cardiovascular and autonomic adjustments occur during and after physical exercise, and exercise intensity can directly influence the magnitude of these adjustments. Therefore, it is important to analyze post-exercise recovery to provide better guidance for prescription strategies.

to analyze autonomic behavior during post-exercise recovery after the Pilates method at different intensity levels.

in total, 24 healthy young men were included in this study. The participants underwent 12 weeks of Pilates training. The exercises were progressive between beginners, intermediate, and advanced levels. Post-exercise autonomic behavior was analyzed using vagal indices of heart rate variability. Descriptive statistics were adopted with Repeated Measures Analysis of Variance and the Bonferroni correction.

for intermediate and advanced levels, a decrease in vagal modulation was observed (p < 0.05) in the first 5 min after exercise compared to rest, represented by the rMSSD and SD1 indices.

intermediate and advanced exercise reduced parasympathetic modulation in the initial minutes of post-exercise recovery. The beginner level did not promote changes in autonomic behavior immediately after the exercise session.

Pulmonary thromboembolism (PTE) is the third most frequent acute cardiovascular syndrome, with serious sequelae in untreated patients. Heart rate variability (HRV) has emerged as a crucial and established prognostic indicator for adverse events. Nevertheless, its correlation with PTE and its prognostic significance in anticipating adverse outcomes warrant additional investigation. This study sought to examine the 30-day prognostic utility of HRV in predicting major adverse cardiovascular events (MACEs) in individuals with PTE.

This retrospective cohort study, conducted at 2 centers, enrolled 170 patients diagnosed with PTE and 174 control subjects who underwent 24-hour Holter recording, with an evaluation of time-domain HRV. PTE patients with simplified-Pulmonary-Embolism-Severity Index = 0 points are classified as a low-risk group, and ≥1 as an intermediate-risk group. The association between HRV and MACE was assessed using receiver operating characteristic curve analysis, Cox-regression, and Kaplan-Meier curve tests.

Time-domain HRV was reduced in all PTE patients compared with the control group and intermediate-risk PTE than in low-risk PTE groups (P < 0.05). A total of 22 PTE patients developed MACE during follow-up. PTE patients with reduced HRV have an increased risk of MACE (log-rank P < 0.05). HRV was an independent predictor of MACE, the standard deviation of all normal-to-normal RR intervals (hazard ratio [HR], 0.968; 95% CI, 0.950-0.986, P = 0.001), and the standard deviation of 5-minute mean N-N interval (HR, 0.974; 95% CI, 0.958-0.990, P = 0.002).

HRV is an independent risk factor and is associated with 30-day poor outcomes in PTE. Thus, HRV can be considered as a tool in the risk stratification of PTE patients.

HRV is clinically considered to be a surrogate measure of the asymmetrical interplay of the sympathetic and parasympathetic nervous system. While HRV has become an increasingly measured variable through commercially-available wearable devices, HRV is not routinely monitored or utilized in healthcare settings at this time. The purpose of this narrative review is to discuss and evaluate the current research and potential future applications of HRV in several medical specialties, including critical care, cardiology, pulmonology, nephrology, gastroenterology, endocrinology, infectious disease, hematology and oncology, neurology and rehabilitation, sports medicine, surgery and anesthesiology, rheumatology and chronic pain, obstetrics and gynecology, pediatrics, and psychiatry/psychology. A narrative literature review was conducted with search terms including HRV and relevant terminology to the medical specialty in question. While HRV has demonstrated promise for some diagnoses as a non-invasive, easy to use, and cost-effective metric for early disease detection, prognosis and mortality prediction, disease monitoring, and biofeedback therapy, several issues plague the current literature. Substantial heterogeneity exists in the current HRV literature which limits its applicability in clinical practice. However, applications of HRV in psychiatry, critical care, and in specific chronic diseases demonstrate sufficient evidence to warrant clinical application regardless of the surmountable research issues. More data is needed to understand the exact impact of standardizing HRV monitoring and treatment protocols on patient outcomes in each of the clinical contexts discussed in this paper.

Sleep architectural disruption is associated with atrial fibrillation (AF); however, associated autonomic influences remain unclear and it is unknown if this detriment persists during wakefulness. We hypothesize sleep disruption and autonomic dysfunction have diurnal patterning in patients with paroxysmal AF.

We analyzed data from the Sleep Apnea and Atrial Fibrillation Biomarkers and Electrophysiologic Atrial Triggers (SAFEBEAT) study designed to examine paroxysmal AF and sleep apnea, including simultaneous collection of continuous electrocardiogram monitoring (Heartrak Telemetry®) and actigraphy (Actiwatch GTX) for 7-21 days. Heart rate variability (HRV) measures in time-domain (standard deviation of normal-to-normal (NN) intervals (SDNN), coefficient of variation (CV)) and frequency-domain (low frequency power (LFP), high frequency power (HFP)) were used as surrogates of autonomic function and averaged per sleep/wake per day. A linear mixed-effects model assuming compound symmetry correlation structure was used to assess the relationship of HRV with actigraphy-derived sleep data.

The analytic sample (age 60.1 ± 12.0 years, body mass index 32.6 ± 6.7 kg/m2, 36% female, 75% White) included 100 participants with paroxysmal AF. Longer sleep latency was associated with lower HFP during wakefulness (coefficient - 0.0501, p = 0.031). Higher sleep efficiency was associated with increased SDNN (coefficient 0.0007, p = 0.014) and CV (coefficient 0.0167, p = 0.047). Higher arousal index was associated with increased CV (coefficient 0.0166, p = 0.007) and LFP (coefficient 0.0232, p = 0.003). During sleep, longer average awakenings duration was associated with increased LFP/HFP ratio (coefficient 0.1977, p < 0.001) and reduced HFP (coefficient - 0.1338, p < 0.001). Significant sleep-wake interactions were observed for sleep latency with HFP (p = 0.024), sleep efficiency with SDNN and CV (both p < 0.01), WASO with SDNN, CV, and LFP (all p < 0.05), and frequency of awakenings with CV and LFP (both p < 0.05).

Actigraphy-based measures of sleep disruption were associated with autonomic function alterations exhibiting diurnal variability in paroxysmal AF. Greater overall HRV and parasympathetic modulation were related to better sleep quality. Increased sympathetic activation was associated with sleep fragmentation. Results provide insights into differential autonomic dysfunction related to sleep disruption that may contribute to atrial arrhythmogenesis.

We assessed the test validity of the Apple Watch series 6 measure of heart rate variability (HRV) by comparing it with the reference measure assessed via a Biopac 3-lead electrocardiogram (ECG). We recruited 78 healthy adults (aged 20-75 years). HRV was measured using an in-lab protocol while resting, talking, watching a movie, before walking, and after walking. We conducted a synchronized countdown for each condition to guarantee that the recordings would be aligned between the two devices by using event markers in the Biopac at the exact time that the Apple Watch Breathe app began and ended. We assessed test validity using the Bland-Altman method, and both precision and accuracy were estimated using Lin's concordance correlation coefficient. The highest level of agreement and concordance between devices occurred during rest. We observed near-perfect agreement for R-R intervals and beats per minute (BPM) measures, with mean absolute percentage errors (MAPE) of 1.15% during resting conditions. We observed moderate levels of agreement and concordance for N-N intervals at rest with a MAPE of 31.31% during resting conditions. The Apple Watch provides a high level of validity for measuring R-R intervals and BPM in healthy adults. Further research is needed to determine if HRV measures with the Apple Watch offer a significant opportunity for the surveillance of CVD risk.

A significant proportion of cancer patients experience autonomic dysfunction, and cancer treatments such as chemotherapy and radiation therapy can exacerbate impairments in the cardiac autonomic nervous system. This study sought to investigate the characteristics of heart rate variability (HRV) in individuals with cancer.

