Absence of low-frequency variability of sympathetic nerve activity in severe heart failure
P Van De Borne, N Montano, M Pagani, R Oren… - Circulation, 1997 - Am Heart Assoc
P Van De Borne, N Montano, M Pagani, R Oren, VK Somers
Circulation, 1997•Am Heart AssocBackground In normal humans, variability of blood pressure, RR interval, and sympathetic
activity occurs predominantly at a low frequency (LF; 0.04 to 0.14 Hz) and a high frequency
(HF;±0.25 Hz). In conditions that increase sympathetic activation in normal humans, the LF
component is increased relative to the HF component. Patients with heart failure have high
levels of sympathetic activity. We tested the hypothesis that the LF component of sympathetic
nerve activity variability is increased in heart failure. Methods and Results. We performed …
activity occurs predominantly at a low frequency (LF; 0.04 to 0.14 Hz) and a high frequency
(HF;±0.25 Hz). In conditions that increase sympathetic activation in normal humans, the LF
component is increased relative to the HF component. Patients with heart failure have high
levels of sympathetic activity. We tested the hypothesis that the LF component of sympathetic
nerve activity variability is increased in heart failure. Methods and Results. We performed …
Background In normal humans, variability of blood pressure, RR interval, and sympathetic activity occurs predominantly at a low frequency (LF; 0.04 to 0.14 Hz) and a high frequency (HF; ±0.25 Hz). In conditions that increase sympathetic activation in normal humans, the LF component is increased relative to the HF component. Patients with heart failure have high levels of sympathetic activity. We tested the hypothesis that the LF component of sympathetic nerve activity variability is increased in heart failure.
Methods and Results. We performed spectral analysis of simultaneous recordings of resting muscle sympathetic nerve activity (MSNA) and RR interval in 21 patients with chronic heart failure and 12 age-matched control subjects. MSNA was higher in patients with heart failure (62±4 bursts per minute) than in the normal subjects (39±4 bursts per minute; P<.01). LF components of RR interval and MSNA variability were lower in the heart failure patients versus the control subjects (P<.01). HF variability of RR interval and MSNA was preserved, at least in part, in heart failure. There was close coherence between variability patterns of RR interval and MSNA. Furthermore, in 14 heart failure patients who had no LF variability in MSNA compared with 7 heart failure patients who did manifest LF variability in MSNA, RR interval was shorter, the variance of RR interval was lower, MSNA was higher, respiratory rate was faster, and left ventricular ejection fraction was lower (all P<.05). At a median follow-up of 12 months, 4 heart failure patients had died, all of whom had had absent LF oscillations in MSNA and RR interval.
Conclusions The LF variability of sympathetic nerve activity is absent in patients with severe heart failure. This disturbed pattern of variability is closely coherent with the abnormal variability of RR interval. These disturbances of rhythmic oscillations of autonomic outflow, evident in both RR interval and MSNA, suggest a central autonomic regulatory impairment in heart failure and may have important prognostic implications.
Am Heart Assoc