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The effects of androgen anabolic steroids (AAS) use on athletes’ cardiac autonomic activity in terms of baroreflex sensitivity (BRS), and heart rate variability (HRV) have not yet been adequately studied. Furthermore, there is no information to describe the possible relationship between the structural and functional cardiac remodeling and the cardiac autonomic nervous system changes caused by AAS abuse. Thus, we aimed to study the effects of long-term AAS abuse on cardiac autonomic efficacy and cardiac adaptations in strength-trained athletes. In total, 80 strength-trained athletes (weightlifters and bodybuilders) participated in the study. Notably, 40 of them using AAS according to their state formed group A, 40 nonuser strength-trained athletes comprised group B, and 40 healthy nonathletes (group C) were used as controls. All subjects underwent a head-up tilt test using the 30 min protocol to evaluate the baroreflex sensitivity and short HRV modulation. Furthermore, all athletes undertook standard echocardiography, a cardiac tissue Doppler imaging (TDI) study, and a maximal spiroergometric test on a treadmill to estimate their maximum oxygen consumption (VO2max). The tilt test results showed that group A presented a significantly lower BRS and baroreflex effectiveness index than group B by 13.8% and 10.7%, respectively (p &lt, 0.05). Regarding short-term HRV analysis, a significant increase was observed in sympathetic activity in AAS users. Moreover, athletes of group A showed increased left ventricular (LV) mass index (LVMI) by 8.9% (p &lt, 0.05), compared to group B. However, no difference was found in LV ejection fraction between the groups. TDI measurements indicated that AAS users had decreased septal and lateral peak E’ by 38.0% (p &lt, 0.05) and 32.1% (p &lt, 0.05), respectively, and increased E/E’ by 32.0% (p &lt, 0.05), compared to group B. This LV diastolic function alteration was correlated with the year of AAS abuse. A significant correlation was established between BRS depression and LV diastolic impairment in AAS users. Cardiopulmonary test results showed that AAS users had significantly higher time to exhaustion by 11.0 % (p &lt, 0.05) and VO2max by 15.1% (p &lt, 0.05), compared to controls. A significant correlation was found between VO2max and LVMI in AAS users. The results of the present study indicated that long-term AAS use in strength-trained athletes led to altered cardiovascular autonomic modulations, which were associated with indices of early LV diastolic dysfunction.

ObjectivesFunctional development of the fetal cardiac autonomic nervous system (cANS) plays a key role in fetal maturation and can be assessed through fetal heart rate variability (fHRV)-analysis, with each HRV parameter representing different aspects of cANS activity. Current available techniques, however, are unable to assess the fHRV parameters accurately throughout the whole pregnancy. This study aims to test the feasibility of color tissue Doppler imaging (cTDI) as a new ultrasound technique for HRV analysis. Secondly, we explored time trends of fHRV parameters using this technique.Methods18 healthy singleton fetuses were examined sequentially every 8 weeks from 10 weeks GA onwards. From each examination, 3 cTDI recordings of the four-chamber view of 10 seconds were retrieved to determine accurate beat-to-beat intervals. The fHRV parameters SDNN, RMSSD, SDNN/RMSSD, and pNN10, each representing different functional aspects of the cANS, were measured, and time trends during pregnancy were explored using spline functions within a linear mixed-effects model.ResultsIn total, 77% (95% Cl 66–87%) of examinations were feasible for fHRV analysis from the first trimester onwards, which is a great improvement compared to other techniques. The technique is able to determine different maturation rates of the fHRV parameters, showing that cANS function, presumably parasympathetic activity, establishes around 20 weeks GA and matures rapidly until 30 weeks GA.ConclusionsThis is the first study able to assess cANS function through fHRV analysis from the first trimester onwards. The use of cTDI to determine beat-to-beat intervals seems feasible in just 3 clips of 10 seconds, which holds promise for future clinical use in assessing fetal well-being.

