Effect of high intensity drive train stimulation on dispersion of atrial refractoriness: Role of autonomic nervous system

Wen Chung Yu, Shih A. Chen, Chern E. Chiang, Ching T. Tai, Shih Huang Lee, Chuen Wang Chiou, Kwo Chang Ueng, Zu Chin Wen, Yi J. Chen, Jin Long Huang, An Ning Feng, Mau Song Chang

Research output: Contribution to journalArticle

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Abstract

Objectives. This study evaluated the effect of high intensity drive train (S1) stimulation on the atrial effective refractory period (ERP) and its relation to the autonomic nervous system. Background. High intensity S1 stimulation was demonstrated to shorten the ventricular ERP and to increase dispersion of refractoriness. These effects may be due to local release of neurotransmitters. The response of the atrium and ventricle to neurotransmitters was different. The effects of high intensity S1 stimulation at the atrial tissue were evaluated. Methods. Forty patients without structural heart disease were studied. In group 1, 20 patients, the atrial ERP was measured at 0, 7, 14, 21 and 28 mm away from the S1 site under both twice diastolic threshold and high intensity (10 mA) S1 stimulation. The same protocol was repeated after sequential administration of propranolol (0.2 mg/kg body weight) and atropine (0.04 mg/kg). In group 2, the other 20 patients, the atrial ERP was studied at three atrial sites (high lateral right atrium [HLRA], right posterior interatrial septum [RPS] and distal coronary sinus [DCS] with twice diastolic threshold and high intensity S1 stimulation at baseline and after sequential autonomic blockade. The three atrial sites were randomly assigned as the S1 location. Results. 1n group 1, high intensity S1 stimulation shortened the atrial effective refractory period most prominently at the site of S1: (mean ± SD) 13.3 ± 6.4% (p <0.001), 8.1 ± 3.8% (p <0.001), 4.8 ± 4.3% (p <0.001), 3.7 ± 4.7% (p <0.001) and 0.5 ± 2.6% at 0, 7, 14, 21 and 28 mm from the S1 site, respectively. The effect of high intensity S1 stimulation was blunted with propranolol and autonomic blockade but persisted after atropine alone. High intensity S1 stimulation also increased dispersion of refractoriness (from 23 ± 11 ms to 31 ± 12 ms, p = 0.01), which was eliminated with autonomic blockade. In group 2, high intensity S1 stimulation had similar effects at different locations (ERP shortening of 10.8 ± 2.7%, 10.8 ± 2.2% and 12.2 ± 4.6% at the HLRA, RPS and DCS, respectively). The responses to sequential autonomic blockade were similar to those in group 1. However, high intensity S1 stimulation at HLRA increased dispersion of refractoriness, but at DCS it reduced dispersion of refractoriness. Conclusions. High intensity S1 stimulation led to local shortening of the atrial ERP and increased dispersion of refractoriness. These effects were blunted with propranolol and autonomic blockade. High intensity S1 stimulation at the HLRA increased dispersion of atrial refractoriness, whereas the same stimulation at the DCS decreased dispersion of atrial refractoriness.

Original languageEnglish
Pages (from-to)1000-1006
Number of pages7
JournalJournal of the American College of Cardiology
Volume29
Issue number5
DOIs
Publication statusPublished - Apr 1997
Externally publishedYes

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Coronary Sinus
Autonomic Nervous System
Heart Atria
Propranolol
Atropine
Neurotransmitter Agents
Heart Diseases
Body Weight

ASJC Scopus subject areas

  • Nursing(all)

Cite this

Effect of high intensity drive train stimulation on dispersion of atrial refractoriness : Role of autonomic nervous system. / Yu, Wen Chung; Chen, Shih A.; Chiang, Chern E.; Tai, Ching T.; Lee, Shih Huang; Chiou, Chuen Wang; Ueng, Kwo Chang; Wen, Zu Chin; Chen, Yi J.; Huang, Jin Long; Feng, An Ning; Chang, Mau Song.

In: Journal of the American College of Cardiology, Vol. 29, No. 5, 04.1997, p. 1000-1006.

