Vagal Modulation Of Heart Rate Research Articles

Hypertension, Sleep Apnea, and Atherosclerosis

Having obstructive sleep apnea (OSA) increases the relative odds of also having coronary artery disease by 27% and of having suffered a stroke by 58%.1 Approximately 50% of individuals with OSA are also hypertensive, and those who are not initially so have an ≈3-fold increase in their likelihood of developing hypertension after 4 years if their apnea-hypopnea index (AHI) is ≥15 events per hour.2–4 Some of this propensity to cardiovascular events may accrue from site-specific consequences of OSA. For example, if transmission of the acoustic energy generated by snoring stimulated the development of carotid atherosclerosis,5 conceivably this action could increase the odds for stroke but not for myocardial infarction. Conversely, during each futile effort to breathe against the occluded pharynx, mechanical strain elicited by the abrupt generation of negative intrathoracic (and, hence, augmented epicardial artery transmural) pressure6 could rupture coronary plaques.7 A parallel increase in left ventricular wall stress, accompanied by oxygen desaturation during apnea, might induce myocardial ischemia, or non-ST segment elevation infarction.3 These cardiac effects of OSA could increase coronary risk but should not affect the likelihood of cerebrovascular events, whereas simultaneous increases in left atrial transmural pressure and concurrent fluctuations in autonomic tone might well raise the odds of developing embolic stroke by triggering atrial fibrillation.8 Over the long term, more important than these local actions may be the immediate and sustained systemic consequences of OSA. These include recurrent cycles of apnea and hyperpnea, sympathetic excitation and withdrawal, hypoxia reoxygenation and oxidative stress, impaired tonic and reflex vagal heart rate modulation, platelet aggregation, activation of inflammatory pathways, oxidation of lipoproteins, expression of adhesion molecules, hyperaldosteronism, impaired endothelial responsiveness and vascular smooth muscle proliferation.3,4 By modifying vascular function or structure, or by initiating or promoting atherosclerosis, these stimuli, acting individually …

Autonome Dysfunktion und Betablocker beim Multiorgandysfunktionssyndrom

The multiple organ dysfunction syndrome (MODS), a failure of two or more organ systems, is the endstage of initial trigger events in diseases such as acute coronary syndrome or sepsis. The mortality is high (40 - 60 %). The present study aimed to detect whether beta-adrenergic blockers (BAB) which may affect sympathetic-parasympathetic balance have a positive influence on outcome. Data on 157 patients with MODS (83 male, 74 female, mean age 61.3 +/- 13.4 years) were retrospectively analysed concerning BAB medication and autonomic dysfunction. A 24-hour-Holter-ECG which had been applied within the initial 48 hours of illness was analysed for heart rate variability (HRV). All patients were followed to determine 28-day mortality. 69 of the 157 MODS patients had received BAB. This treatment was associated with a higher survival probability (hazard ratio [HR] 0.4, 95 % confidence interval [CI] 0.23 - 0.68; p = 0.001). Survival benefit was especially seen in the subgroup of MODS patients who had an ischemically triggered MODS (HR 0.2 [0.1 - 0.5], p = 0.001). HRV was less reduced in the BAB group compared to patients without this medication. MODS patients treated with beta-adrenercic blockers may have a survival benefit which is especially seen in the subgroup of MODS patients with ischemically triggered MODS. Moreover, BAB medication is associated with a less pronounced autonomic dysfunction in MODS (especially the vagal modulation of heart rate) which might result in a lower inflammatory response. Hence, future prospective studies have to show the relevance of beta-adrenergic blockers in MODS.

Association of cardiac autonomic function measures with severity of sleep‐disordered breathing in a community‐based sample

