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Abstract
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.
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.
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.
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.
LF power reflects baroreflex function, not cardiac sympathetic innervation.