To evaluate the relationship between HRV and cancer patients, providing insights and references for cancer treatment.

The study included 127 cancer patients with available 24-hour dynamic electrocardiogram data. HRV differences were analyzed using both time domain and frequency domain methods. These findings were then compared to HRV data from reference individuals, sourced from literature that utilized the same HRV computing algorithm.

Our findings revealed that cancer patients generally exhibited abnormal HRV compared to the reference group. HRV was found to be correlated with age and clinical type (P < 0.05), but no significant correlation was observed with tumor site or gender (P > 0.05).

This study indicates that cancer patients have significantly abnormal HRV compared to reference individuals, suggesting the presence of a certain level of cardiac autonomic dysfunction in this patient population.

The Autonomic Nervous System (ANS) regulates 'automatic' functions such as heart rate, and alterations may have significant impacts on health outcomes. Cardiovascular measures of autonomic function such as heart rate variability are of interest as biological markers in autism spectrum disorder (ASD). The interplay between the ANS and physical health establishes a need to examine cardiovascular autonomic functioning in youth with and without ASD over development. The current study aimed to identify change in autonomic function and balance across the parasympathetic and sympathetic branches over time as a function of diagnosis, age, pubertal development, and physical health status.

The study included 244 ASD (N = 140) or neurotypical (NT) (N = 104) youth, ages 10 to 13 years at enrollment and followed over four years. Resting state autonomic functioning was measured using respiratory sinus arrhythmia (RSA; parasympathetic) and pre-ejection period (PEP; sympathetic). Autonomic balance and regulation were also examined as outcomes. Linear mixed models tested between- and within-group differences in the primary autonomic outcomes as well as the influence of pubertal development, body weight, and medication use.

Baseline models showed diagnostic differences, with lower parasympathetic regulation, in youth with ASD, but no differences were observed for the other three outcomes. Adding body mass index (BMI) percentile and medication use removed the statistically significant diagnostic effect, while both variables were significantly related to lower RSA and overall autonomic regulation. Parasympathetic function (RSA) was stable over age and pubertal stage, while a notable decrease in sympathetic control (increased PEP) was found for age and pubertal stage. BMI percentile at enrollment significantly predicted autonomic function, while change in BMI over time did not.

Minimal research to date has explored physical health (e.g., BMI) and autonomic outcomes in ASD. The current study observed few group differences yet demonstrates important effects of physical health on ANS function in both ASD and neurotypical youth. Findings further emphasize a need to focus on individual traits such as BMI and medication use to elucidate the extent to which autonomic differences are related to health status, irrespective of diagnostic category, across the lifespan.

Arterial stiffness and cardiac autonomic function are crucial indicators of cardiovascular health. Acute exercise and age impact these parameters, but research often focuses on specific exercise activities, lacking ecological validity.

We examined the acute effects of commercially available group fitness classes (indoor cycling, resistance training, combined exercise) on arterial stiffness and vagal-related heart rate variability (HRV) indices in twelve young and twelve middle-aged adults. Participants attended four sessions, including exercise and control conditions, with measurements taken at rest and during recovery.

Middle-aged, but not young adults, showed reductions in central and peripheral systolic blood pressure 20-min into recovery across all exercise modalities (range: -7 to -8 mmHg p < 0.05). However, arterial stiffness remained unchanged. Similarly, vagal-related HRV indices (range: -0.51 to -0.90 ms, p < 0.05) and BRS (-4.03, p < 0.05) were reduced immediately after exercise, with differences persisting 30 min into recovery only after indoor cycling. Resistance and combined exercise elicited similar cardiovagal modulation and delayed baroreflex sensitivity recovery to cycling exercise, despite higher energy expenditure during indoor cycling (+87 to +129 kcal, p < 0.05).

Acute group fitness classes induce age-dependent alterations in blood pressure, but not in arterial stiffness or cardiovagal modulation. While the overall cardiovascular effects were generally consistent, differences in autonomic recovery were observed between exercise modes, with prolonged effects seen after indoor cycling. This suggests that exercise prescription should consider both age and exercise modality, as well as recovery time. The findings also emphasize the importance of ecological validity in exercise interventions, highlighting that acute effects on cardiovascular health in real-world settings may differ from those observed in controlled laboratory environments (ID: NCT06616428).

This investigation determined if an acute bout of low-load knee extension (KE) with intermittent blood flow restriction (BFR) influenced autonomic modulation and skeletal muscle oxygenation (SmO2%).

Fourteen physically active males completed three different sessions: one-repetition maximum (1RM), KE with BFR (BFR-KE) at 20% 1RM (cuff pressure=143 ± 13 mmHg), and KE with free blood flow at 20% 1RM (Control-KE). Heart rate variability (HRV) metrics: logarithmically transformed (ln) square root of the mean differences of successive R-R intervals (lnRMSSD), high frequency power (lnHF), and low frequency power (lnLF), as well as SmO2%, and rating of perceived exertion (RPE) were measured. Repeated measures analyses of variance were used to analyze HRV metrics and SmO2%, while a paired t-test was used to analyze RPE. A significance level of P < 0.05 was used for analyses.

From baseline to 15 min post-exercise lnRMSSD decreased in both BFR-KE and Control-KE (4.34 ± 0.43-3.75 ± 0.82 ms, P = 0.027). Thereafter, lnRMSSD (+7%), lnHF (+8%), and lnLF (+7%) increased from 15 to 30 min post-exercise in both BFR-KE and Control-KE (P < 0.05). BFR-KE reduced SmO2% in the vastus lateralis compared to Control-KE (36% vs. 53%; P < 0.001). RPE was greater in BFR-KE (7.0 AU) compared to Control-KE (4.5 AU; P < 0.001).

Unilateral BFR exercise with individualized cuff pressure and intermittent application facilitated greater localized muscular stress and perceptual effort, but there was no influence of vascular occlusion on post-exercise autonomic modulation compared to volume-matched exercise with free blood flow.

Individuals with posttraumatic stress disorder (PTSD) have high rates of cardiovascular disease (CVD) and increased cardiometabolic CVD risk factors (CVDRFs, e.g., hypertension, hyperlipidemia, or diabetes mellitus). Nevertheless, it remains unknown whether PTSD accelerates CVDRF development and how that impacts the development of major adverse cardiovascular events (MACE) in a broad population. Furthermore, the underlying mechanisms remain incompletely characterized.

We hypothesized that 1) PTSD accelerates CVDRF development, 2) accelerated CVDRF development mediates the PTSD-MACE relationship, and 3) accelerated CVDRF development is partially explained by alterations in neural, autonomic, and inflammatory intermediaries (e.g., stress-associated neural activity [SNA], ventromedial prefrontal cortex [vmPFC] activity, heart rate variability [HRV], and C-reactive protein [CRP]).

Subjects (N = 84,343) in the Mass General Brigham Biobank were studied over 10 years. PTSD, CVDRFs, and MACE were identified by diagnostic codes. From participants with available clinical data, neural, autonomic, and inflammatory mediators (e.g., SNA, vmPFC, HRV, and CRP) were assessed.

PTSD independently predicted incident CVDRFs (hazard ratio [95 % confidence interval] = (1.432 [1.287, 1.592], p < 0.001) and associated with the accelerated development of a new CVDRF by ∼ 4 months versus those without PTSD. The development of new CVDRFs predicted incident MACE (1.736 [1.652, 1.823, p < 0.001) and mediated the link between PTSD and MACE (p < 0.05) by up to 36.4 %. Additionally, lower vmPFC activity, lower HRV, and higher CRP were associated with the development of CVDRFs. HRV and CRP significantly mediated the PTSD-CVDRF link.

