Fibromyalgia (FM) patients present impaired cardiac autonomic regulation during maximal exercise; however, it is unknown whether these alterations also manifest during submaximal exercise. The aim of this study was to compare the on-transient heart rate (HR) response and HR variability during a constant-load submaximal cycling exercise between FM and control (CON) women. Ten women with FM (age: 45.2±9.3 years) and 10 age-matched CON women (age: 48.4±6.1 years) performed a 15-min cycling exercise, with the work rate fixed at 50% of the individual peak power output attained in a maximal graded exercise test. The time intervals between consecutive heartbeats were recorded regularly during the exercise for subsequent analysis of on-transient HR response and HR variability indices. The on-transient HR time constant was similar (P=0.83) between the FM (41.0±14.1 sec) and CON (42.2±10.4 sec). During the 5-10 and 10-15 min of exercise, HR variability indices indicating sympathetic and parasympathetic activities were similar (P>0.05) between FM and CON groups. In conclusion, women with FM presented a normal cardiac autonomic response to submaximal cycling exercise. These findings have clinical relevance, as submaximal exercises are commonly prescribed for FM patients.

Children with obstructive sleep apnea (OSA) frequently experience chronic low-grade systemic inflammation, with the inflammasome playing a central role in OSA. This cross-sectional study evaluated the relationship between weight status, autonomic function, and systemic inflammation in a cohort of 55 children with OSA, predominantly boys (78%) with an average age of 7.4 ± 2.2 years and an apnea-hypopnea index of 14.12 ± 17.05 events/hour. Measurements were taken of body mass index (BMI), sleep heart-rate variability, morning circulatory levels of interleukin-1β, interleukin-1 receptor antagonist, and interleukin-6, and tumor necrosis factor-α, anthropometry, and polysomnography. Multiple linear regression modeling showed that an apnea-hypopnea index was significantly associated with BMI, the standard deviation of successive differences between normal-to-normal intervals during N3 sleep, and the proportion of normal-to-normal interval pairs differing by more than 50 ms during rapid-eye-movement sleep. A moderated mediation model revealed that interleukin-1 receptor antagonist levels mediated the association between BMI and interleukin-6 levels, with sympathovagal balance during N3 sleep and minimum blood oxygen saturation further moderating these relationships. This study highlights the complex relationships between BMI, polysomnographic parameters, sleep heart-rate-variability metrics, and inflammatory markers in children with OSA, underlining the importance of weight management in this context.

Post-stroke patients often experience psychological distress and autonomic nervous system (ANS) dysregulation, impacting their well-being. This study evaluated the effectiveness of heart rate variability (HRV) biofeedback on cognitive, motor, psychological, and ANS functions in sixty-two ischemic stroke patients (43 males, mean age = 60.1) at a Medical Center in southern Taiwan. To prevent interaction, we allocated patients to the HRV biofeedback or control (usual care) group based on their assigned rehabilitation days, with 31 patients in each group. Assessments conducted at baseline, three, and six months included the Montreal Cognitive Assessment (MoCA), Fugl-Meyer Assessment for Upper Extremities (FMA-UE), Perceived Stress Scale, Hospital Anxiety and Depression Scales (HADS), and HRV indices. Mixed-effect models were used to analyze Group by Time interactions. The results revealed significant interactions across all functions. At 3 months, significant improvements in the HRV biofeedback group were observed only in MoCA, FMA-UE, and HADS-depression scores compared to the control group. By 6 months, all measured outcomes demonstrated significant improvements in the biofeedback group relative to the control group. These results suggest that HRV biofeedback may be an effective complementary intervention in post-stroke rehabilitation, warranting further validation.

