluation of the right superior PV-LA junction using an epicardial mapping plaque. In 10, this was performed before and after atrial stretch imposed by rapid volume expansion, and in 5, it was performed with an intervening observation period. Activation was characterized by conduction slowing and electrogram fractionation transversely across the PV-LA junction, with lines of block also demonstrated perpendicular to the junction. Conduction was decremental (plaque activation time 135.8±46.8 ms with programmed extra stimuli at 10 ms above effective refractory period versus 66.1±22.9 ms with pacing at 400 ms; P<0.001) and percentage fractionation was greater with programmed extra stimuli at 10 ms above (33.5%±15.3% versus 20.7%±14.0%, P=0.001). Right atrial pressure increased by 2.5±1.8 mm Hg (P=0.002) with volume expansion. Stretch resulted in conduction slowing across the PV-LA junction (increase in activation time 10.9±14.6 ms in acute stretch group versus -0.1±4.5 ms in control group; P=0.002). Conduction slowing was more marked with programmed extra stimuli at 10 ms above effective refractory period than with stable pacing (13.4±16.5 ms versus 1.7±5.4 ms; P=0.003). Stretch resulted in a significant increase in fractionated electrograms (7.9%±7.0% versus -0.4±3.3; P=0.004). Conclusions: Acute stretch results in conduction slowing across the PV-LA junction, with a greater degree of signal complexity. This substrate may be important in AF initiation and maintenance by promoting re-entry.

AB - Background: The pulmonary vein-left atrial (PV-LA) junction is key in pathogenesis of AF, and acute stretch is an important stimulus to AF. We aimed to characterize the response of the junction to acute stretch, hypothesizing that stretch would result in electrophysiological changes predisposing to re-entry. Methods and Results: Fifteen participants undergoing cardiac surgery underwent evaluation of the right superior PV-LA junction using an epicardial mapping plaque. In 10, this was performed before and after atrial stretch imposed by rapid volume expansion, and in 5, it was performed with an intervening observation period. Activation was characterized by conduction slowing and electrogram fractionation transversely across the PV-LA junction, with lines of block also demonstrated perpendicular to the junction. Conduction was decremental (plaque activation time 135.8±46.8 ms with programmed extra stimuli at 10 ms above effective refractory period versus 66.1±22.9 ms with pacing at 400 ms; P<0.001) and percentage fractionation was greater with programmed extra stimuli at 10 ms above (33.5%±15.3% versus 20.7%±14.0%, P=0.001). Right atrial pressure increased by 2.5±1.8 mm Hg (P=0.002) with volume expansion. Stretch resulted in conduction slowing across the PV-LA junction (increase in activation time 10.9±14.6 ms in acute stretch group versus -0.1±4.5 ms in control group; P=0.002). Conduction slowing was more marked with programmed extra stimuli at 10 ms above effective refractory period than with stable pacing (13.4±16.5 ms versus 1.7±5.4 ms; P=0.003). Stretch resulted in a significant increase in fractionated electrograms (7.9%±7.0% versus -0.4±3.3; P=0.004). Conclusions: Acute stretch results in conduction slowing across the PV-LA junction, with a greater degree of signal complexity. This substrate may be important in AF initiation and maintenance by promoting re-entry.

KW - Atrial fibrillation

KW - Electrophysiology

KW - Pulmonary vein

KW - Stretch

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U2 - 10.1161/CIRCEP.114.001894

DO - 10.1161/CIRCEP.114.001894

M3 - Article

VL - 7

SP - 1189

EP - 1197

JO - Circulation: Arrhythmia and Electrophysiology

JF - Circulation: Arrhythmia and Electrophysiology

SN - 1941-3149

IS - 6

ER -