The PTSD-MACE link was partially explained by the accelerated development of CVDRFs. Alterations in neural, autonomic, and inflammatory intermediaries contributed to this association. These findings suggest that greater clinical attention to CVDRFs in individuals with PTSD may attenuate MACE risk.

Hypothyroidism, a common endocrine disorder, is linked to cardiovascular risks arising from autonomic imbalance and metabolic dysregulation. While overt hypothyroidism (OH) manifests distinct thyroid hormone abnormalities, subclinical hypothyroidism (SCH) presents milder hormonal changes. Levothyroxine therapy is widely used for thyroid function restoration, but its long-term effects on autonomic and cardiovascular health in OH remain understudied. This study investigates the therapeutic effects of six months of levothyroxine treatment on autonomic function and metabolic parameters in OH patients.

A follow-up study was conducted on OH patients receiving levothyroxine therapy. Participants with confounding cardiovascular comorbidities were excluded. Clinical assessments included autonomic function tests, metabolic profiling (lipid and thyroid parameters), and inflammatory/oxidative stress markers. Comparative analyses were performed against healthy controls.

Levothyroxine therapy effectively restored thyroid hormone levels in OH patients. Autonomic function tests demonstrated improved parasympathetic modulation and partial sympathovagal balance recovery, though residual autonomic irregularities persisted. Lipid profiles showed marked improvement but did not fully normalize compared to controls. Inflammatory and oxidative stress markers decreased significantly post-therapy, yet remained elevated relative to healthy individuals. Statistical modeling identified oxidative stress as a key contributor to autonomic dysfunction.

While levothyroxine normalized thyroid function and improved autonomic balance, incomplete resolution of metabolic and inflammatory abnormalities suggests persistent cardiovascular risks in OH patients after six months of therapy. The findings highlight the need for extended treatment durations to achieve comprehensive cardiovascular risk mitigation.

Despite therapeutic benefits, OH patients retain residual cardiovascular risks post-levothyroxine therapy, necessitating long-term monitoring. Future research should investigate optimal treatment durations and adjunct therapies to address persistent autonomic and metabolic dysfunction in this population.

Autonomic rehabilitation using osteopathic manipulative treatment (OMT) to stimulate the vagus nerve may be a good adjunct therapy by physiatrists who treat dysautonomia. Heart rate variability (HRV) may provide quantitative evidence for the benefits of OMT on autonomic nervous system function. Elevated HRV indicates optimal health and reduced mortality risk, whereas low HRV is associated with stress, pain, and chronic disease pathology.

To analyze the impact of modified occipitomastoid suture v-spread OMT technique on vagal tone by measuring HRV.

Within-participant design with 5-minute HRV measurement pre- and post-OMT treatment.

Clinical examination suites.

Thirty healthy osteopathic medical students.

A modified occipitomastoid suture v-spread treating somatic dysfunction by osteopathic physicians trained in osteopathic neuromusculoskeletal medicine.

HRV variables related to vagal tone including root mean square of successive differences (RMSSD), percentage of successive normal sinus RR intervals >50 ms (pNN50), high frequency (HF), Parasympathetic Nervous System Index (PNSI), and Sympathetic Nervous System Index (SNSI). Repeated measures t-test analyzed the difference in mean HRV values after OMT.

There were statistically significant increases in each of the HRV measures after OMT. Participants had a mean (95% confidence interval) RMSSD of 50.5 ms (38.3-62.8) at baseline and 55.0 ms (41.2-68.7, p = .013) post-OMT. pNN50 was 24.5% (17.6-31.3, n = 30) at baseline and 28.2% (20.8-35.6, p = .003) post-OMT. HF was 1549.6 ms2 (389.8-2709.4) at baseline and 1901.8 ms2 (618.2-3185.4, p = .103) post-OMT. PNSI was -0.1 (-0.5 to 0.2) at baseline and 0.1 (-0.3 to 1.5, p < .01) post-OMT, and SNSI was 0.2 (-0.1 to 0.6) at baseline and 0.05 (-0.3 to 0.4, p < .01) post-OMT. Normalization, due to high baseline variance, results include RMSSD 1.1 ms (1.0 to 1.1, p = .012), pNN50 1.3 (1.1 to 1.4, p = .011), and HF 1.2 ms2 (1.1 to 1.4, p = .018).

Modified occipitomastoid suture v-spread may provide clinical benefit through increased vagal tone and decreased sympathetic activity.

Autonomic dysfunction is associated with cardiovascular and neurological diseases, including hypertension, heart failure, anxiety, and stress-related disorders. Prior studies demonstrated that late gestation exposure to dexamethasone (DEX) resulted in female-biased increases in stress-responsive mean arterial pressure (MAP) and heart rate (HR), suggesting a role for glucocorticoid-mediated programming of autonomic dysfunction. The present study investigated the influence of sympathetic (SYM) or parasympathetic (PS) blockade on cardiovascular function in male and female rat offspring of mothers injected with DEX in utero [gestation days (GD) 18-21]. At 11-12-wk of age, MAP, HR, and heart rate variability (HRV) were evaluated at baseline and in response to SYM antagonists (α1-adrenoceptor + β1-adrenoceptor), a PS (muscarinic) antagonist, or saline (SAL). To assess stress-responsive function, rats were exposed to acute restraint. Tyrosine hydroxylase was measured in the adrenals and left ventricle, and expression of the β1 adrenergic receptor, choline acetyltransferase, and acetylcholinesterase were measured in the left ventricle. Maternal DEX injection reduced basal HRV in male and female offspring. SYM blockade attenuated increases in stress-responsive HR and MAP. PS blockade elevated stress-responsive HR and MAP to a greater extent in vehicle females. SYM and PS blockade produced equivalent effects on HR and MAP responses in male offspring, regardless of maternal treatment. Based on these findings, we suggest that maternal DEX injection disrupted autonomic regulation of cardiovascular function in females, resulting in a shift toward greater SYM input and less input from PS. Future studies will investigate whether changes in autonomic function are mediated by changes in central autonomic circuitry.NEW & NOTEWORTHY Pharmacological antagonists are used to characterize the nature of the autonomic dysregulation induced in female offspring exposed to dexamethasone, in utero. The female offspring of dams injected with dexamethasone in late gestation show a reduction in vulnerability to parasympathetic blockade and an increase in responses to acute restraint stress even in the presence of sympathetic blockade. This suggests that late gestation dexamethasone disrupts the normal development of the autonomic function in females, shifting sympathovagal balance.

Adolescents and young adults (AYAs) receiving hematopoietic cell transplantation (HCT) are at high risk for poor psychosocial outcomes. Heart rate variability (HRV), a surrogate for autonomic nervous system activity, is a promising digital biomarker that has been linked to important outcomes. The objectives of this study were to prospectively describe the trajectory of HRV among AYAs receiving HCT and explore the association between HRV and patient-reported outcomes (PROs).

This was a multi-site study embedded in a randomized trial among AYAs receiving HCT (NCT03640325). We collected sequential 24-h HRV metrics, including the standard deviation of normal-to-normal beats (SDNN), root-mean-square of successive differences (RMSSD), as well as frequency domain measures. PRO surveys queried anxiety, depression, quality of life, hope, and resilience at baseline and 3 months. We summarized outcomes using descriptive statistics, and Pearson correlation coefficients were used to examine the relationship between HRV and PROs.

Thirty-nine HRV recordings were collected from n = 16 participants aged 12-21 years. There was a moderately strong correlation between inferior baseline HRV and higher anxiety and depression (anxiety: r = -0.35 (p = 0.18) for SDNN, r = -0.47 (p = 0.07) for RMSSD; depression: r = -0.26 (p = 0.34) for SDNN, r = -0.39 (p = 0.14) for RMSSD). Among participants with elevated baseline anxiety, higher HRV suggested greater improvement in anxiety over time (r = -0.66 (p = 0.08) for SDNN, r = -0.31 (p = 0.45) for RMSSD).