OBJECTIVE: This study aimed to investigate the integrative effects and mechanisms of transcutaneous electrical acustimulation (TEA) on postprocedural recovery from endoscopic retrograde cholangio-pancreatography (ERCP).
METHODS: A total of 86 patients for elective ERCP were randomly ordered to receive TEA (n = 43) at acupoints PC6 and ST36 or Sham-TEA (n = 43) at sham points from 24 hours before ERCP (pre-ERCP) to 24 hours after ERCP (PE24). Scores of gastrointestinal (GI) motility-related symptoms and abdominal pain, gastric slow waves, and autonomic functions were recorded through the spectral analysis of heart rate variability; meanwhile, circulatory levels of inflammation cytokines of tumor necrosis factor-α (TNF-α) and interleukin (IL)-10 and GI hormones of motilin, ghrelin, cholecystokinin (CCK), and vasoactive intestinal peptide (VIP) were assessed by enzyme-linked immunosorbent assay.
RESULTS: 1) TEA, but not Sham-TEA, decreased the post-ERCP GI motility-related symptom score (2.4 ± 2.6 vs 7.9 ± 4.6, p < 0.001) and abdominal pain score (0.5 ± 0.7 vs 4.1 ± 2.7, p < 0.001) at PE24, and decreased the post-ERCP hospital day by 20.0% (p ＜0.05 vs Sham-TEA); 2) TEA improved the average gastric percentage of normal slow waves and dominant frequency by 34.6% and 33.3% at PE24, respectively (both p < 0.001 vs Sham-TEA); 3) TEA, but not Sham-TEA, reversed the ERCP-induced increase of TNF-α but not IL-10 at PE24, reflected as a significantly lower level of TNF-α in the TEA group than in the Sham-TEA group (1.6 ± 0.5 pg/mL vs 2.1 ± 0.9 pg/mL, p ＜ 0.01); 4) compared with Sham-TEA, TEA increased vagal activity by 37.5% (p ＜ 0.001); and 5) TEA caused a significantly higher plasma level of ghrelin (1.5 ± 0.8 ng/ml vs 1.1 ± 0.7 ng/ml, p ＜ 0.05) but not motilin, VIP, or CCK than did Sham-TEA at PE24.
CONCLUSIONS: TEA at PC6 and ST36 accelerates the post-ERCP recovery, reflected as the improvement in GI motility and amelioration of abdominal pain, and suppression of the inflammatory cytokine TNF-α may mediate through both autonomic and ghrelin-related mechanisms.

Loss of regulation of the autonomic nervous system is found in many diseases from the age of 50 to 60 yr and even more so in older patients. The imbalance is usually manifested by an increase in sympathetic tone, long considered to be the most deleterious element in terms of cardiac rhythmic risk, but also by a reduction in the effectiveness of short-term regulation of the baroreflex arc (partial loss of parasympathetic control). Techniques for analysing this autonomic disorder by analysing heart rate regulation are widely available in outpatient clinics and provide interesting indicators of cardiovascular and cerebrovascular risk. Deceleration capacity of cardiac autonomic control has been identified for its prognostic role in high-risk patients and in the general population. Further research is indicated to assess the value of this marker in anaesthetic risk management by targeting procedures with greater risk of intraoperative and postoperative autonomic dysfunction.

