Cardiac arrhythmias affect 1%-5% of the global population, with atrial fibrillation (AF) being the most common and clinically relevant. While AF is traditionally linked to electrical and structural remodeling of the atria, growing evidence highlights a critical yet underexplored contributor: dysfunction of the autonomic nervous system (ANS). The ANS regulates heart rate and rhythm through sympathetic and parasympathetic inputs, and its imbalance can initiate and sustain AF by promoting ectopic activity, shortening refractory periods, and enhancing reentry circuits. Autonomic dysregulation is further impacted by lifestyle and environmental influences. Excessive alcohol intake, chronic stress, sleep deprivation, and extreme physical exertion have all been shown to modulate autonomic activity and elevate the risk of AF. Additionally, social determinants such as socioeconomic status and healthcare access indirectly influence AF susceptibility through chronic activation of neurocardiac stress pathways. Mechanistically, emerging research implicates sympathetic hyperinnervation, neuroinflammation, and dysfunction of intrinsic cardiac ganglionated plexi as key contributors to arrhythmogenic remodeling. However, current animal models often fail to capture the complexity of human neuro-cardiac interactions due to species-specific differences in cardiac anatomy, innervation patterns, and immune responses. Human induced pluripotent stem cell (iPSC)-derived models offer an alternative, patient-specific platform to study ANS-driven mechanisms in AF. This review focuses on the role of the ANS in AF pathophysiology, examining the cellular and molecular mechanisms by which autonomic dysregulation promotes arrhythmia. We explore current therapeutic interventions of autonomic-driven AF and discuss the potential of new models to improve mechanistic insight and therapeutic development.

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Cardiac activity is associated with changes in microstates of the electroencephalogram in healthy adults: A resting state study.

Music is the combination of harmony of melody and rhythm. Music listening have been associated with decrease of physiological arousal, heart rate, blood pressure and reduction of cortisol levels. Pharmacological and non-pharmacological measures have been advocated to minimize the development of stress related diseases. Relaxation techniques and listening to music can prevent cardiovascular complications. Music can affect central and autonomic nervous system as well as endocrine system. This experimental study was conducted in the Department of Physiology, Chittagong Medical College, Chattagram, Bangladesh from January 2020 to December 2021. Total 60 subjects of first year MBBS, with equal number of male and female, studying in Chittagong Medical College, Chattagram, were included by stratified random sampling method according to inclusion and exclusion criteria. A questionnaire along with general information about previous diseases, medical and family history were filled up by the subjects. Stress biomarkers- systolic and diastolic blood pressure, perceived stress scale (PSS) score and serum cortisol were recorded before and after 15 minutes of music intervention for 15 days. Result was compiled and compared after data collection by using SPSS 25.0. Paired 't' tests were done to compare differences between pre and post-intervention values of different outcome parameters. P value <0.05 was considered as statistically significant. Stress biomarkers- systolic and diastolic blood pressure, perceived stress scale (PSS) score and serum cortisol were significantly reduced after 15 days music intervention. This study concludes that regular listening to slow music causes significant reduction of stress and improvement of cardiorespiratory endurance and quality of life.

Methylphenidate is a first-line psychostimulant widely prescribed for the treatment of attention-deficit/hyperactivity disorder (ADHD). Although its therapeutic efficacy is well established, concerns remain regarding its potential effects on cardiovascular regulation, particularly on autonomic nervous system balance. To evaluate the effect of methylphenidate on heart rate variability (HRV) in ADHD children and adolescents. Our review included children and adolescents diagnosed with ADHD, studies wherein the intervention group should receive short- or long-term methylphenidate treatment, studies that evaluated participants under conventional treatment except methylphenidate, single or double-blind, non-blind randomized or non-randomized control studies. No significant changes were observed in time- and frequency-domain HRV indices, with all outcomes presenting very low certainty of evidence. Our results indicate that methylphenidate does not significantly affect resting heart rate HRV in ADHD children and adolescents. The very low certainty of this review's evidence level and high risk of bias warrant further studies to provide stronger scientific and statistical evidence.