The goal of this study was to test the hypothesis that spectral indices of heart rate variability, such as high-frequency power (HFP), low-to-high frequency power (LHR), and their respiration-adjusted counterparts (HFPra, LHRra) are correlated with severity of sleep-disordered breathing (SDB), as quantified by the respiratory disturbance index (RDI). A total of 436 subjects, non-smoking, normotensive, and free of cardiovascular disease and diabetes were selected from the Sleep Heart Health Study (SHHS). Of these, 288 records with sufficiently high quality electrocardiogram signals were selected for further analysis [males/females: 221/67; age: 46.1 to 74.9 years; body mass index (BMI): 21.5 to 46.4 kg m(-2); 0.3 < RDI < 85.0(-1)]. From each polysomnogram, the respiration channels (thoracic and abdominal) and R-R interval (RRI) derived from the electrocardiogram were subjected to spectral analysis and autoregressive moving average modeling in consecutive 5-min segments. After adjusting for age and BMI, mean RRI was found to be negatively correlated with RDI in men in all sleep-wake states (all P < 0.001). HFP and HFPra were negatively correlated with RDI in men only during wakefulness (all P < 0.01). In women, LHR and LHRra were not correlated with RDI during wakefulness, but were positively correlated during non-rapid eye movement Stage 1 and 2 sleep (all P < 0.01). These findings suggest that the indices of cardiac autonomic control are correlated with SDB severity, but gender and state affect the nature of these correlations. In both genders, however, vagal modulation of heart rate increases while sympathetic modulation decreases from wakefulness to sleep.

Letter by Jong et al Regarding Article, “Dietary Fish and ω - 3 Fatty Acid Consumption and Heart Rate Variability in US Adults”

To the Editor: We read with interest the recent report from Mozaffarian et al1 that consumption of ω-3 fatty acid containing fish is associated with increased heart rate variability (HRV) markers of vagal heart rate modulation. Importantly, in their analysis, higher HRV was accompanied by a lower risk of subsequent cardiac death. Their findings, which demonstrate the potential use of HRV indices as surrogate or secondary measures of treatment efficacy when evaluating preventive strategies for cardiovascular disease, raise 2 important questions for research on the HRV response to interventions such as diet. First, how would one characterize the magnitude of treatment effects such …

Continuous positive airway pressure increases heart rate variability in heart failure patients with obstructive sleep apnoea

Patients with heart failure or OSA (obstructive sleep apnoea) have reduced HF-HRV (high-frequency heart rate variability), indicating reduced cardiac vagal modulation, a marker of poor prognosis. CPAP (continuous positive airway pressure) abolishes OSA in patients with heart failure, but effects on daytime HF-HRV have not been determined. We hypothesized that, in patients with heart failure, treatment of coexisting OSA by CPAP would increase morning HF-HRV. In 19 patients with heart failure (left ventricular ejection fraction <45%) and OSA (>/=20 apnoeas and hypopnoeas/h of sleep), HF-HRV was quantified before and 1 month after randomization to a control or CPAP-treated group. In the control group (n=7), there were no changes in HF-HRV over the 1 month study during wakefulness in the morning. In the CPAP-treated group (n=12) HF-HRV increased significantly during wakefulness in the morning [from 2.43+/-0.55 to 2.82+/-0.50 log(ms(2)/Hz); P=0.002] due to an increase in transfer function between changes in lung volume and changes in HF-HRV (92.37+/-96.03 to 219.07+/-177.14 ms/l; P=0.01). In conclusion, treatment of coexisting OSA by nocturnal CPAP in patients with heart failure increases HF-HRV during morning wakefulness, indicating improved vagal modulation of heart rate. This may contribute to improved prognosis.

Impaired serotonergic regulation of heart rate may underlie reduced baroreflex sensitivity in an animal model of depression

Serotonin (5-HT) is crucial to normal reflex vagal modulation of heart rate (HR). Reduced baroreflex sensitivity [spontaneous baroreflex sensitivity (sBRS)] and HR variability (HRV) reflect impaired neural, particularly vagal, control of HR and are independently associated with depression. In conscious, telemetered Flinders-Sensitive Line (FSL) rats, a well-validated animal model of depression, we tested the hypothesis that cardiovascular regulatory abnormalities are present and associated with deficient serotonergic control of reflex cardiovagal function. In FSL rats and control Flinders-Resistant (FRL) and Sprague-Dawley (SD) rat strains, diurnal measurements of HR, arterial pressure (AP), activity, sBRS, and HRV were made. All strains had normal and similar diurnal variations in HR, AP, and activity. In FRL rats, HR was elevated, contributing to the reduced HRV and sBRS in this strain. In FSL rats, sBRS and high-frequency power HRV were reduced during the night, indicating reduced reflex cardiovagal activity. The ratio of low- to high-frequency bands of HRV was increased in FSL rats, suggesting a relative predominance of cardiac sympathetic and/or reflex activity compared with FRL and SD rats. These data show that conscious FSL rats have cardiovascular regulatory abnormalities similar to depressed humans. Acute changes in HR, AP, temperature, and sBRS in response to 8-hydroxy-2-(di-n-propylamino)tetralin, a 5-HT(1A), 5-HT(1B), and 5-HT(7) receptor agonist, were also determined. In FSL rats, despite inducing an exaggerated hypothermic effect, 8-hydroxy-2-(di-n-propylamino)tetralin did not decrease HR and AP or improve sBRS, suggesting impaired serotonergic neural control of cardiovagal activity. These data suggest that impaired serotonergic control of cardiac reflex function could be one mechanism linking reduced sBRS to increased cardiac risk in depression.