There was a correlation between HRV and PROs in this study, and among those with elevated anxiety, HRV predicted improvement over time. Digital biomarkers may augment behavioral intervention design and implementation.

Particulate matter (PM) exposure can reduce heart rate variability (HRV), a cardiovascular health marker. This study examines PM1.0 (aerodynamic diameters <1 μm), PM2.5 (≥1 μm and <2.5 μm), and PM10 (≥2.5 μm and <10 μm) effects on HRV in patients with environmental diseases as chronic disease groups and vulnerable populations as control groups. PM levels were measured indoors and outdoors for five days in 97 participants, with 24-h HRV monitoring via wearable devices. PM exposure was assessed by categorizing daily cumulative PM concentrations into higher and lower exposure days, while daily average PM concentrations were used for analysis. Results showed significant negative associations between exposure to single and mixtures of different PM metrics and HRV across all groups, particularly in chronic airway disease and higher air pollution exposed groups. These findings highlight that even lower PM levels may reduce HRV, suggesting a need for stricter standards to protect sensitive individuals.

Chronic venous insufficiency (CVI) manifests as morphological and functional abnormalities in the venous system, primarily affecting the lower extremities and presenting as leg heaviness, oedema, and varicose veins. CVI is a common vascular disorder characterised by impaired blood flow in the veins, often leading to various clinical manifestations. To better understand the additional underlying mechanisms of CVI, it is essential to explore the role of Wnt proteins, which play a crucial role in regulating signalling processes. This study aimed to investigate the expression levels of the Wnt3a and Wnt5a genes using real-time PCR in patients with venous insufficiency compared to acontrol group.

68 participants were included, comprising 29 controls and 39 patients with venous insufficiency from Near East University Hospital. Real-time PCR was utilised for gene expression analysis on a segment of the great saphenous vein biopsy, encompassing all vascular layers, from each participant in both groups. With a significance threshold of p < 0.05, the analysis revealed a significant difference in Wnt3a gene expression (p ₌ 0.0007) and a nonsignificant difference in Wnt5a expression levels (p ₌ 0.5726) between patients with venous insufficiency and the healthy control group.

This study indicates fluctuations in the Wnt genes in varicose vein biopsies compared to healthy veins. Consequently, further research is essential to elucidate whether the dysregulation of the Wnt pathway induces venous insufficiency or vice versa. This may facilitate targeted interventions addressing its fundamental molecular aberrations.

Stress is ubiquitous in our modern society and contributes to many disease states. This narrative review describes the effect of stress/distress on cancer development and progression. Seminal randomized controlled trials, systematic reviews/meta-analyses, and distress management guidelines from the National Comprehensive Cancer Network (NCCN), the American Society of Clinical Oncology (ASCO), and the Society for Integrative LinearOncology (SIO) are highlighted. We describe the physiological effects of distress, distress assessment, and management. Psychological treatments are summarized. Evidence-based lifestyle modifications and integrative therapies are reviewed in detail, including mindfulness-based techniques, yoga, guided imagery, breathing techniques, hypnosis, exercise, music therapy, qigong/Tai Chi, eye movement desensitization and reprocessing, and improving sleep and heart rate variability. Recognition and treatment of distress can improve quality of life. More research is needed to determine the effects of managing distress on cancer outcomes, as well as the best type and duration of intervention, noting that the benefits of interventions may be specific for patients with different cancer types.

Data on associations between adiposity and heart rate variability (HRV) in prepubertal children are limited. We examined the associations between adiposity indices and HRV, independent of lifestyle behaviors, comparing multiple indicators of adiposity, and explored differences between boys and girls.

Data stem from 469 participants of the QUALITY cohort (630 children aged 8-10 years with a parental history of obesity). Adiposity indices included waist-to-height ratio, body mass index (BMI) percentiles and categories (overweight, obesity), dual-energy x-ray absorptiometry (DEXA) defined fat mass percentage and android/gynoid ratio. HRV indices in the frequency and the spectral domain were derived from a daytime 3-h Holter recording. Multivariable linear regression models were adjusted for age, sex, Tanner stage, physical activity, screen time, and fitness. Interactions between sex and adiposity were tested.

Greater adiposity was associated with decreased parasympathetic modulation and increased sympathetic dominance. Waist-to-height ratio was associated with lower parasympathetic activity: root mean square of the successive differences (RMSSD) [B =  -23.32, 95% confidence interval (CI) -42.42, -4.22], pNN50 (B =  -16.93, 95% CI - 28.58, - 5.27), LF/HF ratio (B = 1.83, 95% CI 0.97-2.70). Patterns of association were similar for android/gynoid ratio. Overweight was not associated with altered HRV. Obesity was negatively associated with RMSSD and pNN50 and positively with LF/HF ratio. Greater fat mass percentage was associated with lower RMSSD, pNN50, and HF, and increased LF/HF ratio. There were no differences between boys and girls.

Specific markers of adiposity relate to altered HRV in childhood, with waist-to-height ratio being potentially a more relevant marker of HRV than BMI and more pragmatic than percent body fat.

NCT03356262, 11 November 2017.

Inhalation of ambient particulate matter (PM) and ozone (O3) has been associated with increased cardiovascular morbidity and mortality. However, the interactive effects of PM and O3 on cardiac dysfunction and disease have not been thoroughly examined, especially at a proteomic level. The purpose of this study was to identify and compare proteome changes in spontaneously hypertensive (SH) rats co-exposed to concentrated ambient particulates (CAPs) and O3, with a focus on investigating inflammatory and metabolic pathways, which are the two major ones implicated in the pathophysiology of cardiac dysfunction. For this, we measured and compared changes in expression status of 9 critical pro- and anti-inflammatory cytokines using multiplexed ELISA and 450 metabolic proteins involved in ATP production, oxidative phosphorylation, cytoskeletal organization, and stress response using two-dimensional electrophoresis (2-DE) and mass spectrometry (MS) in cardiac tissue of SH rats exposed to CAPs alone, O3 alone, and CAPs + O3. Proteomic expression profiling revealed that CAPs alone, O3 alone, and CAPs + O3 differentially altered protein expression patterns, and utilized divergent mechanisms to affect inflammatory and metabolic pathways and responses. Ingenuity Pathway Analysis (IPA) of the proteomic data demonstrated that the metabolic protein network centered by gap junction alpha-1 protein (GJA 1) was interconnected with the inflammatory cytokine network centered by nuclear factor kappa beta (NF-kB) potentially suggesting inflammation-induced alterations in metabolic pathways, or vice versa, collectively contributing to the development of cardiac dysfunction in response to CAPs and O3 exposure. These findings may enhance understanding of the pathophysiology of cardiac dysfunction induced by air pollution and provide testable hypotheses regarding mechanisms of action.

An imbalance between cardiovascular parasympathetic and sympathetic activity towards sympathetic predominance has been implicated in the pathogenesis of treatment-resistant arterial hypertension and heart failure. Arterial baroreceptors control efferent cardiovascular autonomic activity and have, therefore, been recognized as potential treatment targets. Baroreflex activation therapy through electrical carotid sinus stimulation is a device-based approach to modulate cardiovascular autonomic activity. Electrical carotid sinus stimulation lowered blood pressure in various hypertensive animal models and improved cardiac remodeling and survival in preclinical models of heart failure. In human mechanistic profiling studies, electrical carotid sinus stimulation lowered blood pressure through sympathetic inhibition with substantial inter-individual variability. The first-generation device reduced blood pressure in controlled and uncontrolled clinical trials. Controlled clinical trials proving efficacy in blood pressure reduction in patients with hypertension do not exist for the currently available second-generation carotid sinus stimulator. Investigations in heart failure patients showed improved symptoms, quality of life, and natriuretic peptide biomarkers. Electrical carotid sinus stimulation is an interesting technology to modulate cardiovascular autonomic control. However, controlled trials with hard clinical endpoints are required.