The World Health Organization estimates that the number of people living with hypertension [blood pressure (BP) of ≥140 mmHg systolic or ≥90 mmHg diastolic or on medication] doubled between 1990 and 2019, from 650 million to 1.28 billion. Elevated BP is associated with increased risks of stroke, coronary artery disease, heart failure, and chronic kidney disease. Resistant hypertension is defined as office BP ≥140/90 mmHg despite treatment with 3 classes of antihypertensive agents (including a diuretic) at maximally tolerated doses, or the need for 4 or more agents regardless of BP level. Device-based antihypertensive therapies primarily target autonomic nervous system through techniques, such as renal denervation, carotid baroreceptor activation, and carotid body ablation. This review outlines the pathophysiological basis of selected interventions, critically evaluates existing clinical evidence, and highlights future directions for their development and integration into clinical practice.

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Circadian rhythms, governed by the body's endogenous clock mechanism, regulate daily fluctuations in cardiovascular function, optimizing physiological processes like blood pressure regulation, cardiac metabolism, and myocardial repair. Rhythms also align cardiovascular reactivity with predictable environmental and behavioral cycles, enabling normal function and affecting disease susceptibility. Major adverse cardiovascular events, including myocardial infarction, ventricular arrhythmias, and stroke, exhibit a distinct morning peak, with evidence for circadian regulation in cardiovascular health. Indeed, controlled human laboratory studies demonstrate that beyond the influences of sleep and other behaviors, endogenous circadian rhythms independently regulate blood pressure, autonomic nervous system activity, blood clotting, vascular tone, and metabolic function. Additionally, the kidney plays a critical role in circadian sodium handling, fluid balance, and blood pressure control, with disruptions in renal circadian rhythms contributing to hypertension and progression to heart failure. Chronic circadian misalignment resulting from shift work, irregular sleep-wake cycles, or misaligned lifestyle habits is strongly associated with increased cardiovascular risk and disease progression. The emerging field of Circadian Medicine applies circadian principles to clinical care, leveraging interventions such as optimizing light exposure, meal timing, and physical activity to restore biological alignment. Chronotherapy, the strategic timing of medications or procedures to align with a patient's diurnal or circadian rhythms, offers further potential for enhancing treatments and reducing adverse effects. By integrating circadian biology into cardiovascular medicine, novel strategies are emerging to help prevent disease, improve patient outcomes, and enhance therapeutic precision. Understanding the interplay between circadian regulation and cardiovascular physiology provides a foundation for advancing cardiovascular prevention and treatment strategies.

Presynaptic congenital myasthenic syndromes (CMS) encompass a large number of rare neurologic disorders caused by impaired release of acetylcholine (ACh) from motor nerve terminals. There are two main groups of presynaptic CMS: one in which the amount of ACh in synaptic vesicles (SV) is diminished and another in which the mechanism of synaptic vesicle release is impaired. The latter is often referred to as a congenital Lambert-Eaton myasthenic syndrome (LEMS). Presynaptic CMS, like other forms of CMS, is primarily characterized by muscle weakness and fatigue, but is often associated with additional manifestations of central and autonomic nervous system involvement, including episodic apneas, cognitive delay, seizures, and gastrointestinal complications. The most common causes of presynaptic CMS are recessive and dominant mutations in genes encoding proteins participating in the mechanisms of ACh synthesis and SV release. However, at times gene mutations can result in more complex pathogenic mechanisms. The most effective treatment of these conditions is prevention of potentially fatal episodes of apnea and other respiratory complications resulting from bulbar weakness. Pharmacologic treatments are also useful; however, in many cases the response is incomplete, and in other mild cases there is improvement with age that obviates the need for pharmacologic interventions. Preclinical studies in animal models of presynaptic CMS using targeted gene therapies are promising but these new therapies will not be available in the near future.

