Tight mechanism correlation between heart rate turbulence and baroreflex sensitivity

Sequential autonomic blockade analysis

Lian Yu Lin, Ling Ping Lai, Jiunn Lee Lin, Chao Cheng Du, Wen Yi Shau, Hsiao Lung Chan, Yung Zu Tseng, Shoei K. Stephen Huang

Research output: Contribution to journalArticle

96 Citations (Scopus)

Abstract

Introduction: Heart rate turbulence is a powerful de novo risk predictor for patients surviving acute myocardial infarction. However, little is known about its underlying physiologic mechanism. Methods and Results: Hypothesizing that heart rate turbulence is barorceptor reflex related, we studied heart rate and blood pressure fluctuations at rest and after systematically introduced ventricular premature beats in 16 patients without structural heart disease (10 men and 6 women; mean age 45 ± 17 years) before and after sequential sympathetic (esmolol 4-mg bolus followed by 120 μg/kg/min intravenously), parasympathetic (atropine 0.04 mg/kg intravenously), and combined autonomic blockade (esmolol plus atropine). Turbulence onset (%) and turbulence slope (msec/beat) were averaged from 10 respective ventricular premature beats. Spontaneous baroreflex sensitivity (msec/mmHg) was calculated from 5 minutes of sinus rhythm recording. The results showed that turbulence slope decreased after atropine (0.71 ± 0.50 msec/beat vs 5.17 ± 3.96 msec/beat at baseline; P < 0.01) and combined autonomic blockade (1.23 ± 1.02 msec/beat; P < 0.01) but was unchanged after esmolol (4.53 ± 3.30 msec/beat; P > 0.05). Turbulence onset increased after atropine (0.32% ± 0.35% vs -0.45 ± 0.94 at baseline; P < 0.05) and combined sympathetic and parasympathetic blockade (0.58% ± 0.86%; P < 0.05) but was unchanged after esmolol (-0.62% ± 1.33%; P > 0.05). Turbulence slope was positively correlated with baroreflex sensitivity at baseline (r = 0.78, P < 0.01) and after esmolol (r = 0.8, P < 0.01), but dissociated after atropine (r = 0.16, P > 0.05) and combined autonomic blockade (r = 0.31, P > 0.05). Turbulence onset was negatively correlated with baroreflex sensitivity at baseline (r = -0.61, P < 0.05), after esmolol (r = -0.80, P < 0.01), and after atropine (r = -0.53, P < 0.05). Conclusion: Heart rate turbulence of turbulence onset and turbulence slope is critically vagal dependent and highly correlated with spontaneous baroreflex sensitivity, which underscores its clinical importance in cardiovascular risk stratification.

Original languageEnglish
Pages (from-to)427-431
Number of pages5
JournalJournal of Cardiovascular Electrophysiology
Volume13
Issue number5
DOIs
Publication statusPublished - Jan 1 2002
Externally publishedYes

Fingerprint

Baroreflex
Atropine
Heart Rate
Ventricular Premature Complexes
Reflex
Heart Diseases
Myocardial Infarction
Blood Pressure
esmolol

Keywords

  • Autonomic blockade
  • Autonomic nervous system
  • Baroreflex sensitivity
  • Cardiovascular risk stratification
  • Heart rate turbulence

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

Cite this

Tight mechanism correlation between heart rate turbulence and baroreflex sensitivity : Sequential autonomic blockade analysis. / Lin, Lian Yu; Lai, Ling Ping; Lin, Jiunn Lee; Du, Chao Cheng; Shau, Wen Yi; Chan, Hsiao Lung; Tseng, Yung Zu; Stephen Huang, Shoei K.

In: Journal of Cardiovascular Electrophysiology, Vol. 13, No. 5, 01.01.2002, p. 427-431.

