Autonomic Imbalance Research Articles

Sleep-Disordered Breathing and Cardiac Arrhythmias

A narrative review was performed, analyzing peer-reviewed articles from databases such as PubMed, EMBASE, Scopus, and Web of Science to examine the mechanistic links between sleep-disordered breathing (SDB), and cardiac arrhythmias, emphasizing intermittent hypoxia, autonomic imbalance, and intrathoracic pressure swings as key pathways. Studies, including the DREAM and CESAAR trials, consistently demonstrate that SDB patients face elevated risks: more than doubling the likelihood of overall arrhythmias (OR 2.24; 95% CI 1.48–3.39), quadrupling the risk of AF (OR 4.02; 95% CI 1.03–15.74), and tripling the risk of non-sustained ventricular tachycardia (NSVT) with higher apnea-hypopnea index (AHI) values. Additionally, SDB doubles the risk of bradyarrhythmia, such as sinus pause, second and third-degree atrioventricular block, and intraventricular conduction delay (OR 2.50; 95% CI 1.58–3.95). According to meta-analytical findings, continuous positive airway pressure (CPAP) therapy is a pivotal intervention, significantly reducing AF recurrence by 42% and lowering VA incidence by 58%. Moreover, CPAP therapy diminishes sinus bradycardia and occurrences of sinus pause and may reduce the necessity for pacemaker implantation. Recognizing SDB as a modifiable risk factor for cardiac arrhythmias highlights the importance of early diagnosis and effective management, primarily through CPAP therapy, to improve cardiovascular outcomes.

Neuroimmune cross-talk in heart failure.

Heart failure (HF) is characterized by autonomic nervous system (ANS) imbalance and low-grade chronic inflammation. The bidirectional relationship between the ANS and immune system (IS) is named "neuroimmune cross-talk" (NICT), and is based on common signaling molecules, receptors, and pathways. NICT may be altered in HF, and neuroinflammation seems to be a main driver of HF progression. In HF, heightened sympathetic nerve activity triggers inflammatory cascades that lead to cardiomyocyte death and myocardial interstitial fibrosis. Concurrently, parasympathetic withdrawal may impair the cholinergic anti-inflammatory pathway, with a less effective immune response to infections or inflammatory events. Additionally, microglial activation and inflammatory molecules contribute to autonomic imbalance by acting on central nuclei and peripheral visceral feedbacks, which in turn promote adverse cardiac remodeling, HF decompensation, and potentially life-threatening arrhythmias. Therefore, neuroinflammation has been identified as a potential target for treatment. Pharmacological antagonism of the neurohormonal system remains the cornerstone of chronic HF therapy. While some drugs used in HF management may have additional benefits due to their anti-inflammatory properties, clinical trials targeting inflammation in patients with HF have so far produced inconclusive results. Nevertheless, considering the pathophysiological relevance of NICT, its modulation seems an appealing strategy to optimize HF management. Current research is therefore investigating novel pharmacological targets for anti-inflammatory drugs, and the immunomodulatory properties of denervation approaches and bioelectronic medicine devices targeting NICT and neuroinflammation in HF. A deeper understanding of the complex relationship between the ANS and IS, as outlined in this review, could therefore facilitate the design of future studies aimed at improving outcomes by targeting NICT in patients with HF.

Hypertension-induced heart failure disrupts cardiac sympathetic innervation.