Background and aims Cardiovascular disease (CVD) is the leading cause of death in patients with non-alcoholic fatty liver disease (NAFLD), both with and without type 2 diabetes mellitus (T2DM). Cardiac autonomic dysfunction is a risk factor for CVD morbidity and mortality. The aim of this pilot study was to assess whether there is an association between NAFLD and impaired cardiac autonomic function. Methods and results Among the first 4979 participants from the Cooperative Health Research in South Tyrol (CHRIS) study, we randomly recruited 173 individuals with T2DM and 183 age- and sex-matched nondiabetic controls. Participants underwent ultrasonography and vibration-controlled transient elastography (Fibroscan®, Echosens) to assess hepatic steatosis and liver stiffness. The low-to-high-frequency (LF/HF) power ratio and other heart rate variability (HRV) measures were calculated from a 20-min resting electrocardiogram (ECG) to derive a measure of cardiac sympathetic/parasympathetic imbalance. Among the 356 individuals recruited for the study, 117 had NAFLD and T2DM, 56 had T2DM alone, 68 had NAFLD alone, and 115 subjects had neither condition. Individuals with T2DM and NAFLD (adjusted odds ratio [OR] 4.29, 95% confidence intervals [CI] 1.90–10.6) and individuals with NAFLD alone (adjusted OR 3.41, 95% CI 1.59–7.29), but not those with T2DM alone, had a substantially increased risk of having cardiac sympathetic/parasympathetic imbalance, compared with those without NAFLD and T2DM. Logistic regression models were adjusted for age, sex, body mass index (BMI), hypertension, dyslipidemia, insulin resistance, hemoglobin A1c (HbA1c), C-reactive protein (CRP), and Fibroscan®-measured liver stiffness. Conclusions NAFLD was associated with cardiac sympathetic/parasympathetic imbalance, regardless of the presence or absence of T2DM, liver stiffness, and other potential confounding factors.

Background Premature infants may present with damage to the autonomic nervous system (ANS), which may be related to poorer neurological development. Among the techniques used to evaluate the ANS, heart rate variability (HRV) emerged as a simple, non-invasive, and easy to apply tool. The aim of the present study was to analyze and compare HRV in preterm infants at different times of hospitalization in order to verify the possible environmental relationships or clinical evolution with HRV. Methods A longitudinal, prospective, and descriptive study with non-probabilistic sampling composed of 25 collections of preterm infants of HRV at two moments: moment I (within 15 days of birth) and moment II (after 45 days post-birth). The Polar V800 heart rate monitor was used with the Polar H10 cardiac transducer to collect HRV, which was collected in the supine position for 15 min. The HRV data were analyzed by the linear method in frequency domain and time domain and by the nonlinear method using Kubios HRV analysis software, version 3.0.2. Results There was an increase in HRV values at moment II, these being statistically significant in the SD1, ApEn, and SampEn. Data related to increased sympathetic nervous system activity, parasympathetic nervous system activity, and increased index complexity. Conclusions The data demonstrate an increase in HRV values in premature infants at moment II, demonstrating a possible development in the maturation of the ANS during hospitalization. Trial registration: RBR-3x7gz8 retrospectively registered. Electronic supplementary material The online version of this article (10.1186/s12872-019-1166-4) contains supplementary material, which is available to authorized users.

Reduced heart rate (HR) variability in preterm infants compared with full-term infants suggests that autonomic cardiac control is developmentally delayed. However, the association between developmental changes in myocardial repolarization and gestational age remains unknown. This study investigated the association between the myocardial repolarization lability index, namely the QT variability index (QTVI) = log10 [(QTv/QTm2)/(HRv/HRm2)], and the perinatal profile of healthy 1-month-old infants. We included 209 infants (143 boys and 87 girls; mean gestational weeks at birth, 38.6 ± 1.7) who were born in university hospitals between 2014 and 2015 without apparent cardiac disease. We compared the ECG variability indices in 28 infants born before 37 gestational weeks (mean gestational weeks at birth, 35.6 ± 1.1 as preterm) and 181 infants born at the average number of gestational weeks (mean gestational weeks at birth, 38.8 ± 1.1 as controls). There was a negative correlation between the QTVI and gestational weeks (r = - 0.460, p = 0.035). QTVI values in preterm infants were larger than those in the controls (0.01 ± 0.50 vs. -0.26 ± 0.48, p = 0.023). In conclusion, the QTVI is negatively correlated with gestational age. The QTVI can serve as an index of the maturity of the cardiac autonomic nervous system and myocardial depolarization.

The cardiac autonomic nervous system (CANS) is associated with modulation of cardiac electrophysiology and arrhythmogenesis. In this mini review, we will briefly introduce cardiac autonomic anatomy and autonomic activity in ventricular arrhythmias (VAs) and discuss novel approaches of CANS modulation for treating VAs. Studies over the decades have provided a better understanding of cardiac autonomic innervation and revealed overwhelming evidence of the relationship between autonomic tone and VAs. A high sympathetic tone and low parasympathetic (vagal) tone are considered as the major triggers of VAs in patients with myocardial ischemia, which can cause sudden cardiac death. In recent years, novel methods of autonomic neuromodulation have been investigated to prevent VAs, and they have been verified as being beneficial for malignant VAs in animal models and humans. The clinical outcome of autonomic neuromodulation depends on the level of cardiac neuraxis, stimulation parameters, and patient's pathological status. Since autonomic modulation for VA treatment is still in the early stage of clinical application, more basic and clinical studies should be performed to clarify these mechanisms and optimize autonomic neuromodulation therapies for patients with VAs in the future.