UNASSIGNED: Degenerative aortic stenosis is an atherosclerotic-like process associated with impaired endothelial and autonomic function. Transcatheter aortic valve implantation (TAVI) has become a treatment of choice for patient with severe degenerative aortic stenosis at high surgical risk. The effect of this procedure on endothelial function measured with flow mediated dilatation (FMD) and autonomic function measured with heart rate variability (HRV) at different time-points of disease management (early and late follow-up) remains unknown.
UNASSIGNED: We prospectively included 50 patients with severe aortic stenosis who were deemed suitable for TAVI by the Heart Team. FMD and HRV parameters were collected at baseline ( < 24 h pre-TAVI), at early follow-up (up to 48 h post-TAVI) and at late follow-up (3-6 months post-TAVI).
UNASSIGNED: 43 patients (mean age 81 (75-85); 60% women) completed the study. FMD significantly improved from 2.8 ± 1.5% before TAVI to 4.7 ± 2.7% early after TAVI (p < 0.001) and was later maintained on late follow-up (4.8 ± 2.7%, p = 0.936). Conversely, high-resolution ECG parameters remained preserved at early and improved at late follow-up after TAVI. Significant improvement was detected in a high frequency-domain parameter-HF (from 5231 ± 1783 to 6507 ± 1789 ms 2 ; p = 0.029) and in two Poincare plot parameters: ratio of the short- and long-term R-R variability in the Poincare plot-SD1/SD2 (from 0.682 to 0.884 ms 2 ; p = 0.003) and short-term R-R variability in the Poincare plot-SDRR (from 9.6 to 23.9 ms; p = 0.001). Echocardiographic parameters comprising baseline maximal aortic valve velocity (R = 0.415; p = 0.011), mean aortic gradient (R = 0.373; p = 0.018), indexed stroke volume (R = 0.503; p = 0.006), change in aortic valve maximal velocity (R = 0.365; p = 0.031), change in mean aortic gradient (R = 0.394; p = 0.019) and NT-proBNP (R = 0.491; p = 0.001) were found as significant predictors of change in FMD.
UNASSIGNED: Endothelial function measured with FMD and autonomic function obtained with HRV parameters significantly improve after TAVI. While endothelial function improves early and is maintained later after TAVI, autonomic function remains stable and improves on late follow-up. This is most likely caused by early hemodynamic changes after resolution of aortic valve obstruction and gradual left ventricular remodeling.
UNASSIGNED: www.clinicaltrials.gov, identifier NCT04286893.

Background: Individuals with posttraumatic stress disorder (PTSD) are at heightened risk for cardiovascular disease (CVD) compared to the general population. Inflammation and autonomic dysfunction are candidate mechanisms of CVD risk in PTSD; however, these mechanisms have not been well-characterised in the PTSD-CVD link. Further, these mechanisms may operate through altered stress-related neural activity (SNA). Yet, it remains unknown if changes in PTSD are associated with changes in CVD risk mechanisms.Objective: This manuscript describes the design and procedures of a pilot randomised controlled trial to assess the impact of a first-line treatment for PTSD (Cognitive Processing Therapy; CPT) versus waitlist control on mechanisms of CVD risk. Further, this study will test the hypothesis that CPT reduces CVD risk through its effects on inflammation and autonomic function and that these changes are driven by changes in SNA.Methods: Adults with PTSD and CVD risk (N = 30) will be randomised to CPT or waitlist control. Participants complete two laboratory visits (baseline and post-treatment) that include surveys, brain and peripheral imaging via 18F-fluorodeoxyglucose positron emission tomography (FDG-PET), and resting measures of autonomic function. Primary outcomes include arterial inflammation and heart rate variability. Secondary outcomes include leukopoiesis (bone marrow uptake), heart rate, and blood pressure. The indirect effects of PTSD treatment on changes in inflammation and autonomic function through SNA will also be examined.Conclusions: This study seeks to characterise candidate neuroimmune mechanisms of the PTSD-CVD link to identify treatment targets and develop personalised interventions to reduce CVD events in PTSD populations.Trial registration: ClinicalTrials.gov identifier: NCT06429293..
Individuals with posttraumatic stress disorder (PTSD) have greater risk for cardiovascular disease (CVD) than the general population.Autonomic dysfunction and inflammation are candidate mechanisms of the PTSD-CVD link, which may be driven by changes in neural activity.This pilot randomised controlled trial will test the impact of a first-line PTSD treatment on autonomic dysfunction and inflammation, and whether neural alterations are associated with changes in these mechanisms.