Research output: Contribution to journalArticle

Lin, Lian Yu ; Lai, Ling Ping ; Lin, Jiunn Lee ; Du, Chao Cheng ; Shau, Wen Yi ; Chan, Hsiao Lung ; Tseng, Yung Zu ; Stephen Huang, Shoei K. / Tight mechanism correlation between heart rate turbulence and baroreflex sensitivity : Sequential autonomic blockade analysis. In: Journal of Cardiovascular Electrophysiology. 2002 ; Vol. 13, No. 5. pp. 427-431.
@article{8db06c4585c445df888aac74bed745fc,
title = "Tight mechanism correlation between heart rate turbulence and baroreflex sensitivity: Sequential autonomic blockade analysis",
abstract = "Introduction: Heart rate turbulence is a powerful de novo risk predictor for patients surviving acute myocardial infarction. However, little is known about its underlying physiologic mechanism. Methods and Results: Hypothesizing that heart rate turbulence is barorceptor reflex related, we studied heart rate and blood pressure fluctuations at rest and after systematically introduced ventricular premature beats in 16 patients without structural heart disease (10 men and 6 women; mean age 45 ± 17 years) before and after sequential sympathetic (esmolol 4-mg bolus followed by 120 μg/kg/min intravenously), parasympathetic (atropine 0.04 mg/kg intravenously), and combined autonomic blockade (esmolol plus atropine). Turbulence onset ({\%}) and turbulence slope (msec/beat) were averaged from 10 respective ventricular premature beats. Spontaneous baroreflex sensitivity (msec/mmHg) was calculated from 5 minutes of sinus rhythm recording. The results showed that turbulence slope decreased after atropine (0.71 ± 0.50 msec/beat vs 5.17 ± 3.96 msec/beat at baseline; P < 0.01) and combined autonomic blockade (1.23 ± 1.02 msec/beat; P < 0.01) but was unchanged after esmolol (4.53 ± 3.30 msec/beat; P > 0.05). Turbulence onset increased after atropine (0.32{\%} ± 0.35{\%} vs -0.45 ± 0.94 at baseline; P < 0.05) and combined sympathetic and parasympathetic blockade (0.58{\%} ± 0.86{\%}; P < 0.05) but was unchanged after esmolol (-0.62{\%} ± 1.33{\%}; P > 0.05). Turbulence slope was positively correlated with baroreflex sensitivity at baseline (r = 0.78, P < 0.01) and after esmolol (r = 0.8, P < 0.01), but dissociated after atropine (r = 0.16, P > 0.05) and combined autonomic blockade (r = 0.31, P > 0.05). Turbulence onset was negatively correlated with baroreflex sensitivity at baseline (r = -0.61, P < 0.05), after esmolol (r = -0.80, P < 0.01), and after atropine (r = -0.53, P < 0.05). Conclusion: Heart rate turbulence of turbulence onset and turbulence slope is critically vagal dependent and highly correlated with spontaneous baroreflex sensitivity, which underscores its clinical importance in cardiovascular risk stratification.",
keywords = "Autonomic blockade, Autonomic nervous system, Baroreflex sensitivity, Cardiovascular risk stratification, Heart rate turbulence",
author = "Lin, {Lian Yu} and Lai, {Ling Ping} and Lin, {Jiunn Lee} and Du, {Chao Cheng} and Shau, {Wen Yi} and Chan, {Hsiao Lung} and Tseng, {Yung Zu} and {Stephen Huang}, {Shoei K.}",
year = "2002",
month = "1",
day = "1",
doi = "10.1046/j.1540-8167.2002.00427.x",
language = "English",
volume = "13",
pages = "427--431",
journal = "Journal of Cardiovascular Electrophysiology",
issn = "1045-3873",
publisher = "Wiley-Blackwell",
number = "5",

}

TY - JOUR

T1 - Tight mechanism correlation between heart rate turbulence and baroreflex sensitivity

T2 - Sequential autonomic blockade analysis

AU - Lin, Lian Yu

AU - Lai, Ling Ping

AU - Lin, Jiunn Lee

AU - Du, Chao Cheng

AU - Shau, Wen Yi

AU - Chan, Hsiao Lung

AU - Tseng, Yung Zu

AU - Stephen Huang, Shoei K.