PURPOSE OF REVIEW: This review aims to describe the latest advances in autonomic neuromodulation approaches to treating cardiac arrhythmias, with a focus on ventricular arrhythmias. RECENT FINDINGS: The increasing understanding of neuronal remodeling in cardiac diseases has led to the development and improvement of novel neuromodulation therapies targeting multiple levels of the autonomic nervous system. Thoracic epidural anesthesia, spinal cord stimulation, stellate ganglion modulatory therapies, vagal stimulation, renal denervation, and interventions on the intracardiac nervous system have all been studied in preclinical models, with encouraging preliminary clinical data. SUMMARY: The autonomic nervous system regulates all the electrical processes of the heart and plays an important role in the pathophysiology of cardiac arrhythmias. Despite recent advances in the clinical application of cardiac neuromodulation, our comprehension of the anatomy and function of the cardiac autonomic nervous system is still limited. Hopefully in the near future, more preclinical data combined with larger clinical trials will lead to further improvements in neuromodulatory treatment for heart rhythm disorders.

Left cardiac sympathetic denervation (LCSD) is a surgical antiadrenergic intervention with a strong antiarrhythmic effect, supported by preclinical as well as clinical data. The mechanism of action of LCSD in structurally normal hearts with increased arrhythmic susceptibility (such as those of patients with channelopathies) is not limited to the antagonism of acute catecholamines release in the heart. LCSD also conveys a strong anti-fibrillatory action that was first demonstrated over 40 years ago and provides the rationale for its use in almost any cardiac condition at increased risk of ventricular fibrillation. The molecular mechanisms involved in the final antiarrhythmic effect of LCSD turned out to be much broader than anticipated. Beside the vagotonic effect at different levels of the neuraxis, other new mechanisms have been recently proposed, such as the antagonism of neuronal remodeling, the antagonism of neuropeptide Y effects, and the correction of neuronal nitric oxide synthase (nNOS) imbalance. The beneficial effects of LCSD have never been associated with a detectable deterioration of cardiac performance. Finally, patients express a high degree of satisfaction with the procedure. In this review, we focus on the rationale, results and our personal approach to LCSD in patients with channelopathies such as long QT syndrome and catecholaminergic polymorphic ventricular tachycardia.

An exploratory multivariate analysis of factors of echocardiographic variables and those of the Holter test of 38 dogs with MVMD staged in three classes (class 1a, class 1b, class 2) of congestive heart failure proposed by the ISACHC. The purpose of this analysis was learning the processes that would explain the behavior of the variables described, using exploratory multivariate techniques of factors. Five independent factors were determined (PNS to SF) which altogether explain 82.17% of the shared variance of the data. It was identified that among the five factors, the first process (PNS) is the first factor in importance, recruiting the highest percentage of variance (37.96%) and represents the participation of the cardiac autonomic nervous system. RESUMO Foi realizada análise multivariada exploratória de fatores das variáveis ecocardiográficas e do exame Holter de 38 cães com DMVM estadiados em três classes (classe 1a, classe 1b, classe 2) da insuficiência cardíaca congestiva proposta pela ISACHC. O objetivo desta análise foi conhecer os processos que explicariam o comportamento das variáveis descritas, utilizando-se para esse fim técnicas multivariadas exploratórias de fatores. Foram determinados cinco fatores independentes (PNS até SF) que, em conjunto, explicam 82,17% da variância compartilhada dos dados. O primeiro processo (PNS) é o primeiro fator em importância, recrutando a maior porcentagem da variância total (37,96%) e representa a participação do sistema nervoso autônomo cardíaco.

Background Cardiac sympathetic blockade is a therapeutic approach for arrhythmias and heart failure and may be a beneficial effect of high thoracic epidural anesthesia. These treatments require detailed knowledge of the spatial location and distribution of cardiac autonomic nerves, however, there are controversies on this subject in humans. Objective To provide a systematic overview of current knowledge on human anatomy of the cardiac autonomic nervous system. Results In contrast to the often claimed assumption that human preganglionic sympathetic cardiac neurons originate mainly from thoracic spinal segments T1–T4 or T5, there is ample evidence indicating involvement of cervical spinal segment C8 and thoracic spinal segments below T5. Whether cervical ganglia besides the stellate ganglion play a role in transmission of cardiac sympathetic signals is unclear. Similarly, there is debate on the origin of cardiac nerves from different thoracic ganglia. Most human studies report thoracic cardiac nerves emerging from the first to fourth thoracic paravertebral ganglia; others report contributions from the fifth, sixth and even the seventh thoracic ganglia. There is no agreement on the precise composition of nerve plexuses at the cardiac level. After years of debate, it is generally accepted that the vagal nerve contributes to ventricular innervation. Vagal distribution appears higher in atria, whereas adrenergic fibers exceed the number of vagal fibers in the ventricles. Conclusion Anatomy of the human cardiac autonomic nervous system is highly variable and likely extends beyond generally assumed boundaries. This information is relevant for thoracic epidural anesthesia and procedures targeting neuronal modulation of cardiac sympathetic innervation.