BACKGROUND: Conflicting results have been published considering the diagnostic performance of head-up tilt test (HUTT) in patients with hypertrophic cardiomyopathy (HCM). We aimed to conduct a meta-analysis to evaluate the diagnostic value of HUTT in the evaluation of unexplained syncope in patients with HCM.
METHODS: We performed a structured systematic database search using the following keywords: hypertrophic cardiomyopathy, syncope, unexplained syncope, head-up tilt test, tilt table test, tilt testing, orthostatic stress, autonomic function, autonomic response. Studies in which the HUTT was used to define autonomic dysfunction in patients with syncope at baseline or without syncope were included in the final analysis.
RESULTS: A total of 252 HCM patients from 6 studies (159 patients without a history of syncope and 93 with a history of syncope, respectively) were evaluated. HUTT was positive in 50 (19.84%) of 252 patients (in 21 of 93 patients (22.58%) with a history of syncope and in 29 of 159 patients (18.24%) without a history of syncope, respectively). The pooled total sensitivity and specificity of the HUTT for detecting syncope were 22.1% (14.8-35.1%) and 83.6% (73.2-91.6%), respectively. The summary receiver operator curve showed that HUTT had an only modest discriminative ability for syncope with an area under the curve value of 0.565 (0.246-0.794).
CONCLUSIONS: Although HUTT has significant limitations in diagnosis of unexplained syncope in patients with HCM, it may still be used to determine hypotensive susceptibility. Other autonomic tests can be used in diagnostic workflow in this population.

BACKGROUND: Concussion is known to cause transient autonomic and cerebrovascular dysregulation that generally recovers; however, few studies have focused on individuals with an extensive concussion history.
METHODS: The case was a 26-year-old male with a history of 10 concussions, diagnosed for bipolar type II disorder, mild attention-deficit hyperactivity disorder, and a history of migraines/headaches. The case was medicated with Valproic Acid and Escitalopram. Sensor-based baseline data were collected within six months of his injury and on days 1-5, 10, and 14 post-injury. Symptom reporting, heart rate variability (HRV), neurovascular coupling (NVC), and dynamic cerebral autoregulation (dCA) assessments were completed using numerous biomedical devices (i.e., transcranial Doppler ultrasound, 3-lead electrocardiography, finger photoplethysmography).
RESULTS: Total symptom and symptom severity scores were higher for the first-week post-injury, with physical and emotional symptoms being the most impacted. The NVC response showed lowered activation in the first three days post-injury, while autonomic (HRV) and autoregulation (dCA) were impaired across all testing visits occurring in the first 14 days following his concussion.
CONCLUSIONS: Despite symptom resolution, the case demonstrated ongoing autonomic and autoregulatory dysfunction. Larger samples examining individuals with an extensive history of concussion are warranted to understand the chronic physiological changes that occur following cumulative concussions through biosensing devices.

BACKGROUND: Long-COVID-19 syndrome (LCS) exhibits neurological problems such as peripheral neuropathy and autonomic nervous system (ANS) dysfunction. Exercise intolerance and, consequently, low cardiorespiratory fitness (CRF) are some of the most common symptoms of LCS. We describe a series of individuals exhibiting LCS symptoms compared to a control group and posit that this condition may be related to the exercise capacity-mediated disruption of the ANS resulting particularly in exercise intolerance.
METHODS: This study included 87 individuals with LCS and 71 control participants without COVID-19 diagnoses. Heart rate variability (HRV) in supine position is commonly measured to diagnose autonomic dysregulation and subsequently analyzed using the Kubios software (Kuopio, Finland). CRF (peak VO2), post-COVID-19 patient-reported symptoms, maximal muscle strength (grip strength, bilateral leg press, leg extension, pectoral press, and back press exercises), and body composition were also measured. Analysis of covariance (ANCOVA) and mediation analysis were employed to assess the associations among LCS, peak VO2, and HRV indicators. Two-sided p < 0.05 was considered as significant.
RESULTS: The HRV parameters-RR interval, RMSSD, SDNN, PNS index, LF, HF, total power, SD1, and SD2-were significantly elevated (p < 0.05) in the control group when compared to the LCS patients. In contrast, the HR, stress index, and SNS index parameters were significantly higher (p < 0.05) in the LCS group. When adjusted for RR intervals, these parameters remained statistically significant (p < 0.05). A partially mediated effect was found between peak VO2 and RMSSD (mediation effect = 24.4%) as well as peak VO2 and SDNN (mediation effect = 25.1%) in the LCS patients.
CONCLUSIONS: These findings contribute new insights on the interplay between CRF and HRV indicators as well as endorse that dysautonomia may be related to the low peak VO2 observed in long COVID-19 patients.