About 26 million people worldwide live with heart failure (HF), and hypertension is the primary cause in 25% of these cases. Autonomic dysfunction and sympathetic hyperactivity accompany cardiovascular diseases, including HF. However, changes in cardiac sympathetic innervation in HF are not well understood. We hypothesized that cardiac sympathetic innervation is disrupted in hypertension-induced HF. Male and female C57BL6/J mice were infused with Angiotensin II (AngII) for 4 weeks to generate hypertension leading to HF; controls were infused with saline. AngII-treated mice displayed HF phenotype including reduced cardiac function, hypertrophy, and fibrosis. AngII-treated mice also had significantly reduced sympathetic nerve density in the left ventricle, intraventricular septum, and right ventricle. In the left ventricle, the subepicardium remained normally innervated, while the subendocardium was almost devoid of sympathetic nerves. Loss of sympathetic fibers led to loss of norepinephrine content in the left ventricle. Several potential triggers for axon degeneration were tested and ruled out. AngII-treated mice had increased premature ventricular contractions after isoproterenol and caffeine injection. Although HF can induce a cholinergic phenotype and neuronal hypertrophy in stellate ganglia, AngII treatment did not induce a cholinergic phenotype or activation of trophic factors in this study. Cardiac neurons in the left stellate ganglion were significantly smaller in AngII-treated mice, while neurons in the right stellate were unchanged. Our findings show that AngII-induced HF disrupts sympathetic innervation, particularly in the left ventricle. Further investigations are imperative to unveil the mechanisms of denervation in HF and to develop neuromodulatory therapies for patients with autonomic imbalance.

Baroreflex activation therapy in heart failure patients with reduced ejection fraction: a long-term follow up

Abstract Introduction Heart failure with reduced ejection fraction (HFrEF) is a major public health concern with substantial morbidity and mortality. Overactivation of the sympathetic nervous system is a key pathophysiological process driving heart failure progression. Baroreceptor activation therapy (BAT) targets this autonomic imbalance and is a promising treatment strategy for patients with HFrEF. Current short-term studies indicate that BAT provides symptomatic relief, improvement in left ventricular function and cardiac biomarkers. However, data regarding the long-term effect of BAT on HFrEF are scarce. Purpose This study aims to assess long-term outcome in HFrEF patients who underwent BAT. Methods Patients with HFrEF who received BAT between 2014-2023 were followed until latest available follow-up. Symptom burden, echocardiography and laboratory testing were assessed before BAT implantation and in subsequent follow ups. Results 23 patients (mean age 66±10 years, 83% men) with HFrEF were included in the study. Etiology of heart failure was ischemic in 70%. The majority of patients (96%) suffered from NYHA III with a mean left ventricular ejection fraction (LVEF) of 23±8% and NTproBNP of 2463±2922pg/ml. Complication occurred in one patient during BAT implantation (4%). Mean follow-up was 3±2 (max. 7.5) years. BAT reduced NYHA classification in 12 patients (52%) after 1 year, of which 1 patient remained in ameliorated NYHA for 7.5 years. Evolution of NYHA functional class over time is shown in Figure 1. Echocardiographic evaluation revealed significant improvement in LVEF of 9±9% after 1 year (p<0.001) and by 11±9% after 2 years (p=0.005). In long-term a trend towards improved LVEF could be observed (Figure 2). In addition, BAT mildly reduced NTproBNP in the first 2 years (after 1 year non-significantly by -396±1006pg/ml and significantly after 2 years by -566±651pg/ml (p=0.039)). Seven patients reaching recommended replacement time underwent device exchange. Four patients deceased during observation time. Conclusion BAT resulted in a substantial reduction in NYHA classification, improvement in LVEF, and a delayed reduction in NTproBNP levels. These findings highlight the long-term efficacy and potential benefits of BAT as a therapeutic intervention for patients with HFrEF.Sankey plot of NYHA class over timeAlteration of LVEF over time

Examining the acute cardiovagal consequences of supine recovery during high-intensity interval exercise.