Chronic heart failure (CHF) is a condition affecting millions worldwide, characterized by the heart's reduced ability to pump blood efficiently. Conventional diagnostics, such as imaging and ECG assessments, can be time-consuming and expensive, often identifying CHF only after significant progression. Early detection is crucial for improving treatment options and reducing healthcare costs. Heart rate variability (HRV), which measures the variation in time intervals between heartbeats, is emerging as a non-invasive and cost-effective biomarker for CHF detection. HRV reflects the autonomic nervous system's regulatory functions, often impaired in CHF patients. This study aims to assess advanced HRV measures for earlier CHF detection. The research involved examining CHF patients (N = 934, Age 65 ± 12) compared to healthy controls (N = 274, Age 43 ± 17). Data was sourced from Physionet and the Telemetric and Holter ECG Warehouse, with RR interval (RRI) data extracted from 24-h Holter recordings. The study utilized dynamical detrended fluctuation analysis (DDFA), which considers changes in RRI correlations over time and scale, resulting in scaling exponent α(t,s). This was further aggregated into scale and heart rate (HR)-dependent forms, α(HR,s), classified using XGBoost ensemble method with 10-fold nested cross-validation. The classifier achieved 97% sensitivity and 90% specificity for distinguishing between CHF and control groups. Sensitivity and specificity remained consistent across subgroup analyses based on beta blocker medication and NYHA class. This method demonstrated high classification accuracy, suggesting potential utility for early CHF detection, independent of CHF severity.

Purpose Post-exercise recovery is a critical window for physiological adaptation, with the autonomic nervous system (ANS) playing a key regulatory role. However, whether long-term training with different modalities systematically influences post-exercise ANS recovery remains unclear. This study investigated the long-term effects of moderate-intensity continuous training (MICT), high-intensity interval training (HIIT), and resistance training (RT) on post-exercise ANS recovery assessed by heart rate variability (HRV) in healthy adults. Methods Three independent cohorts completed 12 weeks of MICT, HIIT, or RT (3 sessions per week). 5-minute continuous HRV data were collected immediately after each session. Recovery slopes of the root mean square of successive differences (RMSSD) and low-frequency/high-frequency power (LF/HF) ratio were calculated. Linear mixed-effects models analyzed trends in recovery slopes across training weeks, with pre-exercise resting HRV and prior-night insomnia score as covariates. Results A total of 43 participants (MICT: n = 13; HIIT: n = 16; RT: n = 14) completed the intervention, yielding 1393 training observations. RMSSD recovery slope decreased significantly in MICT (b=-0.165, P = 0.003), but not in HIIT (b = 0.019, P = 0.680) or RT (b=-0.037, P = 0.452). Between-group comparisons showed a significant difference between HIIT and MICT (Δb = 0.184, P = 0.030). Pre-exercise resting RMSSD (β = 0.022, P < 0.001) and prior-night insomnia score (β = 0.052, P = 0.021) significantly influenced RMSSD recovery slope. No observable trend was detected in LF/HF ratio recovery slopes. Conclusion Long-term training with different exercise modalities differentially affects post-exercise ANS recovery. MICT potentially promotes economical autonomic adaptation; HIIT maintains rapid recovery capacity; RT exerts weaker effects. Pre-exercise resting RMSSD and sleep quality may serve as practical markers for daily training monitoring.

Circadian rhythms, fundamental biological oscillations aligning physiological functions with the Earth’s 24-h cycle, profoundly influence blood pressure (BP) regulation. In this review, we first consolidates current understanding the systemic and cellular organizations of circadian clocks. Next, we delve into the intricate relationship between BP and circadian rhythms, examining how environmental cues like light, sleep, and diet disrupt these rhythms, leading to BP disorders. Crucially, we emphasize the ANS’s central role as a dynamic integrator, mediating the influence of central and peripheral circadian clocks on BP, and facilitating crosstalk with other major BP regulatory systems like the renin-angiotensin-aldosterone system (RAAS), natriuretic peptides (NP), and the immune system. Finally, we presented a future perspective of research on ANS function in the circadian rhythm of BP, identifying key unresolved questions and proposed therapies based on mechanisms for hypertension induced by ANS disorders. Overall, this is a comprehensive review elucidating ANS tone as a pivotal mechanism underlying the circadian rhythm of blood pressure.

