title: Supine low-frequency power of heart rate variability reflects baroreflex function, not cardiac sympathetic innervation.
abstract: BACKGROUND
  Power spectral analysis of heart rate variability (HRV) has been used to indicate cardiac autonomic function. High-frequency power relates to respiratory sinus arrhythmia and therefore to parasympathetic cardiovagal tone; however, the relationship of low-frequency (LF) power to cardiac sympathetic innervation and function has been controversial. Alternatively, LF power might reflect baroreflexive modulation of autonomic outflows.
  
  
  OBJECTIVE
  We studied normal volunteers and chronic autonomic failure syndrome patients with and without loss of cardiac noradrenergic nerves to examine the relationships of LF power with cardiac sympathetic innervation and baroreflex function.
  
  
  METHODS
  We compared LF power of HRV in patients with cardiac sympathetic denervation, as indicated by low myocardial concentrations of 6-[(18)F] fluorodopamine-derived radioactivity or low rates of norepinephrine entry into coronary sinus plasma (cardiac norepinephrine spillover) to values in patients with intact innervation, at baseline, during infusion of yohimbine, which increases exocytotic norepinephrine release from sympathetic nerves, or during infusion of tyramine, which increases non-exocytotic release. Baroreflex-cardiovagal slope (BRS) was calculated from the cardiac interbeat interval and systolic pressure during the Valsalva maneuver.
  
  
  RESULTS
  LF power was unrelated to myocardial 6-[(18)F] fluorodopamine-derived radioactivity or cardiac norepinephrine spillover. In contrast, the log of LF power correlated positively with the log of BRS (r=0.72, P <0.0001). Patients with a low BRS (<or=3 msec/mm Hg) had low LF power, regardless of cardiac innervation. Tyramine and yohimbine increased LF power in subjects with normal BRS but not in those with low BRS. BRS at baseline predicted LF responses to tyramine and yohimbine.
  
  
  CONCLUSIONS
  LF power reflects baroreflex function, not cardiac sympathetic innervation.
authors.affiliation: Children's National Medical Center, Washington, DC, USA. moakj@mail.nih.gov
authors.forename: Jeffrey P
authors.initials: JP
authors.lastname: Moak
authors.forename: David S
authors.initials: DS
authors.lastname: Goldstein
authors.forename: Basil A
authors.initials: BA
authors.lastname: Eldadah
authors.forename: Ahmed
authors.initials: A
authors.lastname: Saleem
authors.forename: Courtney
authors.initials: C
authors.lastname: Holmes
authors.forename: Sandra
authors.initials: S
authors.lastname: Pechnik
authors.forename: Yehonatan
authors.initials: Y
authors.lastname: Sharabi
mesh_terms: D000320:Adrenergic Fibers / Q000502:physiology*; D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D001342:Autonomic Nervous System Diseases; D017704:Baroreflex / Q000502:physiology*; D006321:Heart / Q000294:innervation* / Q000502:physiology*; D006339:Heart Rate / Q000187:drug effects / Q000502:physiology*; D006801:Humans; D007024:Hypotension, Orthostatic; D016683:Supine Position; D013566:Sympathomimetics / Q000494:pharmacology; D014439:Tyramine / Q000494:pharmacology; D015016:Yohimbine / Q000494:pharmacology
chemical_list: D000317:Adrenergic alpha-Antagonists; D013566:Sympathomimetics; D015016:Yohimbine; D014439:Tyramine