scholarly journals Depressed low frequency power of heart rate variability as an independent predictor of sudden death in chronic heart failure

2000 ◽  
Vol 21 (6) ◽  
pp. 475-482 ◽  
Author(s):  
M Galinier
1996 ◽  
Vol 91 (4) ◽  
pp. 391-398 ◽  
Author(s):  
Piotr Ponikowski ◽  
Massimo Piepoli ◽  
Aham A. Amadi ◽  
Tuan Peng Chua ◽  
Derek Harrington ◽  
...  

1. In patients with chronic heart failure, heart rate variability is reduced with relative preservation of very-low-frequency power (< 0.04 Hz). Heart rate variability has been measured without acceptable information on its stability and the optimal recording periods for enhancing this reproducibility. 2. To this aim and to establish the optimal length of recording for the evaluation of the very-low-frequency power, we analysed 40, 20, 10 and 5 min ECG recordings obtained on two separate occasions in 16 patients with chronic heart failure. The repeatability coefficient and the variation coefficient were calculated for the heart rate variability parameters, in the time-domain (mean RR, SDRR and pNN50), and in the frequency-domain: very low frequency (< 0.04 Hz), low frequency (0.04–0.15 Hz), high frequency (0.15–0.40 Hz), total power (0–0.5 Hz). 3. Mean RR remained virtually identical over time (variation coefficient 8%). The reproducibility of time-domain (variation coefficient 25–139%) and of spectral measures (variation coefficient 45–111%) was very low. The stability of the heart rate variability parameters was only apparently improved after square root and after log transformation. 4. Very-low-frequency values derived from 5 and 10 min intervals were significantly lower than those calculated from 40 and 20 min intervals (P < 0.005). Discrete very-low-frequency peaks were detected in 11 out of 16 patients on the first 40, 20 and 10 min recording, but only in seven out of 16 when 5 min segments were analysed. 5. The reproducibility of both time or frequency-domain measures of heart rate variability in patients with chronic heart failure may vary significantly. Square root or log-transformed parameters may be considered rather than absolute units in studies assessing the influence of management on heart rate variability profile. Recordings of at least 20 min in stable, controlled conditions are to be recommended to optimize signal acquisition in patients with chronic heart failure, if very-low-frequency power in particular is to be studied.


CHEST Journal ◽  
2011 ◽  
Vol 140 (4) ◽  
pp. 427A
Author(s):  
Subhasis Behera ◽  
Samuel Brown ◽  
Jason Jones ◽  
Michael Lanspa ◽  
Kathryn Kuttler ◽  
...  

2009 ◽  
Vol 76 (4 suppl 2) ◽  
pp. S51-S59 ◽  
Author(s):  
Jeffrey P. Moak ◽  
David S. Goldstein ◽  
Basil A. Eldadah ◽  
Ahmed Saleem ◽  
Courtney Holmes ◽  
...  

1995 ◽  
Vol 89 (2) ◽  
pp. 155-164 ◽  
Author(s):  
Massimo Piepoli ◽  
Stamatis Adamopoulos ◽  
Luciano Bernardi ◽  
Peter Sleight ◽  
Andrew J. S. Coats

1. Heart rate variability can be used to evaluate autonomic balance, but it is unclear how inotropic therapy may affect the findings. The aim of the study was to assess whether heart rate variability can differentiate between sympathetic stimulation induced by inotrope infusion or by physical exercise. 2. Ten patients with chronic heart failure (64.3 ± 5.4 years of age) underwent four dobutamine infusions (8-min steps of 5 μg min−1 kg−1) and four supine bicycle exercise tests (5-min steps of 25 W). Plasma noradrenaline was evaluated, as well as the SD of R—R intervals, together with low-frequency (0.03–0.14 Hz) and high-frequency (0.15–0.4 Hz) components of heart rate variability using autoregressive spectral analysis. 3. Exercise and inotrope infusion produced similar changes in heart rate variability. An exercise load of 50 W and a dobutamine infusion of 15 μg min−1 kg−1 gave the following results respectively: heart rate, 120.3 ± 3.0 beats/min versus 110.2 ± 3.0 beats/min; SD, 16.0 ± 1.1 ms versus 16.3 ± 2.5 ms; low-frequency component, 4.3 ± 0.3 ln-ms2 versus 4.4 ± 0.3 ln-ms2 and high-frequency component, 2.6 ± 0.3 ln-ms2 versus 2.2 ± 0.3 ln-ms2. All comparisons were non-significant. The variables of heart rate variability showed high reproducibility in the same subject during different conditions. Noradrenaline was elevated by exercise from 326.0 ± 35.2 pg/ml to 860.1 ± 180.4 pg/ml (P < 0.05), but was unchanged by dobutamine infusion. 4. Heart rate variability changes cannot differentiate between dobutamine infusions and physical exercise, indicating that we should be cautious in evaluating patients undergoing inotropic therapy. The degree of receptor stimulations, rather than the level of sympathetic drive, would appear to determine the changes in heart rate variability.