Menstrual cycle disorders (MCD) in adolescent girls frequently co-occur with autonomic dysfunction (AD), forming a persistent clinico-functional complex that compromises quality of life and increases the risk of chronic reproductive and psychosomatic disorders. Objective. To investigate the clinical and diagnostic interdependence of autonomic dysfunction and menstrual cycle disorders in adolescent girls, identifying clinical and functional markers of autonomic regulation associated with the pattern and severity of menstrual irregularities. Materials and methods. The study cohort comprised 79 adolescent girls aged 13–18 years presenting with MCD and signs of AD (study group), alongside 29 apparently healthy adolescents serving as controls. Autonomic status was evaluated using the Wayne scale and the Kerdo index. All patients underwent pelvic ultrasonography; brain magnetic resonance imaging was performed when clinically indicated Hormonal evaluation included thyroid-stimulating hormone, prolactin, luteinizing hormone, follicle-stimulating hormone, and testosterone levels. Receiver operating characteristic (ROC) analysis was employed. The study was conducted following the ethical principles for biomedical research, and the protocol was approved by the Local Ethics Committee of Samarkand State Medical University. All procedures were performed in accordance with the 2013 revision of the Declaration of Helsinki of the World Medical Association. Written informed consent was obtained from all participants or their legal representatives prior to enrollment. Patient data confidentiality was strictly maintained throughout the study. Statistical analyses were performed using the Statistica and SPSS software packages, with statistical significance set at p &lt; 0.05. This work was conducted as part of the research program of Samarkand State Medical University, titled "Optimization of early diagnostic, therapeutic, and preventive strategies for pathological conditions affecting public health in the Samarkand Region" (2022–2026). Results. Asthenic complaints were reported by 63.3% of patients in the study group compared with 13.8% in the control group (p &lt; 0,001). Ovarian abnormalities were detected by ultrasonography in 57.0% of patients. Elevated prolactin levels were recorded in 32.9%, thyroid-stimulating hormone abnormalities in 29.1%, and increased testosterone concentrations in 24.1% of cases. Receiver operating characteristic analysis indicated that the Wayne scale (area under the curve [AUC] = 0.82; 95% confidence interval [CI]: 0.73–0.91) and the Kerdo index (AUC = 0.79; 95% CI: 0.69–0.88) exhibited the highest prognostic value. These findings corroborate the predominant role of the autonomic nervous system and neuroendocrine mechanisms in the pathogenesis of menstrual cycle disorders in adolescent girls. The severity of clinical and autonomic manifestations was significantly greater in the study group than in the control group, underscoring the significance of autonomic dysfunction as a primary pathogenetic factor of reproductive disorders during adolescence. Instrumental and laboratory data demonstrated a close association between functional alterations in autonomic regulation and hormonal disturbances of the hypothalamic-pituitary-ovarian and thyroid axes. The absence of structural alterations in the hypothalamic-pituitary region on magnetic resonance imaging among the examined patients emphasizes the predominantly functional nature of the identified disorders. The substantial prognostic value of hormonal and ultrasonographic parameters justifies their inclusion in a comprehensive diagnostic algorithm for adolescents presenting with this condition. Conclusions. Autonomic dysfunction and neuroendocrine dysregulation play a pivotal role in the development and progression of menstrual cycle disorders in adolescent girls. The Wayne scale and the Kerdo index serve as informative prognostic tools with high sensitivity and specificity. An integrative diagnostic approach incorporating clinical, autonomic, hormonal, and instrumental data is justified for this patient population.