OBJECTIVES: Survival after surgical repair of a ventricular septal defect (VSD) is good, but, as in almost all congenital heart diseases, late complications are frequent in adulthood. The exact mechanisms, timing and who is at risk are not fully understood. Altered cardiac autonomic nervous system (ANS) activity might play a role in these long-term sequelae. The aim of this study was to extensively evaluate children late after VSD repair including their cardiac ANS activity, cardiac function and exercise capacity.METHODS: Thirty-three patients after surgical VSD repair and 66 healthy age-matched controls underwent 24-h monitoring of ANS control and cardiac output using impedance cardiography, detailed echocardiography and cardiopulmonary exercise testing.RESULTS: Ambulatory cardiac ANS control was not different between the patients and the controls. Right ventricular function, exercise capacity and ambulatory cardiac output were decreased in patients compared with the controls. No relationships were found between cardiac ANS activity and cardiac function.CONCLUSIONS: Long (average time after repair was 9.9 years) after successful surgical correction of a VSD, cardiac ANS control is not different from the controls. Right ventricular function and exercise capacity are impaired in VSD patients. Post-surgical outcome in these patients may be less benign than presently assumed; therefore, follow-up should be continued into adulthood to detect adverse outcomes in a timely fashion.

KEY TEACHING POINTS In the electrically nonisolated pulmonary veins, the cardiac autonomic system has been shown to play an important role in initiating pulmonary vein (PV) ectopy and triggering atrial fibrillation (AF).1, 2, 3 However, the effects of the cardiac autonomic system on the isolated PV are not currently known. We present the observations from a case where opportunistic stimulation of the autonomic system was performed in the presence of dissociated pulmonary vein potentials (PVPd).

Background: Recent studies have claimed a positive effect of physical activity and body composition on vagal tone. In pediatric populations, there is a pronounced decrease in heart rate with age. While this decrease is often interpreted as an age-related increase in vagal tone, there is some evidence that it may be related to a decrease in intrinsic heart rate. This factor has not been taken into account in most previous studies. The aim of the present study was to assess the association between physical activity and/or body composition and heart rate variability (HRV) independently of the decline in heart rate in young children. Methods: Anthropometric measurements were taken in 309 children aged 2-6 years. Ambulatory electrocardiograms were collected over 14-18 h comprising a full night and accelerometry over 7 days. HRV was determined of three different night segments: (1) over 5 min during deep sleep identified automatically based on HRV characteristics; (2) during a 20 min segment starting 15 min after sleep onset; (3) over a 4-h segment between midnight and 4 a.m. Linear models were computed for HRV parameters with anthropometric and physical activity variables adjusted for heart rate and other confounding variables (e.g., age for physical activity models). Results: We found a decline in heart rate with increasing physical activity and decreasing skinfold thickness. HRV parameters decreased with increasing age, height, and weight in HR-adjusted regression models. These relationships were only found in segments of deep sleep detected automatically based on HRV or manually 15 min after sleep onset, but not in the 4-h segment with random sleep phases. Conclusions: Contrary to most previous studies, we found no increase of standard HRV parameters with age, however, when adjusted for heart rate, there was a significant decrease of HRV parameters with increasing age. Without knowing intrinsic heart rate correct interpretation of HRV in growing children is impossible.