Studies have found that sleep disorders and autonomic dysfunction are associated with several metabolic diseases. Moreover, these factors also been reported to be related with the development of atherosclerosis and cardiovascular disease independent of other known factors, and details related to their pathogenesis have recently received increased attention. Additionally, the rates of incidence of heart and renal failure are showing an increasing trend.

A literature search was conducted to explore the interrelationship between sleep disorders, autonomic dysfunction, and cardio-renal function.

Sleep disorders and autonomic dysfunction have been shown to be strongly and directly linked to cardio-renal function, as well as various metabolic disorders, while cardiac and renal diseases themselves have been found to have a bidirectional relationship, and can also cause sleep disorders and autonomic dysfunction.

Reported findings indicate that sleep disorders and autonomic dysfunction cause metabolic abnormalities, thus are directly or indirectly related to cardio-renal function. With increased attention given to this research field and more focused studies performed, sleep conditions and autonomic function are expected to receive greater recognition as promising clinical targets for the prevention of heart failure and chronic kidney disease in the future.

Management of opioid dependence requires titrating medication doses based on withdrawal symptoms, but its clinical assessment presents challenges when it comes to subjective reporting. This study aimed to find out the relationship between heart rate variability (HRV) and opioid withdrawal in patients with opioid dependence.

Three groups of adult males were recruited: (a) patients with opioid dependence undergoing inpatient detoxification, (b) patients with opioid dependence stabilized on buprenorphine-based opioid substitution treatment, and (c) healthy controls. Frequency and time-domain parameters of HRV were used in the analysis. The opioid withdrawal was assessed using the Subjective Opiate Withdrawal Scale (SOWS).

Resting heart rate was found to be significantly different across the three groups (higher in patients stabilized on buprenorphine than the other two groups). In time-domain parameters, the detoxification group had the highest beat-to-beat variability. In frequency-domain parameters, the total power was highest for the detoxification group and lowest for the opioid substitution treatment group. In contrast, the relative power of frequency bands (very low, low, and high) did not vary across the groups at baseline. The SOWS had a weak negative correlation with root mean square of successive differences (RMSSD) in the opioid substitution group and did not have any relationship with HRV parameters in the detoxification group.

This exploratory study did not find HRV parameters to be robustly associated with subjective withdrawal, except for a negative association with the beat-to-beat variability among patients on opioid substitution treatment. This study adds to information on HRV in patients with opioid dependence.

The pathophysiology of gastro esophageal reflux disease (GERD) implicates autonomic dysregulation of the lower esophageal sphincter tone. Our goal is to investigate whether this dysregulation of the autonomic nervous system (ANS) function observed in isolated GERD cases can affect other systems, such as cardiovascular regulation.

Twenty-five participants were included in the study, 11 patients with isolated GERD and 14 controls. All patients and 7 controls responded to a COMposite Autonomic Symptoms Score 31 (COMPASS 31) questionnaire and underwent functional explorations including EMLA test, sympathetic skin response (SSR), 24-hour heart rate recording and ambulatory blood pressure measurement (ABPM). Seven additional controls underwent a 24-hour heart rate recording only.

GERD patients (Age: mean 36.81±7.82; SR= 0.22) showed high clinically dysautonomic scores (COMPASS 31) (p = 0.015), increased Heart rate variability (HRV) parameters (daytime, nighttime, 24-hour SDNN (standard deviation of the RR interval (NN)), respectively p = 0.003, p < 0.001, p = 0.001; daytime and nighttime very low frequencies (VLF) respectively p = 0.03 and p = 0.007), impaired nocturnal dipping of blood pressure (3/11 patients) and high positivity of EMLA test (7/11, p = 0.037). These outcomes were strongly correlated with clinical dysautonomic assessment. No difference was observed between patients and controls regarding SSR.

Our data suggests a high parasympathetic tone amongst patients with GERD and a dysregulation of parasympathetic and sympathetic balance in the cardiovascular system with an impairment of the peripheral sympathetic fibers of cutaneous microcirculation, assessed by the EMLA test. GERD may be an inaugural symptom of autonomic neuropathy. Further functional exploration of peripheral small fibers seems to be necessary.

Traditional electrocardiography (ECG)-derived heart rate variability (HRV) and photoplethysmography (PPG)-derived "HRV" (termed PRV) have been reported interchangeably. Any potential dissociation between HRV and PRV could be due to the variability in pulse arrival time (PAT; time between heartbeat and peripheral pulse).

This study examined if PRV is equivalent to ECG-derived HRV and if PRV's innate error makes it a high-quality measurement separate from HRV.

ECG data from 1084 subjects were obtained from the PhysioNet Autonomic Aging dataset, and individual PAT dispersions for both the wrist (n = 42) and finger (n = 49) were derived from Mol et al. (Exp Gerontol. 2020; 135: 110938). A Bayesian simulation was constructed whereby the individual arrival times of the PPG wave were calculated by placing a Gaussian prior on the individual QRS-wave timings of each ECG series. The standard deviation (σ) of the prior corresponds to the PAT dispersion from Mol et al. This was simulated 10,000 times for each PAT σ. The root mean square of successive differences (RMSSD) and standard deviation of N-N intervals (SDNN) were calculated for both HRV and PRV. The Region of Practical Equivalence bounds (ROPE) were set a priori at ± 0.2% of true HRV. The highest density interval (HDI) width, encompassing 95% of the posterior distribution, was calculated for each PAT σ.

The lowest PAT σ (2.0 SD) corresponded to 88.4% within ROPE for SDNN and 21.4% for RMSSD. As the σ of PAT increases, the equivalence of PRV and HRV decreases for both SDNN and RMSSD. The HDI interval width increases with increasing PAT σ, with the HDI width increasing at a higher rate for RMSSD than SDNN.

For individuals with greater PAT variability, PRV is not a surrogate for HRV. When considering PRV as a unique biometric measure, SDNN may have more favorable measurement properties than RMSSD, though both exhibit a non-uniform measurement error.

This review explores the various pathophysiological factors influencing antihypertensive effects, involving the regulation of vascular resistance, plasma volume, cardiac function, and the autonomic nervous system, emphasizing the interconnected processes regulating blood pressure (BP). The kidney's pivotal role in BP control and its potential contribution to hypertension is complicated but important to understand the effective mechanisms of renal denervation (RDN), which may be a promising treatment for resistant hypertension. Excessive stimulation of the sympathetic nervous system or the renin-angiotensin-aldosterone system (RAAS) can elevate BP through various physiological changes, contributing to chronic hypertension. Renal sympathetic efferent nerve activation leads to elevated norepinephrine levels and subsequent cascading effects on vasoconstriction, renin release, and sodium reabsorption. RDN reduces BP in resistant hypertension by potentially disrupting sensory afferent nerves, decreasing feedback activation to the central nervous system, and reducing efferent sympathetic nerve activity in the heart and other structures. RDN may also modulate central sympathetic outflow and inhibit renal renin-angiotensin system overactivation. While evidence for RDN efficacy in hypertension is increasing, accurate patient selection becomes crucial, considering complex interactions that vary among patients. This review also discusses methods to evaluate autonomic nerve activity from the golden standard to new potential examination for finding out optimization in stimulation parameters or rigorous patient selection based on appropriate biomarkers.

Stress associated with manipulation during electrocardiography (ECG) recording in cats potentially limits the assessment of autonomic function through heart rate variability (HRV) in the feline population. This study proposed an alternative, cat friendly, stethoscopic approach to evaluate HRV with an easily acquired vasovagal tonus index (VVTI).