Anxiety disorders are prevalent mental health conditions with complex pathogenesis and limited treatment efficacy. While links between patent foramen ovale (PFO) and migraine, and between migraine and anxiety are established, no study has explored PFO-anxiety association in non-migraine populations. We conducted a retrospective observational study to examine PFO-anxiety correlation in anxiety disorder patients and propose potential mechanistic pathways. A total of 103 consecutive patients with ICD-10-confirmed anxiety disorders were recruited from Hebei General Hospital. Anxiety severity was stratified into mild-to-moderate and severe groups using the Hamilton Anxiety Rating Scale (HAMA). The grade of right-to-left shunt (RLS) through patent foramen ovale (PFO) was quantified via agitated saline contrast echocardiography (ASCE). Correlation analysis and multiple linear regression were applied to identify factors associated with anxiety severity. Fifty-four patients had mild to moderate anxiety, and forty-nine patients had severe anxiety. Eighty (77.67%) patients with anxiety were positive for patent foramen ovale. Furthermore, the anxiety level of inpatients was greater than that of outpatients and the anxiety level of patients with a positive right-to-left shunt via patent foramen ovale was greater than that of patients with a negative shunt. Spearman correlation analysis revealed a strong positive association between RLS grade and anxiety severity (r = 0.817, p < 0.001). This preliminary observational study identifies a statistically significant association between anxiety severity, PFO presence and RLS grade in patients with anxiety disorders. A key limitation of this work is its retrospective design, which precludes confirmation of causal relationships between the observed variables. Potential underlying mechanisms including neurohumoral dysregulation, cerebrovascular compromise, and autonomic nervous system dysfunction are proposed for future investigation. These findings provide a novel perspective for anxiety pathophysiology research, and further validation in large, well-controlled cohort studies is warranted.

Aging-related autonomic nervous system imbalance and adrenergic regulation of immunity: Implications for inflammaging, autoimmunity, and long COVID.

Long COVID-19 is recognized as a condition associated with autonomic nervous system (ANS) dysfunction. However, quantitative evidence of its impact on heart rate variability (HRV) and blood pressure (BP) regulation during postural changes remains limited. This study assessed autonomic imbalance in post-COVID-19 patients by evaluating HRV and BP responses during tilt table testing, comparing long COVID-19 patients with healthy controls. A total of 61 participants were enrolled, 39 long COVID-19 patients (Study Group, SG) and 22 healthy controls (Control Group, CG). HRV was analyzed using time- and frequency-domain parameters. BP monitoring evaluated systolic, and diastolic blood pressure (SBP, and DBP respectively), and Pulse pressure (PP = SBP-DBP) was calculated for each phase. SG participants exhibited marked autonomic dysfunction during tilt. In the upright phase, they showed a significant increase in mean RR intervals (p = 0.0136), reduced normalized low-frequency (LF†) with p = 0.0316, increased normalized high-frequency (HF†) with p = 0.0315, and a decreased low-frequency/high-frequency (LF/HF) ratio (p = 0.0316), indicating a blunted sympathetic response and impaired autonomic adaptation to orthostatic stress. BP responses were also impaired: SG demonstrated attenuated changes in PP (ΔPP) when transitioning from the upright position to the recovery phase (p < 0.037). Within-group analysis confirmed persistent RR interval instability (p < 0.0001), incomplete normalization of LF and HF components (both p < 0.0001), and delayed recovery of PP after return to supine position. BP responses were also diminished: SG showed smaller ΔPP when moving from standing upright to the recovery phase (p < 0.037). Baroreflex sensitivity values did not differ between groups. Long COVID-19 patients display significant autonomic dysregulation, characterized by reduced HRV, abnormal BP responses. These findings highlight the value of tilt testing in uncovering hidden dysautonomia and support the need for targeted interventions, including pharmacologic modulation and long-term HRV/BP monitoring, to improve cardiovascular stability in long COVID-19.

Cardiorespiratory functional disorders: A transnosologic approach