Highlights • Exercise intolerance is a hallmark in COPD patients. • Changes in HRV dynamics are early and sensitive indices of impaired health. • 6MWD provides relevant information about functional (in)capacity in COPD patients. • A system with loss of complexity interferes with exercise performance. • HRV modulation to submaximal exercise may reflect ventilatory and hemodynamic abnormalities., Background Poor exercise capacity is an important negative prognostic marker in patients with chronic obstructive pulmonary disease (COPD). Heart rate variability (HRV) responses can indicate alterations in cardiac autonomic control. Nevertheless, it remains unclear whether these abnormalities are related to cardiorespiratory responses to exercise in these patients. Objective To evaluate whether HRV at rest and submaximal exercise are related to impaired cardiopulmonary responses to exercise in COPD patients. Methods Fifteen men (66.2 ± 8.7 years) with COPD (FEV1: 55.1 ± 19.2%) were assessed. The R-R interval (RRi) data collection was performed at rest (stand position) and during the six-minute walk test (6MWT). All patients performed a symptom-limited cardiopulmonary exercise test on a cycle ergometer. The HRV changes from rest to submaximal exercise (Δ rest-6MWT) were calculated. Results We found significant correlations between low frequency (LF) and high frequency (HF) Δ rest-6MWT with Δ oxyhemoglobin saturation by pulse oximetry (r = −0.64 and r = 0.65, respectively; p

Adriana Mazzuco,1 Wladimir Musetti Medeiros,2 Milena Pelosi Rizk Sperling,1 Aline Soares de Souza,2 Maria Clara Noman Alencar,2 Flávio Ferlin Arbex,2 José Alberto Neder,2,3 Ross Arena,4 Audrey Borghi-Silva1 1Cardiopulmonary Physiotherapy Laboratory, Federal University of São Carlos, São Carlos, 2Pulmonary Function and Clinical Exercise Physiology Unit, Respiratory Division, Department of Medicine, Federal University of São Paulo, São Paulo, Brazil; 3Laboratory of Clinical Exercise Physiology, Division of Respiratory and Critical Care Medicine, Department of Medicine, Queen’s University, Kingston, ON, Canada; 4Department of Physical Therapy and Integrative Physiology Laboratory, College of Applied Health Sciences, University of Illinois Chicago, Chicago, IL, USA Background: In chronic obstructive pulmonary disease (COPD), functional and structural impairment of lung function can negatively impact heart rate variability (HRV); however, it is unknown if static lung volumes and lung diffusion capacity negatively impacts HRV responses. We investigated whether impairment of static lung volumes and lung diffusion capacity could be related to HRV indices in patients with moderate to severe COPD. Methods: Sixteen sedentary males with COPD were enrolled in this study. Resting blood gases, static lung volumes, and lung diffusion capacity for carbon monoxide (DLCO) were measured. The RR interval (RRi) was registered in the supine, standing, and seated positions (10 minutes each) and during 4 minutes of a respiratory sinus arrhythmia maneuver (M-RSA). Delta changes (Δsupine-standing and Δsupine-M-RSA) of the standard deviation of normal RRi, low frequency (LF, normalized units [nu]) and high frequency (HF [nu]), SD1, SD2, alpha1, alpha2, and approximate entropy (ApEn) indices were calculated. Results: HF, LF, SD1, SD2, and alpha1 deltas significantly correlated with forced expiratory volume in 1 second, DLCO, airway resistance, residual volume, inspiratory capacity/total lung capacity ratio, and residual volume/total lung capacity ratio. Significant and moderate associations were also observed between LF/HF ratio versus total gas volume (%), r=0.53; LF/HF ratio versus residual volume, %, r=0.52; and HF versus total gas volume (%), r=-0.53 (P

Background Depression is an independent risk factor for coronary artery disease. Autonomic instability may play a mediating or moderating role in this relationship; however this is not well understood. The objective of this study was to explore cardiac autonomic function and cardiac arrhythmia in depression, the correlation between depression severity and Heart Rate Variability (HRV) related indices, and the prevalence of arrhythmia. Methods Individuals (n = 53) with major depression as assessed by the Diagnostic and Statistical Manual of Mental Disorders, who had a Hamilton Rating Scale for Depression (HAMD) score ≥20 and a Zung Self-Rating Depression Scale score > 53 were compared to 53 healthy individuals, matched for age and gender. Multichannel Electrocardiograph ECG-92C data were collected over 24 hours. Long-term changes in HRV were used to assess the following vagally mediated changes in autonomic tone, expressed as time domain indices: Standard deviation of the NN intervals (SDNN), standard deviation of 5 min averaged NN intervals (SDANN), Root Mean Square of the Successive Differences (RMSSD) and percentage of NN intervals > 50 ms different from preceding interval (pNN50). Pearson’s correlations were conducted to explore the strength of the association between depression severity (using the SDS and HRV related indices, specifically SDNN and low frequency domain / high frequency domain (LF/HF)). Results The values of SDNN, SDANN, RMSSD, PNN50 and HF were lower in the depression group compared to the control group (PPPP Conclusions Our findings suggest that depression is accompanied by dysfunction of the cardiac autonomic nervous system, and further, that depression severity is linked to severity of this dysfunction. Individuals with depression appear to be susceptible to premature atrial and/or ventricular disease.