Conditions of autonomic reciprocal interplay versus autonomic co-activation: Effects on non-linear heart rate dynamics

The present study was aimed at investigating the autonomic nervous system influences on the fractal organization of human heart rate during sympathovagal interactions, with special emphasize on the short-term fractal organization in heart rate variability (HRV), as assessed by the scaling exponent ( α 1) of the detrended fluctuation analysis. Linear and non-linear HRV analyses were used to study the sympathetic and vagal modulation of heart rate in ten healthy men (mean ± SEM; age 26 ± 1 years) during conditions of 1) increased sympathetic activity and vagal withdrawal (head-up tilt), 2) decreased sympathetic activity and increased vagal outflow (thermoneutral upright head-out water immersion, WIn), and 3) simultaneous activation of the two arms of the autonomic nervous activity (upright head-out immersion in cold water, WIc). Hemodynamic and linear HRV results were consistent with previous reports during similar physiological conditions. α 1 increased significantly during head-up tilt (from 0.71 ± 0.13 supine to 0.90 ± 0.15 upright) and WIn (0.86 ± 0.10) and was significantly decreased during WIc (0.61 ± 0.15). Thus, α 1 increased when the cardiac autonomic interplay was altered in a reciprocal fashion, whatever the direction of the balance change. Conversely, α 1 decreased during the concomitant activation of both vagal and sympathetic activities. The results of linear analysis were necessary to precisely define the direction of change in autonomic control revealed by an increase in α 1, while the direction of change in α 1 indicated whether an increased vagal activity is coupled with a decreased or increased sympathetic activation. Using both linear and non-linear analysis of HRV may increase the understanding of changes in cardiac autonomic status.

Fetal body weight and the development of the control of the cardiovascular system in fetal sheep

Reduced birth weight predisposes to cardiovascular diseases in later life. We examined in fetal sheep at 0.76 (n = 18) and 0.87 (n = 17) gestation whether spontaneously occurring variations in fetal weight affect maturation of autonomic control of cardiovascular function. Fetal weights at both gestational ages were grouped statistically in low (LW) and normal weights (NW) (P < 0.01). LW fetuses were within the normal weight span showing minor growth dysproportionality at 0.76 gestation favouring heart and brain, with a primary growth of carcass between 0.76 and 0.87 gestation (P < 0.05). While twins largely contributed to LW fetuses, weight differences between singletons and twins were absent at 0.76 and modest at 0.87 gestation, underscoring the fact that twins belong to normality in fetal sheep not constituting a major malnutritive condition. Mean fetal blood pressure (FBP) of all fetuses was negatively correlated to fetal weight at 0.76 but not 0.87 gestation (P < 0.05). At this age, FBP and baroreceptor reflex sensitivity were increased in LW fetuses (P < 0.05), suggesting increased sympathetic activity and immaturity of circulatory control. Development of vagal modulation of fetal heart rate depended on fetal weight (P < 0.01). These functional associations were largely independent of twin pregnancies. We conclude, low fetal weight within the normal weight span is accompanied by a different trajectory of development of sympathetic blood pressure and vagal heart rate control. This may contribute to the development of elevated blood pressure in later life. Examination of the underlying mechanisms and consequences may contribute to the understanding of programming of cardiovascular diseases.