The aim of this prospective study was to evaluate whether VVTI derived from heart sound signals could distinguish between relaxed and stimulated states. A total of 29 cats with 56 recordings of heart sound and ECG on 31 occasions were included. In 25 cats in their home environment, a stethoscope connected to a digital recording device was used to record 2 mins of heart sounds twice - with the cats in a relaxed state and immediately after stimulation. The VVTI was calculated from 20, 60 and 120 consecutive beat-to-beat intervals on the heart sound spectrogram (stethoscopic-VVTI 20, 60 and 120), using the natural logarithm of the variance of the intervals based on previous literature. A 2-min ECG recording was obtained at home with the intention of avoiding strict restraint. To demonstrate the feasibility of the stethoscopic approach in a hospital setting, six cats (two of which were also recorded at home) underwent heart sound and ECG recordings during planned veterinary visits.

Stethoscopic-VVTI 20 (5.43 to 4.79, P = 0.001), 60 (6.20 to 5.18, P <0.001) and 120 (6.24 to 5.60, P = 0.02) all significantly decreased after stimulation, indicating a reduced vasovagal tone as expected. Calculations of stethoscopic-VVTI from different sections of the recording yielded statistically similar results. Stethoscopic-VVTI showed a negative correlation with the corresponding heart rate. Bland-Altman analysis revealed a mean bias for the differences between stethoscopic-VVTI and ECG-VVTI of 0.50 and 1.07 at home and in the hospital, respectively.

VVTI can be successfully detected through a stethoscopic approach, serving as a less stressful tool for HRV evaluation in cats during routine auscultation.

Background: An intricate physiological and pathophysiological connection exists between the heart and lungs, which is especially important in individuals with spinal cord injury (SCI). While an exercise intervention may seem the best approach to leverage this relationship, the prior work has shown that, despite numerous health benefits, regular exercise training does not improve cardiorespiratory control in individuals with SCI. Breath training presents an alternative intervention that is uniquely accessible, with yogic breathing directly engaging linked fluctuations in respiration and cardiovascular control. In addition, there is evidence across a range of populations that regular yogic breathing reduces cardiovascular disease risk. It is possible that the chronic decrease in breathing frequency associated with regular yogic breathing, rather than the specific yogic breathing techniques themselves, is the primary contributor to the observed risk reduction. Methods: Therefore, in 12 individuals with traumatic SCI from C4 to T8, the authors compared Unpaced and conventional 0.083 Hz (Slow) paced breathing with various yogic breathing techniques including: (1) inspiratory-expiratory breath holds (i.e., Kumbhaka or "Box Breathing"), (2) extended exhalation (1:2 duty cycle), and (3) expiratory resistance via throat constriction (i.e., Ujjayi). Beat-to-beat heart rate and blood pressure were measured as well as end-tidal CO2 and O2 saturation were measured. Statistical analysis was performed using a one-way repeated-measures analysis of variance with post hoc pairwise t tests corrected for multiple comparisons. Results: As expected, all slow breathing patterns markedly increased respiratory sinus arrhythmia (RSA) compared with Unpaced in all (n = 12) individuals. More importantly, Ujjayi breathing appeared to improve ventilatory efficiency over Unpaced breathing in individuals with SCI by increasing O2 saturation (97.6% vs. 96.1%; p = 0.042) and tended to decrease end-tidal CO2 (32 mmHg vs. 35 mmHg; p = 0.08). While other slow breathing patterns demonstrated similar effects, only Ujjayi improved RSA while increasing heart rate and improving ventilatory efficiency. Conclusions: Hence, slow breathing per se can result in important cardiorespiratory changes, but the yogic breathing practice of Ujjayi, with glottic throat resistance, may hold the greatest promise for improving cardiorespiratory control in individuals with SCI (CTR ID No. NCT05480618).

To establish reference values and clinically relevant determinants for measures of heart rate variability (HRV) and to assess their relevance for clinical outcome prediction in individuals with heart failure.

Data from the MyoVasc study (NCT04064450; N = 3289), a prospective cohort on chronic heart failure with a highly standardized, 5 h examination, and Holter ECG recording were investigated. HRV markers were selected using a systematic literature screen and a data-driven approach. Reference values were determined from a healthy subsample. Clinical determinants of HRV were investigated via multivariable linear regression analyses, while their relationship with mortality was investigated by multivariable Cox regression analyses.

Holter ECG recordings were available for analysis in 1001 study participants (mean age 64.5 ± 10.5 years; female sex 35.4%). While the most frequently reported HRV markers in literature were from time and frequency domains, the data-driven approach revealed predominantly non-linear HRV measures. Age, sex, dyslipidemia, family history of myocardial infarction or stroke, peripheral artery disease, and heart failure were strongly related to HRV in multivariable models. In a follow-up period of 6.5 years, acceleration capacity [HRperSD 1.53 (95% CI 1.21/1.93), p = 0.0004], deceleration capacity [HRperSD: 0.70 (95% CI 0.55/0.88), p = 0.002], and time lag [HRperSD 1.22 (95% CI 1.03/1.44), p = 0.018] were the strongest predictors of all-cause mortality in individuals with heart failure independently of cardiovascular risk factors, comorbidities, and medication.

HRV markers are associated with the cardiovascular clinical profile and are strong and independent predictors of survival in heart failure. This underscores clinical relevance and interventional potential for individuals with heart failure.

NCT04064450.

Background: Preserving health and physical fitness is critical to ensure independent living across the lifespan. Lower levels of physical fitness are associated with age-related cognitive decline and a higher prevalence of mild cognitive impairment (MCI). Thus, this study investigates the influence of a six-month dance intervention on selected measures of physical fitness in older adults with MCI. Methods: In this randomized controlled trial, 55 patients with MCI were randomized into a sportive dance training (IG; n = 26; age: 70.7 ± 5.6 years; 62% female) or an inactive control group (CG; n = 24; age: 69.1 ± 6.8 years; 46% female). The dance group received two 90 min dance training sessions per week over a duration of six-months, which focused on learning dance movement patterns. During the training sessions, heart rate was measured to control exercise intensity. Physical fitness was assessed using cardiopulmonary exercise testing (CPET), lower limb functional fitness via sit-to-stand test, handgrip strength, and heart rate variability (HRV). Results: We observed that the dance intervention preserved the cardiorespiratory fitness as measured by maximal oxygen uptake (VO2max) during CPET, which decreased in the CG. Furthermore, participants in the IG demonstrated increases in leg and handgrip strength, although these were not statistically significant. HRV displayed a non-significant decrease following the intervention. Conclusions: The results of this randomized controlled trial suggest that sportive dance training can preserve elements of physical fitness (i.e., cardiorespiratory fitness) in older adults with MCI. Although improvements in the other parameters (i.e., leg and handgrip strength) were statistically non-significant, likely due to the small sample size, stabilizing muscular fitness and preventing age-related decline in older adults with MCI is important for maintaining functional independence. For future studies, we recommend a longer training duration paired with precise control of regular physical activity levels, an important confounding factor.

Although both aging and menopause influence cardiovascular autonomic control, the effect of menopause per se remains unclear. The current study was undertaken to test the hypothesis that post-menopausal women (PMW) have a blunted cardiovascular autonomic adjustment to active standing compared to pre-menopausal women. Thus, we compared the heart rate variability (HRV) indexes from supine (SUP) to orthostatic (ORT) positions among young women (YW), young men (YM), older men (OM), and PMW.

The participants rested for 10 min in SUP and then stood up and remained for 5 min in ORT. ECG was continuously recorded, and R-R time series of about 300 beats were analyzed using linear (spectral analysis) and non-linear (symbolic analysis) methods. The variation from SUP to ORT was calculated (Δ = ORT-SUP) for each HRV index.