Research output: Contribution to journalArticle

Yu, WC, Chen, SA, Chiang, CE, Tai, CT, Lee, SH, Chiou, CW, Ueng, KC, Wen, ZC, Chen, YJ, Huang, JL, Feng, AN & Chang, MS 1997, 'Effect of high intensity drive train stimulation on dispersion of atrial refractoriness: Role of autonomic nervous system', Journal of the American College of Cardiology, vol. 29, no. 5, pp. 1000-1006. https://doi.org/10.1016/S0735-1097(97)00036-3
Yu, Wen Chung ; Chen, Shih A. ; Chiang, Chern E. ; Tai, Ching T. ; Lee, Shih Huang ; Chiou, Chuen Wang ; Ueng, Kwo Chang ; Wen, Zu Chin ; Chen, Yi J. ; Huang, Jin Long ; Feng, An Ning ; Chang, Mau Song. / Effect of high intensity drive train stimulation on dispersion of atrial refractoriness : Role of autonomic nervous system. In: Journal of the American College of Cardiology. 1997 ; Vol. 29, No. 5. pp. 1000-1006.
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title = "Effect of high intensity drive train stimulation on dispersion of atrial refractoriness: Role of autonomic nervous system",
abstract = "Objectives. This study evaluated the effect of high intensity drive train (S1) stimulation on the atrial effective refractory period (ERP) and its relation to the autonomic nervous system. Background. High intensity S1 stimulation was demonstrated to shorten the ventricular ERP and to increase dispersion of refractoriness. These effects may be due to local release of neurotransmitters. The response of the atrium and ventricle to neurotransmitters was different. The effects of high intensity S1 stimulation at the atrial tissue were evaluated. Methods. Forty patients without structural heart disease were studied. In group 1, 20 patients, the atrial ERP was measured at 0, 7, 14, 21 and 28 mm away from the S1 site under both twice diastolic threshold and high intensity (10 mA) S1 stimulation. The same protocol was repeated after sequential administration of propranolol (0.2 mg/kg body weight) and atropine (0.04 mg/kg). In group 2, the other 20 patients, the atrial ERP was studied at three atrial sites (high lateral right atrium [HLRA], right posterior interatrial septum [RPS] and distal coronary sinus [DCS] with twice diastolic threshold and high intensity S1 stimulation at baseline and after sequential autonomic blockade. The three atrial sites were randomly assigned as the S1 location. Results. 1n group 1, high intensity S1 stimulation shortened the atrial effective refractory period most prominently at the site of S1: (mean ± SD) 13.3 ± 6.4{\%} (p <0.001), 8.1 ± 3.8{\%} (p <0.001), 4.8 ± 4.3{\%} (p <0.001), 3.7 ± 4.7{\%} (p <0.001) and 0.5 ± 2.6{\%} at 0, 7, 14, 21 and 28 mm from the S1 site, respectively. The effect of high intensity S1 stimulation was blunted with propranolol and autonomic blockade but persisted after atropine alone. High intensity S1 stimulation also increased dispersion of refractoriness (from 23 ± 11 ms to 31 ± 12 ms, p = 0.01), which was eliminated with autonomic blockade. In group 2, high intensity S1 stimulation had similar effects at different locations (ERP shortening of 10.8 ± 2.7{\%}, 10.8 ± 2.2{\%} and 12.2 ± 4.6{\%} at the HLRA, RPS and DCS, respectively). The responses to sequential autonomic blockade were similar to those in group 1. However, high intensity S1 stimulation at HLRA increased dispersion of refractoriness, but at DCS it reduced dispersion of refractoriness. Conclusions. High intensity S1 stimulation led to local shortening of the atrial ERP and increased dispersion of refractoriness. These effects were blunted with propranolol and autonomic blockade. High intensity S1 stimulation at the HLRA increased dispersion of atrial refractoriness, whereas the same stimulation at the DCS decreased dispersion of atrial refractoriness.",
author = "Yu, {Wen Chung} and Chen, {Shih A.} and Chiang, {Chern E.} and Tai, {Ching T.} and Lee, {Shih Huang} and Chiou, {Chuen Wang} and Ueng, {Kwo Chang} and Wen, {Zu Chin} and Chen, {Yi J.} and Huang, {Jin Long} and Feng, {An Ning} and Chang, {Mau Song}",
year = "1997",
month = "4",
doi = "10.1016/S0735-1097(97)00036-3",
language = "English",
volume = "29",
pages = "1000--1006",
journal = "Journal of the American College of Cardiology",
issn = "0735-1097",
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}

TY - JOUR

T1 - Effect of high intensity drive train stimulation on dispersion of atrial refractoriness

T2 - Role of autonomic nervous system

AU - Yu, Wen Chung

AU - Chen, Shih A.

AU - Chiang, Chern E.

AU - Tai, Ching T.

AU - Lee, Shih Huang

AU - Chiou, Chuen Wang

AU - Ueng, Kwo Chang

AU - Wen, Zu Chin

AU - Chen, Yi J.