C-reactive protein modulates vagal heart rate control in patients with coronary artery disease

Systemic inflammation is associated with sympathetic cardiac activation and decreased HRV (heart rate variability) in subjects at high risk of CAD (coronary artery disease). In the present study, we examined the influence of systemic inflammation, measured by CRP (C-reactive protein), on vagal HR (heart rate) control during behavioural relaxation in patients with CAD. It was hypothesized that CRP would be associated with decreased vagal HR modulation. Consecutive patients were screened 2 weeks prior to elective PTCA (percutaneous transluminal coronary angioplasty). The study was comprised of 29 subjects who represented the first and fourth quartiles of the CRP distribution: Low (0.47+/-0.07 microg/ml)- and High (8.19+/-1.95 microg/ml)-CRP groups respectively. Vagal HR control was quantified as RR high-frequency spectral power (0.15 to 0.40 Hz), and was assessed in log-transformed absolute units (logHF power). Near-IR particle immunoassay was used to determine high-sensitivity CRP concentration. Assessment entailed 5 min of silent reading and self-guided behavioural relaxation. RR logHF power was decreased in the High-CRP group across both assessment procedures (P=0.032). Behavioural relaxation increased RR logHF power for both the Low- and High-CRP groups (P=0.033). Hierarchical linear regression determined that CRP accounted for 18.9% of the variance in RR logHF power during behavioural relaxation (P=0.03), independent of baseline RR interval, cardiac medication, respiratory logHF power and body mass index. In conclusion, patients with CAD had augmented vagal HR control with behavioural relaxation, but this effect was moderated by the severity of CRP. Therefore it may be advisable to assess systemic inflammation in interventions aimed at improving neurocardiac regulation in patients with CAD.

The Autonomic Nervous System Activity and Osteopathic Manipulation

The Osteopathic medical profession generally accepts that Osteopathic manual therapy (OMT) can be used to influence sympathovagal balance. However, there is little quantitative data evaluating this relationship. This study tested the hypothesis that cervical myofascial release increases vagal modulation of heart rate. The protocol lasted 30 minutes. Changes in body position were incorporated into the study to facilitate interpretation of autonomic tone measures. The protocol consisted of studying 17 human subjects in three positions; 10 min - horizontal, 10 min - 50 deg head-up, and 10 min - horizontal. Each subject was studied three times (control, sham, OMT) separated by at least one day. The OMT (cervical myofascial release) was applied while subjects were head-up. Sympathovagal balance was assessed by using spectral analysis of heart rate variability. In the control group, head-up tilt increased heart rate and the LF/HF ratio. The ratio increased from 1.45±0.23 (mean±SE) to 4.85±0.60 reflecting an increase in sympathetic and decrease in vagal tone. Sham treatment was not distinguishable from the control group. OMT caused a significant decrease in LH/HF ratio. The ratio decreased from 4.85±0.6 to 1.80±0.35. The results support the hypothesis that OMT can be used to modulate vagal tone. This study was approved by the institutional IRB; all subjects signed consent forms prior to participation in the study.

Hyperthyroidism is characterized by both increased sympathetic and decreased vagal modulation of heart rate: evidence from spectral analysis of heart rate variability

The clinical manifestations of hyperthyroidism resemble those of the hyperadrenergic state. This study was designed to evaluate the impact of hyperthyroidism on the autonomic nervous system (ANS) and to investigate the relationship between serum thyroid hormone concentrations and parameters of spectral heart rate variability (HRV) analysis in hyperthyroidism. Thirty-two hyperthyroid Graves' disease patients (mean age 31 years) and 32 sex-, age-, and body mass index (BMI)-matched normal control subjects were recruited to receive one-channel electrocardiogram (ECG) recording. The cardiac autonomic nervous function was evaluated by the spectral analysis of HRV, which indicates the autonomic modulation of the sinus node. The correlation coefficients between serum thyroid hormone concentrations and parameters of the spectral HRV analysis were also computed. The hyperthyroid patients revealed significant differences (P < 0.001) compared with the controls in the following HRV parameters: a decrease in total power (TP), very low frequency power (VLF), low frequency power (LF), high frequency power (HF), and HF in normalized units (HF%); and an increase in LF in normalized units (LF%) and in the ratio of LF to HF (LF/HF). After correction of hyperthyroidism in 28 patients, all of the above parameters were restored to levels comparable to those of the controls. In addition, serum thyroid hormone concentrations showed significant correlations with spectral HRV parameters. Hyperthyroidism is in a sympathovagal imbalanced state, characterized by both increased sympathetic and decreased vagal modulation of the heart rate. These autonomic dysfunctions can be detected simultaneously by spectral analysis of HRV, and the spectral HRV parameters could reflect the disease severity in hyperthyroid patients.

