Heart rate variability at 0.1 Hz did not directly reflect cardiac sympathetic nerve firing, as cardiac failure patients showed elevated norepinephrine spillover but reduced HRV (49 vs 243 ms2; P<0.05).
Observational (n=91)
Does heart rate variability at 0.1 Hz accurately reflect cardiac sympathetic nerve firing compared to cardiac norepinephrine spillover in various states of sympathetic activation and failure?
Heart rate variability at 0.1 Hz is not a direct or reliable measure of cardiac sympathetic nerve firing rates, as it dissociates from cardiac norepinephrine spillover in conditions like aging and heart failure.
Absolute Event Rate: 59% vs 18%
p-value: p=<0.01
BACKGROUND: Although heart rate variability (HRV) at 0.1 Hz has been proposed as a noninvasive clinical measure of cardiac sympathetic nerve firing, this premise has not been sufficiently validated by comparison with techniques such as microneurography and the measurement of norepinephrine spillover from the heart that more directly reflect presynaptic sympathetic activity. METHODS AND RESULTS: We compared the three techniques under conditions of effective cardiac sympathetic denervation, pure autonomic failure (n = 4), dopamine beta-hydroxylase deficiency (n = 1), and after cardiac transplantation (n = 9) as well as in the context of sympathetic nervous activation in cardiac failure (n = 15) and with aging (n = 10). Age-matched comparisons were made in each case with healthy individuals drawn from a pool of 52 volunteers. In pure autonomic failure and early after transplantation, cardiac norepinephrine spillover was negligible, and HRV was low. Late after transplantation, however, cardiac norepinephrine spillover returned to normal levels, and HRV remained low. In comparison to younger subjects (18 to 35 years old), older individuals (60 to 75 years old) had higher muscle sympathetic nerve activity (young, 22.9 +/- 1.9; old, 31.3 +/- 5.8 bursts per minute; P < .05) and cardiac norepinephrine spillover (young, 14.3 +/- 2.5; old, 20.1 +/- 3.0 ng/min; P < .05). In contrast, total HRV was reduced by 89%, and at 0.1 Hz it was reduced by 93% (P < .05). Cardiac failure was also characterized by elevated cardiac norepinephrine spillover (cardiac failure patients, 59 +/- 4; healthy volunteers, 18 +/- 3 ng/min; P < .01) but reduced 0.1 Hz HRV (cardiac failure patients, 49 +/- 17; healthy volunteers, 243 +/- 4 ms2; P < .05). CONCLUSIONS: HRV at 0.1 Hz depends on factors in addition to cardiac sympathetic nerve firing rates, including multiple neural reflexes, cardiac adrenergic receptor sensitivity, postsynaptic signal transduction, and electrochemical coupling, and is not directly related to cardiac norepinephrine spillover, which is a more direct measure of the sympathetic nerve firing rate.
Kingwell et al. (1994) conducted an observational in Sympathetic nervous activation and failure (n=91). Heart rate variability (HRV) at 0.1 Hz vs. Cardiac norepinephrine spillover and muscle sympathetic nerve activity was evaluated on Cardiac norepinephrine spillover in cardiac failure patients versus healthy volunteers (p=<0.01). Heart rate variability at 0.1 Hz did not directly reflect cardiac sympathetic nerve firing, as cardiac failure patients showed elevated norepinephrine spillover but reduced HRV (49 vs 243 ms2; P<0.05).