Document Detail


Low frequency power of heart rate variability reflects baroreflex function, not cardiac sympathetic innervation.
MedLine Citation:
PMID:  21279414     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: Power spectral analysis of heart rate variability is used to assess cardiac autonomic function. The relationship of low frequency (LF) power to cardiac sympathetic tone has been unclear. We reported previously that LF power may reflect baroreflex modulation. In this study we attempted to replicate our findings in additional subject cohorts, taking into account possible influences of respiration and using different methods to measure baroreflex-cardiovagal gain (BCG).
OBJECTIVE: We assessed relationships of LF power, including respiration-adjusted LF power (LFa), with cardiac sympathetic innervation and baroreflex function in subjects with or without neuroimaging evidence of cardiac sympathetic denervation.
METHODS: Values for LF power at baseline supine, seated, and during the Valsalva maneuver were compared between subject groups with low or normal myocardial concentrations of 6-[(18)F]fluorodopamine-derived radioactivity. BCG was calculated from the slope of cardiac interbeat interval vs. systolic pressure during Phase II of the Valsalva maneuver or after i.v. nitroglycerine injection (the Oxford technique).
RESULTS: LF and LFa were unrelated to myocardial 6-[(18)F]fluorodopamine-derived radioactivity. During sitting rest and the Valsalva maneuver logs of LF and LFa correlated positively with the log of Phase II BCG (r = 0.61, p = 0.0005; r = 0.47, p = 0.009; r = 0.69, p < 0.0001; r = 0.60, p = 0.0006). Groups with Low BCG (≤ 3 ms/mmHg) had low LF and LFa regardless of cardiac innervation. The log of LF power during supine rest correlated with the log of Oxford BCG (r = 0.74, p < 0.0001).
CONCLUSION: LF power, with or without respiratory adjustment, reflects baroreflex modulation and not cardiac sympathetic tone.
Authors:
Faisal Rahman; Sandra Pechnik; Daniel Gross; LaToya Sewell; David S Goldstein
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Intramural     Date:  2011-01-29
Journal Detail:
Title:  Clinical autonomic research : official journal of the Clinical Autonomic Research Society     Volume:  21     ISSN:  1619-1560     ISO Abbreviation:  Clin. Auton. Res.     Publication Date:  2011 Jun 
Date Detail:
Created Date:  2011-05-13     Completed Date:  2011-09-29     Revised Date:  2013-06-30    
Medline Journal Info:
Nlm Unique ID:  9106549     Medline TA:  Clin Auton Res     Country:  Germany    
Other Details:
Languages:  eng     Pagination:  133-41     Citation Subset:  IM    
Affiliation:
Clinical Neurocardiology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, 10 Center Drive MSC-1620, Bethesda, MD 20892-1620, USA.
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MeSH Terms
Descriptor/Qualifier:
Baroreflex / physiology*
Case-Control Studies
Electrophysiologic Techniques, Cardiac / methods*
Heart / innervation*,  physiology
Heart Rate / drug effects,  physiology*
Humans
Hypotension, Orthostatic / physiopathology
Multiple System Atrophy / physiopathology
Nitroglycerin / pharmacology
Parkinson Disease / physiopathology
Pure Autonomic Failure / physiopathology
Sympathetic Nervous System / physiology*
Tomography, Emission-Computed
Valsalva Maneuver / physiology
Vasodilator Agents / pharmacology
Grant Support
ID/Acronym/Agency:
Z99 NS999999/NS/NINDS NIH HHS; ZIA NS003033-04/NS/NINDS NIH HHS
Chemical
Reg. No./Substance:
0/Vasodilator Agents; 55-63-0/Nitroglycerin
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