In SUP, no difference was found for any HRV index among groups. However, Δ0V% and ΔLFn (cardiac sympathetic modulation) were reduced in PWM compared to all groups (OM, YW, and YM), while Δ2UV% and ΔHFn (cardiac vagal modulation) were reduced in PMW than the younger group (YW and YM). No differences were found among the male groups (OM and YM).

In light of our results, the cardiac autonomic dynamic response to orthostatic stress is blunted in post-menopausal women compared to younger women and older men, a finding that might be influenced not only by aging.

Cardiovascular morbidity and mortality are high in people with serious mental illness (SMI). This problem is mediated, at least in part, by metabolic side effects of second-generation antipsychotics (SGAs) and by unhealthy lifestyle behaviors. We asked whether oral glucose tolerance testing (oGTT) or hemoglobin A1c (HbA1c) is superior in identifying people with SMI at high cardiometabolic risk and whether this risk is shaped by mood, cognition, or lifestyle habits.

We evaluated 40 patients with schizophrenia, schizoaffective, or bipolar disorder receiving SGAs by oGTT, HbA1c, comprehensive metabolic and lipid panels, and CRP. Mood was assessed using the Patient Health Questionnaire (PHQ-9), and cognition was assessed using the Saint Louis University Mental Status examination. Diet was assessed using the UK Diabetes and Diet Questionnaire (UKDDQ), and physical activity was assessed using daily step counts.

Most patients had prediabetes (preDM) or diabetes mellitus (DM), 72.5% by oGTT, and 52.5% by HbA1c criteria. Pulse rates and insulin resistance indices (Homeostatic Model Assessment of Insulin Resistance, HOMA IR; Matsuda) were significantly different between patients classified as normal or with preDM/DM, using either oGTT or HbA1c criteria. Patients with preDM/DM by HbA1c but not oGTT criteria also had higher waist/hip ratios, triglyceride, and CRP levels (p<0.05). A strong negative correlation was found between average daily step counts and CRP levels (rho = -0.62, p<0.001). Higher UKDDQ scores, or unhealthier diet habits, were associated with higher fasting plasma glucose (rho = 0.28, p = 0.08), triglyceride levels (rho = 0.31, p = 0.05), and insulin resistance (HOMA IR: rho = 0.31, p = 0.06). Higher PHQ-9 scores correlated with lower 2h-oGTT glucose levels (rho = -0.37, p<0.05).

OGTT screening is superior to HbA1c screening in detecting preDM and DM early. Patients identified with preDM/DM by oGTT or HbA1c screening are insulin-resistant and have higher pulse rates. Abdominal obesity, unfavorable lipid profiles, and higher CRP levels were noted in patients screened by HbA1c, but not by oGTT. Low physical activity, low depression scores, and unhealthy diet habits were associated with higher CRP and higher glucose and triglyceride levels, respectively. Future studies should assess the impact of specifically tailored individual lifestyle counseling and medical management interventions in this high-risk population.

Autonomic dysfunction is associated with cardiovascular and neurological disease, including hypertension, heart failure, anxiety, and stress-related disorders. Prior studies demonstrated that late gestation exposure to dexamethasone (DEX) resulted in female-biased increases in stress-responsive mean arterial pressure (MAP) and heart rate (HR), suggesting a role for glucocorticoid-mediated programming of autonomic dysfunction. The present study investigated the influence of sympathetic (SYM) or parasympathetic (PS) blockade on cardiovascular function in male and female rat offspring of mothers injected with DEX in utero (gestation days [GD]18-21). At 11-12-weeks of age, MAP, HR, and heart rate variability (HRV) were evaluated at baseline and in response to SYM antagonists (α 1 -adrenoceptor + β 1 -adrenoceptor), a PS (muscarinic) antagonist, or saline (SAL). To assess stress-responsive function, rats were exposed to acute restraint. Tyrosine hydroxylase was measured in adrenals and left ventricle, and gene expression for the β 1 adrenergic receptor was measured in left ventricle. Maternal DEX injection reduced basal HRV in male and female offspring. SYM blockade attenuated increases in stress-responsive HR and MAP. PS blockade elevated stress-responsive HR and MAP to a greater extent in Vehicle females. SYM and PS blockade produced equivalent effects on HR and MAP responses in male offspring, regardless of maternal treatment. Based on these findings, we suggest that maternal DEX injection disrupted autonomic regulation of cardiovascular function in females, resulting in a shift toward greater SYM input and less input from PS. Future studies will investigate whether changes in autonomic function are mediated by changes in central autonomic circuitry.

These studies use pharmacological antagonists to characterize the nature of the autonomic dysregulation induced in female offspring exposed to the synthetic glucocorticoid, dexamethasone, in utero . The female offspring of dams injected with dexamethasone in late gestation show a reduction in vulnerability to parasympathetic blockade and an increase in responses to acute restraint stress even in the presence of sympathetic blockade. This suggests that late gestation dexamethasone disrupts the normal development of the autonomic function in females leading to a shift in the sympathovagal balance.

We summarise the physiological changes and risk factors for hypertension in females, potential sex-specific management approaches, and long-term prognosis.

Pregnancy and menopause are two key phases of the life cycle where females undergo significant biological and physical changes, making them more prone to developing hypertension. Gestational hypertension occurs from changes in maternal cardiac output, kidney function, metabolism, or placental vasculature, with one in ten experiencing pregnancy complications such as intrauterine growth restriction and delivery complications such as premature birth. Post-menopausal hypertension occurs as the protective effects of oestrogen are reduced and the sympathetic nervous system becomes over-activated with ageing. Increasing evidence suggests that post-menopausal females with high blood pressure (BP) experience greater risk of cardiovascular events at lower BP thresholds, and greater vulnerability to treatment-related adverse effects. Hypertension is a key risk factor for cardiovascular disease in females. Current BP treatment guidelines and recommendations are similar for both sexes, without addressing sex-specific factors. Future investigations into ideal diagnostic thresholds, BP control targets and treatment regimens in females are needed.

Rett syndrome (RTT) is a rare neurological disorder primarily associated with mutations in the methyl-CpG-binding protein 2 (MECP2) gene. The syndrome is characterized by cognitive, social, and physical impairments, as well as sleep disorders and epilepsy. Notably, dysfunction of the autonomic nervous system is a key feature of the syndrome. Although Heart Rate Variability (HRV) has been used to investigate autonomic nervous system dysfunction in RTT during wakefulness, there is still a significant lack of information regarding the same during sleep. Therefore, our aim was to investigate cardiovascular autonomic modulation during sleep in subjects with RTT compared to an age-matched healthy control group (HC).

A complete overnight polysomnographic (PSG) recording was obtained from 11 patients with Rett syndrome (all females, 10 ± 4 years old) and 11 HC (all females, 11 ± 4 years old; p = 0.48). Electrocardiogram and breathing data were extracted from PSG and divided into wake, non-REM, and REM sleep stages. Cardiac autonomic control was assessed using symbolic non-linear heart rate variability analysis. The symbolic analysis identified three patterns: 0 V% (sympathetic), 2UV%, and 2LV% (vagal).

The 0 V% was higher in the RTT group than in the HC group during wake, non-REM, and REM stages (p < 0.01), while the 2LV and 2UV% were lower during wake and sleep stages (p < 0.01). However, the 0 V% increased similarly from the wake to the REM stage in both RTT and HC groups.

Therefore, the sympatho-vagal balance shifted towards sympathetic predominance and vagal withdrawal during wake and sleep in RTT, although cardiac autonomic dynamics were preserved during sleep.