Assessing Arterial Baroreflex Control of Heart Rate During General Anesthesia

To the Editor: We read with interest the article by Drs. Tanaka and Nishikawa on spontaneous baroreflex indices (SBRI) during general anesthesia (GA) (1). They suggested that SBRI inadequately estimate the pharmacological gain during sevoflurane anesthesia, even though these indices have frequently been used in their own recent articles. We agree, in part, that SBRI may not reflect complex physiology of baroreflex during GA. However, unfortunately, there are significant limitations in the methodology of this study. First, we question why they did not choose high-frequency transfer function gain, which is believed to be of vagal origin and has sufficiently high coherence during positive pressure ventilation (2), despite the authors' claim that “SBRI may be useful simply for quantitative assessments of beat-to-beat vagal modulation of heart rate.” Furthermore, we wonder how low-frequency transfer function gain remained unchanged, or increased, during GA when compared with that at conscious baseline. Second, because the SBRI measured at conscious baseline had already shown a large mean difference (Figs. 1 and 2; up to approximately 300 to 500% higher; n = 9), compared with that by Lipman et al. (3), who reported 13 to 46% higher (n = 97), we respectfully question the consistency of SBRI methods used before further assessment of Bland-Altman plot during GA. Moreover, for calculating the α-index, they incorrectly used the spectral power at 0.25 Hz, although mechanical ventilation was at 0.2 Hz. Taken together, these issues may contribute to the increased bias and broad limit of agreement between indices. Therefore, we believe that this article would be best served by eliminating the issues noted above, and it would be worthwhile to perform additional investigations with a larger sample size using different methodology, such as choosing different SBRI and changing thresholds in the sequence method (4,5). Gyu-Sam Hwang, MD, PhD Young-Kug Kim, MD, PhD In-Young Huh, MD, PhD Su-Jin Kang, MD, MS Department of Anesthesiology and Pain Medicine Asan Medical Center University of Ulsan College of Medicine Seoul, Korea [email protected]

Cardiac vagal modulation of heart rate during prolonged submaximal exercise in animals with healed myocardial infarctions: effects of training

The present study investigated the effects of long-duration exercise on heart rate variability [as a marker of cardiac vagal tone (VT)]. Heart rate variability (time series analysis) was measured in mongrel dogs (n = 24) with healed myocardial infarctions during 1 h of submaximal exercise (treadmill running at 6.4 km/h at 10% grade). Long-duration exercise provoked a significant (ANOVA, all P < 0.01, means +/- SD) increase in heart rate (1st min, 165.3 +/- 15.6 vs. last min, 197.5 +/- 21.5 beats/min) and significant reductions in high frequency (0.24 to 1.04 Hz) power (VT: 1st min, 3.7 +/- 1.5 vs. last min, 1.0 +/- 0.9 ln ms(2)), R-R interval range (1st min, 107.9 +/- 38.3 vs. last min, 28.8 +/- 13.2 ms), and R-R interval SD (1st min, 24.3 +/- 7.7 vs. last min 6.3 +/- 1.7 ms). Because endurance exercise training can increase cardiac vagal regulation, the studies were repeated after either a 10-wk exercise training (n = 9) or a 10-wk sedentary period (n = 7). After training was completed, long-duration exercise elicited smaller increases in heart rate (pretraining: 1st min, 156.0 +/- 13.8 vs. last min, 189.6 +/- 21.9 beats/min; and posttraining: 1st min, 149.8 +/- 14.6 vs. last min, 172.7 +/- 8.8 beats/min) and smaller reductions in heart rate variability (e.g., VT, pretraining: 1st min, 4.2 +/- 1.7 vs. last min, 0.9 +/- 1.1 ln ms(2); and posttraining: 1st min, 4.8 +/- 1.1 vs. last min, 2.0 +/- 0.6 ln ms(2)). The response to long-duration exercise did not change in the sedentary animals. Thus the heart rate increase that accompanies long-duration exercise results, at least in part, from reductions in cardiac vagal regulation. Furthermore, exercise training attenuated these exercise-induced reductions in heart rate variability, suggesting maintenance of a higher cardiac vagal activity during exercise in the trained state.