PY - 2002/1/1

Y1 - 2002/1/1

N2 - Introduction: Heart rate turbulence is a powerful de novo risk predictor for patients surviving acute myocardial infarction. However, little is known about its underlying physiologic mechanism. Methods and Results: Hypothesizing that heart rate turbulence is barorceptor reflex related, we studied heart rate and blood pressure fluctuations at rest and after systematically introduced ventricular premature beats in 16 patients without structural heart disease (10 men and 6 women; mean age 45 ± 17 years) before and after sequential sympathetic (esmolol 4-mg bolus followed by 120 μg/kg/min intravenously), parasympathetic (atropine 0.04 mg/kg intravenously), and combined autonomic blockade (esmolol plus atropine). Turbulence onset (%) and turbulence slope (msec/beat) were averaged from 10 respective ventricular premature beats. Spontaneous baroreflex sensitivity (msec/mmHg) was calculated from 5 minutes of sinus rhythm recording. The results showed that turbulence slope decreased after atropine (0.71 ± 0.50 msec/beat vs 5.17 ± 3.96 msec/beat at baseline; P < 0.01) and combined autonomic blockade (1.23 ± 1.02 msec/beat; P < 0.01) but was unchanged after esmolol (4.53 ± 3.30 msec/beat; P > 0.05). Turbulence onset increased after atropine (0.32% ± 0.35% vs -0.45 ± 0.94 at baseline; P < 0.05) and combined sympathetic and parasympathetic blockade (0.58% ± 0.86%; P < 0.05) but was unchanged after esmolol (-0.62% ± 1.33%; P > 0.05). Turbulence slope was positively correlated with baroreflex sensitivity at baseline (r = 0.78, P < 0.01) and after esmolol (r = 0.8, P < 0.01), but dissociated after atropine (r = 0.16, P > 0.05) and combined autonomic blockade (r = 0.31, P > 0.05). Turbulence onset was negatively correlated with baroreflex sensitivity at baseline (r = -0.61, P < 0.05), after esmolol (r = -0.80, P < 0.01), and after atropine (r = -0.53, P < 0.05). Conclusion: Heart rate turbulence of turbulence onset and turbulence slope is critically vagal dependent and highly correlated with spontaneous baroreflex sensitivity, which underscores its clinical importance in cardiovascular risk stratification.

AB - Introduction: Heart rate turbulence is a powerful de novo risk predictor for patients surviving acute myocardial infarction. However, little is known about its underlying physiologic mechanism. Methods and Results: Hypothesizing that heart rate turbulence is barorceptor reflex related, we studied heart rate and blood pressure fluctuations at rest and after systematically introduced ventricular premature beats in 16 patients without structural heart disease (10 men and 6 women; mean age 45 ± 17 years) before and after sequential sympathetic (esmolol 4-mg bolus followed by 120 μg/kg/min intravenously), parasympathetic (atropine 0.04 mg/kg intravenously), and combined autonomic blockade (esmolol plus atropine). Turbulence onset (%) and turbulence slope (msec/beat) were averaged from 10 respective ventricular premature beats. Spontaneous baroreflex sensitivity (msec/mmHg) was calculated from 5 minutes of sinus rhythm recording. The results showed that turbulence slope decreased after atropine (0.71 ± 0.50 msec/beat vs 5.17 ± 3.96 msec/beat at baseline; P < 0.01) and combined autonomic blockade (1.23 ± 1.02 msec/beat; P < 0.01) but was unchanged after esmolol (4.53 ± 3.30 msec/beat; P > 0.05). Turbulence onset increased after atropine (0.32% ± 0.35% vs -0.45 ± 0.94 at baseline; P < 0.05) and combined sympathetic and parasympathetic blockade (0.58% ± 0.86%; P < 0.05) but was unchanged after esmolol (-0.62% ± 1.33%; P > 0.05). Turbulence slope was positively correlated with baroreflex sensitivity at baseline (r = 0.78, P < 0.01) and after esmolol (r = 0.8, P < 0.01), but dissociated after atropine (r = 0.16, P > 0.05) and combined autonomic blockade (r = 0.31, P > 0.05). Turbulence onset was negatively correlated with baroreflex sensitivity at baseline (r = -0.61, P < 0.05), after esmolol (r = -0.80, P < 0.01), and after atropine (r = -0.53, P < 0.05). Conclusion: Heart rate turbulence of turbulence onset and turbulence slope is critically vagal dependent and highly correlated with spontaneous baroreflex sensitivity, which underscores its clinical importance in cardiovascular risk stratification.

KW - Autonomic blockade

KW - Autonomic nervous system

KW - Baroreflex sensitivity

KW - Cardiovascular risk stratification

KW - Heart rate turbulence

UR - http://www.scopus.com/inward/record.url?scp=0036257826&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0036257826&partnerID=8YFLogxK

U2 - 10.1046/j.1540-8167.2002.00427.x

DO - 10.1046/j.1540-8167.2002.00427.x

M3 - Article

VL - 13

SP - 427

EP - 431

JO - Journal of Cardiovascular Electrophysiology

JF - Journal of Cardiovascular Electrophysiology

SN - 1045-3873

IS - 5

ER -