1999 ◽  
Vol 276 (1) ◽  
pp. H215-H223 ◽  
Author(s):  
Melanie S. Houle ◽  
George E. Billman

The low-frequency component of the heart rate variability spectrum (0.06–0.10 Hz) is often used as an accurate reflection of sympathetic activity. Therefore, interventions that enhance cardiac sympathetic drive, e.g., exercise and myocardial ischemia, should elicit increases in the low-frequency power. Furthermore, because an enhanced sympathetic activation has been linked to an increased propensity for malignant arrhythmias, one might also predict a greater low-frequency power in animals that are susceptible to ventricular fibrillation than in resistant animals. To test these hypotheses, a 2-min coronary occlusion was made during the last minute of exercise in 71 dogs with healed myocardial infarctions: 43 had ventricular fibrillation (susceptible) and 28 did not experience arrhythmias (resistant). Exercise or ischemia alone provoked significant heart rate increases in both groups of animals, with the largest increase in the susceptible animals. These heart rate increases were attenuated by β-adrenergic receptor blockade. Despite the sympathetically mediated increases in heart rate, the low-frequency power decreased, rather than increased, in both groups, with the largest decrease again in the susceptible animals: 4.0 ± 0.2 (susceptible) vs. 4.1 ± 0.2 ln ms2 (resistant) in preexercise control and 2.2 ± 0.2 (susceptible) vs. 2.9 ± 0.2 ln ms2 (resistant) at highest exercise level. In a similar manner the parasympathetic antagonist atropine sulfate elicited significant reductions in the low-frequency power. Although sympathetic nerve activity was not directly recorded, these data suggest that the low-frequency component of the heart rate power spectrum probably results from an interaction of the sympathetic and parasympathetic nervous systems and, as such, does not accurately reflect changes in the sympathetic activity.


2015 ◽  
Vol 24 (2) ◽  
pp. 118-127 ◽  
Author(s):  
Muna H. Hammash ◽  
Debra K. Moser ◽  
Susan K. Frazier ◽  
Terry A. Lennie ◽  
Melanie Hardin-Pierce

BackgroundWeaning from mechanical ventilation to spontaneous breathing is associated with changes in the hemodynamic and autonomic nervous systems that are reflected by heart rate variability. Although cardiac dysrhythmias are an important manifestation of hemodynamic alterations, the impact of heart rate variability on the occurrence of dysrhythmias during weaning has not been specifically studied.ObjectivesTo describe differences in heart rate variability spectral power and occurrence of cardiac dysrhythmias at baseline and during the initial trial of weaning from mechanical ventilation and to evaluate the impact of heart rate variability during weaning on occurrence of dysrhythmias.MethodContinuous 3-lead electrocardiographic recordings were collected from 35 patients receiving mechanical ventilation for 24 hours at baseline and during the initial weaning trial. Heart rate variability was evaluated by using spectral power analysis.ResultsLow-frequency power increased (P = .04) and high-frequency and very-low-frequency power did not change during weaning. The mean number of supraventricular ectopic beats per hour during weaning was higher than the mean at baseline (P &lt; .001); the mean of ventricular ectopic beats did not change. Low-frequency power was a predictor of ventricular and supraventricular ectopic beats during weaning (P &lt; .001). High-frequency power was predictive of ventricular and supraventricular (P = .02) ectopic beats during weaning. Very-low-frequency power was predictive of ventricular ectopic beats (P &lt; .001) only.ConclusionHeart rate variability power spectra during weaning were predictive of dysrhythmias. (American Journal of Critical Care. 2015;24:118–127)


2013 ◽  
Vol 2013 ◽  
pp. 1-4 ◽  
Author(s):  
Ming-Ying Lan ◽  
Guo-She Lee ◽  
An-Suey Shiao ◽  
Jen-Hung Ko ◽  
Chih-Hung Shu

Background. Very few studies investigate the role of the autonomic nervous system in allergic rhinitis. In this study, we evaluated the autonomic nervous system in allergic rhinitis patients using heart rate variability (HRV) analysis.Methods. Eleven patients with allergic rhinitis and 13 healthy controls, aged between 19 and 40 years old, were enrolled in the study. Diagnosis of allergic rhinitis was based on clinical history, symptoms, and positive Phadiatop test. Electrocardiographic recordings on the sitting and supine positions were obtained for HRV analysis.Results. In the supine position, there were no significant statistical differences in very-low-frequency power (VLF, ≤0.04 Hz), low-frequency power (LF, 0.04–0.15 Hz), high-frequency power (HF, 0.15–0.40 Hz), and the ratio of LF to HF (LF/HF) between the patient and control groups. The mean RR intervals significantly increased, while LF% and LF/HF significantly decreased in the patient group in the sitting position. Moreover, mean RR intervals, LF, and LF/HF, which were significantly different between the two positions in the control group, did not show a significant change with the posture change in the patient group.Conclusion. These suggest that patients with allergic rhinitis may have poor sympathetic modulation in the sitting position. Autonomic dysfunction may therefore play a role in the pathophysiology of allergic rhinitis.


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