Clinical Epilepsy: Adult

Clinical Epilepsy: Adult

Heart rate variability biofeedback as a behavioral neurocardiac intervention to enhance vagal heart rate control

Patients with coronary heart disease (CHD) who experience depressed mood or psychological stress exhibit decreased vagal control of heart rate (HR), as assessed by spectral analysis of HR variability (HRV). Myocardial infarction and sudden cardiac death are independently associated with depression and stress, as well as impaired vagal HR control. This study examined whether a behavioral neurocardiac intervention to reduce stress or depression can augment cardiovagal modulation in CHD patients. We hypothesized that (1) cognitive-behavioral training with HRV biofeedback would augment vagal recovery from acute stress, and (2) vagal regulation of HR would be inversely associated with stress and depression after treatment. This randomized controlled trial enrolled 46 CHD patients from 3 clinics of CHD risk reduction in Toronto and Vancouver, Canada. Subjects were randomized to five 1.5-hour sessions of HRV biofeedback or an active control condition. Outcome was assessed by absolute and normalized high-frequency spectral components (0.15-0.50 Hz) of HRV, and by the Perceived Stress Scale and Centre for Epidemiologic Studies in Depression scale. Both groups reduced symptoms on the Perceived Stress Scale (P = .001) and Centre for Epidemiologic Studies in Depression scale (P = .004). Hierarchical linear regression determined that improved psychological adjustment was significantly associated with the high-frequency index of vagal HR modulation only in the HRV biofeedback group. Adjusted R 2 was as follows: HRV biofeedback group, 0.86 for stress (P = .02) and 0.81 for depression (P = .03); versus the active control group, 0.04 (P = .57) and 0.13 (P = .95), respectively. A novel behavioral neurocardiac intervention, HRV biofeedback, can augment vagal HR regulation while facilitating psychological adjustment to CHD.

Changes in cardiovascular autonomic regulation among elderly subjects: Follow‐up of sixteen years

BACKGROUND. Previous cross‐sectional studies have suggested that cardiac autonomic regulation, measured as heart rate (HR) variability, is altered upon ageing, and that altered HR variability may predict mortality. However, there are no longitudinal follow‐up reports of the changes of HR dynamics in elderly subjects.AIM & METHOD. This study was designed to examine the longitudinal changes in the spectral, fractal, and complexity measures of HR variability in a random sample of 41 elderly subjects (mean age 69±4 years), who underwent repeated 24‐hour Holter recordings at the baseline and after 16 years' follow‐up. Several cardiovascular risk factors were determined at the baseline.RESULTS. A time‐domain index, standard deviation of N‐N intervals (SDNN) (142±34 msec versus 133±50 msec, not significant (NS)), and the high frequency spectral component of HR variability (219±222 msec2 versus 268±287 msec2, NS) did not change during the follow‐up. The low frequency power (LF) of HR variability decreased from 678±654 msec2 to 436±651 msec2 (P<0.01). Among the fractal HR variability indexes, the power‐law slope (β) (−1.31±0.20 versus −1.47±0.21, P<0.001) and the short‐term fractal exponent α1 (1.16±0.19 versus 1.06±0.18, P<0.01) decreased significantly. Approximate entropy remained unchanged.CONCLUSIONS. The magnitude of total HR variability and the respiratory vagal modulation of HR do not change over time in the elderly. However, the spectral and fractal characteristics of HR behavior still undergo alterations upon ageing.

Impaired vagal modulation of heart rate in individuals with Down syndrome

The attenuated heart rate (HR) and blood pressure (BP) response to exercise in individuals with Down syndrome (DS) has been attributed to autonomic dysfunction, which has been associated with obesity. Our purpose was to determine the role of autonomic control of HR to the attenuated chronotropic response observed in individuals with DS. We evaluated spectral analysis of HR variability (HRV) in 13 individuals with (BMI 32+/-5 kg/m(2), P<0.05) and 14 without DS (BMI 26+/-3 kg/m(2)) by means of 2 min isometric handgrip at 30% of maximal force followed by recovery. Noninvasive measures of HR (ECG) and systolic BP (SBP) (Portapres) were recorded continuously. The increases in HR and SBP, and decrease in high frequency (HF) component were significantly greater in controls than in individuals with DS (P<0.05) during handgrip. The increase in LF/HF ratio was not significantly affected by handgrip and was comparable in both groups. During recovery, the decreases in HR, SBP, and LF/HF ratio, and the increase in HF were significantly greater in controls than in individuals with DS (P<0.05). Controlling for BMI did not alter these results. The attenuated HR and SBP response to the handgrip test in individuals with DS is explained by blunted vagal modulation. Our study suggests that autonomic dysfunction in individuals with DS might be independent of obesity.

The effects of cervical and lumbar epidural anesthesia on heart rate variability and spontaneous sequence baroreflex sensitivity.