AU - Huang, Jin Long

AU - Feng, An Ning

AU - Chang, Mau Song

PY - 1997/4

Y1 - 1997/4

N2 - Objectives. This study evaluated the effect of high intensity drive train (S1) stimulation on the atrial effective refractory period (ERP) and its relation to the autonomic nervous system. Background. High intensity S1 stimulation was demonstrated to shorten the ventricular ERP and to increase dispersion of refractoriness. These effects may be due to local release of neurotransmitters. The response of the atrium and ventricle to neurotransmitters was different. The effects of high intensity S1 stimulation at the atrial tissue were evaluated. Methods. Forty patients without structural heart disease were studied. In group 1, 20 patients, the atrial ERP was measured at 0, 7, 14, 21 and 28 mm away from the S1 site under both twice diastolic threshold and high intensity (10 mA) S1 stimulation. The same protocol was repeated after sequential administration of propranolol (0.2 mg/kg body weight) and atropine (0.04 mg/kg). In group 2, the other 20 patients, the atrial ERP was studied at three atrial sites (high lateral right atrium [HLRA], right posterior interatrial septum [RPS] and distal coronary sinus [DCS] with twice diastolic threshold and high intensity S1 stimulation at baseline and after sequential autonomic blockade. The three atrial sites were randomly assigned as the S1 location. Results. 1n group 1, high intensity S1 stimulation shortened the atrial effective refractory period most prominently at the site of S1: (mean ± SD) 13.3 ± 6.4% (p <0.001), 8.1 ± 3.8% (p <0.001), 4.8 ± 4.3% (p <0.001), 3.7 ± 4.7% (p <0.001) and 0.5 ± 2.6% at 0, 7, 14, 21 and 28 mm from the S1 site, respectively. The effect of high intensity S1 stimulation was blunted with propranolol and autonomic blockade but persisted after atropine alone. High intensity S1 stimulation also increased dispersion of refractoriness (from 23 ± 11 ms to 31 ± 12 ms, p = 0.01), which was eliminated with autonomic blockade. In group 2, high intensity S1 stimulation had similar effects at different locations (ERP shortening of 10.8 ± 2.7%, 10.8 ± 2.2% and 12.2 ± 4.6% at the HLRA, RPS and DCS, respectively). The responses to sequential autonomic blockade were similar to those in group 1. However, high intensity S1 stimulation at HLRA increased dispersion of refractoriness, but at DCS it reduced dispersion of refractoriness. Conclusions. High intensity S1 stimulation led to local shortening of the atrial ERP and increased dispersion of refractoriness. These effects were blunted with propranolol and autonomic blockade. High intensity S1 stimulation at the HLRA increased dispersion of atrial refractoriness, whereas the same stimulation at the DCS decreased dispersion of atrial refractoriness.

AB - Objectives. This study evaluated the effect of high intensity drive train (S1) stimulation on the atrial effective refractory period (ERP) and its relation to the autonomic nervous system. Background. High intensity S1 stimulation was demonstrated to shorten the ventricular ERP and to increase dispersion of refractoriness. These effects may be due to local release of neurotransmitters. The response of the atrium and ventricle to neurotransmitters was different. The effects of high intensity S1 stimulation at the atrial tissue were evaluated. Methods. Forty patients without structural heart disease were studied. In group 1, 20 patients, the atrial ERP was measured at 0, 7, 14, 21 and 28 mm away from the S1 site under both twice diastolic threshold and high intensity (10 mA) S1 stimulation. The same protocol was repeated after sequential administration of propranolol (0.2 mg/kg body weight) and atropine (0.04 mg/kg). In group 2, the other 20 patients, the atrial ERP was studied at three atrial sites (high lateral right atrium [HLRA], right posterior interatrial septum [RPS] and distal coronary sinus [DCS] with twice diastolic threshold and high intensity S1 stimulation at baseline and after sequential autonomic blockade. The three atrial sites were randomly assigned as the S1 location. Results. 1n group 1, high intensity S1 stimulation shortened the atrial effective refractory period most prominently at the site of S1: (mean ± SD) 13.3 ± 6.4% (p <0.001), 8.1 ± 3.8% (p <0.001), 4.8 ± 4.3% (p <0.001), 3.7 ± 4.7% (p <0.001) and 0.5 ± 2.6% at 0, 7, 14, 21 and 28 mm from the S1 site, respectively. The effect of high intensity S1 stimulation was blunted with propranolol and autonomic blockade but persisted after atropine alone. High intensity S1 stimulation also increased dispersion of refractoriness (from 23 ± 11 ms to 31 ± 12 ms, p = 0.01), which was eliminated with autonomic blockade. In group 2, high intensity S1 stimulation had similar effects at different locations (ERP shortening of 10.8 ± 2.7%, 10.8 ± 2.2% and 12.2 ± 4.6% at the HLRA, RPS and DCS, respectively). The responses to sequential autonomic blockade were similar to those in group 1. However, high intensity S1 stimulation at HLRA increased dispersion of refractoriness, but at DCS it reduced dispersion of refractoriness. Conclusions. High intensity S1 stimulation led to local shortening of the atrial ERP and increased dispersion of refractoriness. These effects were blunted with propranolol and autonomic blockade. High intensity S1 stimulation at the HLRA increased dispersion of atrial refractoriness, whereas the same stimulation at the DCS decreased dispersion of atrial refractoriness.

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