The leading cause of death in people living with HIV (PLWH) is cardiovascular disease, and the high prevalence of tobacco cigarette (TC) smoking is a major contributor. Switching to electronic cigarettes (ECs) has been promoted as a harm reduction strategy. We sought to determine if acute EC compared to TC smoking had less harmful effects on arrhythmogenic risk factors including acute changes in hemodynamics, heart rate variability (HRV), and ventricular repolarization (VR). In PLWH who smoke, changes in hemodynamics, HRV, and VR were compared pre/post acutely using an EC, TC, or puffing on an empty straw on different days in random order, in a crossover study. Thirty-seven PLWH (36 males, mean age 40.5 ± 9.1 years) participated. Plasma nicotine was greater after TC versus EC use (10.12 ± 0.96 vs. 6.18 ± 0.99 ng/mL, respectively, p = 0.004). HR increased significantly, and similarly, after acute EC and TC smoking compared to control. Changes in HRV that confer increased cardiac risk (LF/HF ratio) were significantly smaller after acute EC versus TC use, consistent with a harm reduction effect. In a post-hoc analysis of PLWH with and without positive concurrent recreational drug use as indicated by point of care urine toxicology testing, this differential effect was only seen in PLWH not currently using recreational drugs. Changes in VR were not different among the three exposures. In PLWH who smoke, EC compared to TC smoking resulted in smaller adverse changes in HRV. This differential effect was accompanied by a smaller increase in plasma nicotine, and was negated by concurrent recreational drug use. Additional studies are warranted in this vulnerable population disproportionately affected by tobacco-related health disparities.

Heart rate variability, a marker of autonomic function, has shown promising prognostic results in specific populations, but has not been tested in a general medical population. We hypothesized that heart rate variability identifies high-risk medical patients early after admission to the hospital.

This was a single-center prospective cohort study of acutely admitted medical patients aged ≥18 years with a life expectancy ≥3 months, included between 2019-2023. Unstable patients needing direct admission to the intensive care unit were excluded. Heart rate variability was recorded within 24 hours of admission for 10 minutes. The standard deviation of normal-normal beats (SDNN) was the primary heart rate variability marker. Low SDNN was defined as the lowest tertile (≤22 ms). The primary outcome was 30-day all-cause mortality. The secondary outcome was 30-day readmission or mortality.

Among 721 patients included, low SDNN carried an 8-fold greater risk of 30-day mortality in univariate analysis (hazard ratio [HR] 8.3; P = .001); in multivariate analyses a 4-fold greater risk (HR 3.8; P = .037). Low SDNN was associated with the combined outcome of 30-day mortality or readmission (HR 1.5; P = .03) in multivariate analysis. In receiver operating characteristics analyses, low SDNN improved the predictive accuracy of early warning score for 30-day mortality or readmission from 0.63 to 0.71 (P = .008) but did not improve the accuracy for 30-day mortality alone.

In patients admitted due to acute medical illness, low heart rate variability predicted 30-day mortality and readmission, suggesting heart rate variability as a tool to identify patients at high and low risk of relevant endpoints.

Chronic stress can cause an imbalance within the autonomic nervous system, thereby affecting cardiovascular and mental health. Physical activity (PA) may have a positive effect on the autonomic nervous system and stress-related disorders, such as depression and burnout. Heart rate variability (HRV) is a non-invasive marker of the autonomic nervous system. However, limited and inconsistent data exist on the exact relationship between HRV, PA and depression and burnout symptoms. The HARMODI study aims to explore whether HRV is a feasible marker of depression and burnout symptoms and aims to evaluate the role of PA in the treatment of stress-related disorders.

This is an observational study with a cross-sectional up to 8 week follow-up study design. A total of 153 patients, undergoing psychiatric inpatient treatment with burnout syndrome (Z73) and depressive episode (F32 or F33) or adjustment disorder (F43.2), will be recruited. Data on depression and burnout symptoms, HRV recordings (24-hour, supine, standing and exercise stress test), cognitive function, cardiorespiratory fitness, cardiovascular health, balance and strength will be collected at baseline (T1) and after up to 8 weeks (T2). Continuous data on PA and Ecological Momentary Assessments of exhaustion, mood and tension will be monitored daily throughout inpatient treatment. Multiple regression models, adjusted for potential confounders, will assess the association between HRV as the primary outcome, PA and depression and burnout severity score.

The protocol has been approved by Swiss Ethics Committee, Cantonal Ethics Committee Zürich. Results of HARMODI will be disseminated through peer-reviewed journals and conference presentations.

NCT05874856.

Heart rate variability (HRV) is a crucial metric that provides valuable insight into the balance between relaxation and stress. Previous research has shown that most HRV parameters improve during periods of mental relaxation, while decreasing during tasks involving cognitive workload. Although a comprehensive analysis of both linear and non-linear HRV parameters has been carried out in existing literature, there still exists a need for further research in this area. Additionally, limited knowledge exists regarding how specific interventions may influence the interpretation of these parameters and how the different parameters correlate under different interventions. This study aims to address these gaps by conducting a thorough comparison of different linear and non-linear HRV parameters under mentally relaxed versus stressful states.

Participants were randomly and equally divided among two between-subjects groups: relaxed-stress (RS) (N = 22) and stress-relaxed (SR) (N = 22). In the RS group, a paced breathing task was given for 5 min to create relaxation, and was followed by a 5-min time-based mental calculation task to create stress. In the SR group, the order of the stress and relaxed tasks was reversed. There was a washout period of 15 min after the first task in both groups.

Of the 37 HRV parameters, 33 differed significantly between the two interventions. The majority of the parameters exhibited an improving and degrading tendency of HRV parameters in the relaxed and stressed states, respectively. The correlation of the majority of HRV parameters decreases during stress, while prominent time domain and geometric domain parameters stand out in the correlation.

Overall, HRV parameters can be reliably used to assess a person's relaxed and stressed mental states during paced breathing and mental arithmetic task respectively. Furthermore, non-linear HRV parameters provide accurate estimators of the mental state, in addition to the commonly used linear parameters.

Several cardiovascular disease (CVD) risk factors (e.g., hypertension, poor glycemic control) can affect and be affected by autonomic nervous system (ANS) activity. Since excess adiposity can influence CVD development through its effect on hypertension and diabetes mellitus, it is important to determine how adiposity and altered ANS activity are related. The present study employed structural equation modeling to investigate the relation between adiposity and ANS activity both directly and indirectly through biological variables typically associated with glycemic impairment and cardiac stress in older adults. Utilizing the Atherosclerosis Risk in Communities (ARIC) dataset, 1,145 non-smoking adults (74±4.8 yrs, 62.8% female) free from known CVD, hypertension, and diabetes and not currently taking beta-blockers were evaluated for fasting blood glucose (FBG), insulin, and HbA1c concentrations, waist circumference (WC), blood pressure (BP), and markers of ANS activity. WC was recorded just above the iliac crest and was used to reflect central adiposity. Resting 2-minute electrocardiograph recordings, pulse wave velocity, and ankle-brachial index data were used to assess the root mean square of successive differences in RR intervals (RMSSD) and the pre-ejection period (PEP), markers of parasympathetic and sympathetic activity, respectively. FBG, insulin, and HbA1c inferred a latent variable termed glycemic impairment (GI), whereas heart rate and diastolic BP inferred a latent variable termed cardiac stress (CS). The structural equation model fit was acceptable [root mean square error of approximation = 0.050 (90% CI = .036, .066), comparative fit index = .970, Tucker Lewis Index = 0.929], with adiposity having both significant direct (β = 0.208, p = 0.018) and indirect (β = -.217, p = .041) effects on PEP through GI. Adiposity displayed no significant direct effect on RMSSD. CS displayed a significant pathway (β = -0.524, p = 0.035) on RMSSD, but the indirect effect of WC on RMSSD through CS did not reach statistical significance (β = -0.094, p = 0.137). These results suggest that adiposity's relation to ANS activity is multifaceted, as increased central adiposity had opposing direct and indirect effects on markers of sympathetic activity in this population of older adults.