A high level of neuroaxial block may produce profound bradycardia and hypotension, possibly as a result of an imbalance between sympathetic and parasympathetic control of heart rate. We designed this study to test the hypothesis that cervical epidural anesthesia would increase the high-frequency (HF) component of heart rate variability (HRV) as a result of cardiac sympathectomy, whereas lumbar epidural anesthesia would cause sympathetic predominance. HRV and spontaneous baroreflex (SBR) sensitivity were assessed before and after cervical and lumbar epidural anesthesia by using plain 1.5% lidocaine (median upper/lower sensory block: C3/T8 for cervical and T11/L5 for lumbar) in healthy patients (n = 10 each). Electrocardiogram and noninvasive beat-to-beat arterial blood pressure were monitored. HRV was analyzed by using fast Fourier transformation. Least-square regression analysis relating R-R interval and systolic blood pressure during spontaneous fluctuation was performed to obtain SBR sensitivities. Cervical epidural group patients were significantly older (P < 0.01) and taller (P < 0.01). Cervical epidural anesthesia attenuated HF (0.15-0.4 Hz) and low-frequency (0.04-0.15 Hz) power of HRV with concomitant reductions in up- and down-sequence SBR sensitivities, suggesting decreased vagal modulation of heart rate. Lumbar epidural anesthesia resulted in a significant increase in the low-frequency/HF ratio of HRV and unchanged SBR indices, suggesting sympathetic predominance. HF power correlated well with SBR sensitivities under most of our study conditions. Respiratory rates and Paco(2) were unchanged by either epidural technique. Our results indicate that cervical, but not lumbar, epidural anesthesia depresses phasic and tonic dynamic modulation of the cardiac cycle by the vagal nerve in conscious humans.

Effect of posture on heart rate variability spectral measures in children and young adults with heart disease

Background: Reduction of heart rate variability as a consequence of heart disease and postural change has been well documented. However, the data on the effect of postural change in pediatric patients are incomplete and the effect is not fully understood. The aim of the study was to investigate effect of postural change on heart rate variability in relation to the extent of severity of heart disease. Methods: The dependence of heart rate variability on posture in 41 children and young adults (8–20 years) with heart disease has been investigated and compared with control. Short-term electrocardiograms (ECGs) were assessed in supine rest and active standing, and spectral measures of heart rate variability were determined. Results: Two types of response to the change of supine to standing posture were determined in both healthy and diseased subjects. In majority of subjects, the increased heart rate induced by standing was accompanied by a decrease in high-frequency power. However, in about 30% of all subjects, increased heart rate during standing was accompanied by an increased high-frequency power. Independently of posture and disease, high-frequency and low-frequency power were positively correlated. In subjects characterized by a reduction of heart rate variability in standing, the high-frequency power in both postures is reduced in diseased subjects compared to control. Conclusions: These results demonstrate that in this age range, the response to posture is not unique because of the difference in high-frequency power, which implies a variety of vagal modulations of heart rate.

Restoration of heart rate turbulence by titrated beta-blocker therapy in patients with advanced congestive heart failure: positive correlation with enhanced vagal modulation of heart rate.

Heart rate turbulence (HRT) is a powerful novel predictor for cardiovascular mortality. Chronic congestive heart failure is associated with abnormal HRT. Whether antiadrenergic beta-blocker therapy can restore control of HRT in patients with chronic congestive heart failure is unknown. A 24-hour Holter ECG recording was obtained before and 1 and 3 months after titrated addition of atenolol therapy in 10 consecutive patients with advanced congestive heart failure. Two parameters derived from HRT, turbulence slope (TS) and turbulence onset (TO), and time- and frequency-domain heart rate variability (HRV) parameters (SDNN, RMSSD, VLF, LF, HF) from 24-hour ECG were compared before and after beta-blocker therapy, together with the same parameters in age-matched normal control. Results showed that TS (3.1 +/- 2.2 vs 6.2 +/- 3.0; P = 0.001) and all HRV parameters were increased after 3 months of atenolol treatment. No changes in TO were evident (0.6 +/- 0.5 vs -0.2 +/- 1.3; P = 0.13). The improvement of TS and the vagally mediated parameters of mean R-R interval, RMSSD, and the HF component of HRV were positively correlated. Abnormal HRT caused by chronic congestive heart failure can be restored by beta-blocker therapy. The evolution of TS was positively correlated with measures of vagal modulation of heart rate.