Exercise training requires the careful application of training dose to maximize adaptation while minimizing the risk of illness and injury. High-intensity interval training (HIIT) is a potent method for improving health and fitness but generates substantial autonomic imbalance. Assuming a supine posture between intervals is a novel strategy that could enhance physiological readiness and training adaptations. This study aimed to establish the safety and feasibility of supine recovery within a HIIT session and explore its acute effects. Fifteen healthy, active males (18-34years) underwent assessment of cardiopulmonary fitness. Participants completed two identical HIIT treadmill sessions (4 x [3min at 95% VO2max, 3min recovery]) employing passive recovery in standing (STANDard) or supine (SUPER) posture between intervals. Heart rate variability (HRV), HRV recovery (HRVrec; lnRMSSD) and heart rate recovery at 1min (HRrec) were assessed using submaximal constant speed running tests (CST) completed prior to, immediately after and 24h following HIIT. No severe adverse events occurred with SUPER, and compliance was similar between conditions (100 ± 0%). The change in HRVrec from the CST pre-to-post-HIIT was not different between conditions (p = 0.38); however, HRrec was faster following SUPER (39 ± 7bpm) vs. STANDard (36 ± 5bpm). HRV 24h post-SUPER was also greater (3.56 ± 0.57ms) compared to STANDard (3.37 ± 0.42ms). Despite no differences in perceived exertion (p = 0.23) and blood lactate levels (p = 0.35) between SUPER and STANDard, average running HRs were lower (p = 0.04) with SUPER (174 ± 7bpm) vs. STANDard (176 ± 7bpm). Supine recovery within HIIT attenuates acute cardioautonomic perturbation and accelerates post-exercise vagal reactivation. SUPER enhances recovery of vagal modulation, potentially improving physiological preparedness 24h post-HIIT. Further research exploring the chronic effects of SUPER are now warranted.

Exploring the link between comorbid insomnia and sleep apnea (COMISA) and erectile dysfunction: implications for male sexual health.

This review explores the interplay between comorbid insomnia and sleep apnea (COMISA) and erectile dysfunction (ED), 2 conditions that significantly impact men's health. COMISA, a recently recognized condition characterized by the coexistence of insomnia and obstructive sleep apnea, has been shown to disrupt sleep architecture and cause intermittent hypoxia. These disturbances are increasingly linked to the exacerbation of ED, a prevalent issue among men. Understanding the connection between COMISA and ED is crucial for developing integrated treatment approaches that address both sleep and sexual health. We aim to explore the epidemiological, physiological, and potential therapeutic intersections of COMISA and ED. This review sets out to develop a better understanding of the relationship between these conditions and to emphasize the need for an integrated diagnostic and therapeutic approach that addresses both sleep and sexual health. Through a comprehensive analysis, including a detailed examination of extant studies, we address the hormonal imbalances and alterations in neural pathways that collectively contribute to the complex pathophysiology of ED and how these are particularly susceptible to the concurrent presence of COMISA. Our analysis indicates that disruptions in sleep architecture and intermittent hypoxia associated with COMISA can exacerbate ED. Hormonal imbalances, endothelial dysfunction, autonomic imbalance, and increased inflammation and oxidative stress are key mechanisms through which COMISA influences ED. These factors collectively impair vascular health, reduce testosterone levels, disrupt neural control of erections, and contribute to the severity of ED. This review underscores the necessity for an integrated approach to diagnosis and therapy that considers both sleep and sexual health to improve overall outcomes. These insights should foster a deeper understanding of the relationship between COMISA and ED, encourage further research in this area, and potentially lead to the development of innovative treatment strategies to manage these closely intertwined health concerns.

Nasal lymphatic obstruction of CSF drainage as a possible cause of Alzheimer's disease and dementia.

Alzheimer's disease, the most common form of dementia among older adults, slowly destroys memory and thinking skills. In recent years, scientists have made tremendous progress in understanding Alzheimer's disease, still, they do not yet fully understand what causes the disease. This article proposes a novel etiology for Alzheimer's disease. Our hypothesis developed from a review of nuclear medicine scans, in which the authors observed a significant increase in nasal turbinate vasodilation and blood pooling in patients with hypertension, sleep apnea, diabetes and/or obesity, all risk factors for Alzheimer's disease. The authors propose that nasal turbinate vasodilation and resultant blood pooling lead to the obstruction of normal nasal lymphatic clearance of cerebrospinal fluid and its waste products from the brain. The nasal turbinate vasodilation, due to increased parasympathetic activity, occurs alongside the well-established increased sympathetic activity of the cardiovascular system as seen in patients with hypertension. The increased parasympathetic activity is likely due to an autonomic imbalance secondary to the increase in worldwide consumption of highly processed food associated with dysregulation of the glucose regulatory system. The authors' hypothesis offers a novel mechanism and a new paradigm for the etiology of Alzheimer's disease and helps explain the rapid worldwide rise in the disease and other dementias which are expected to double in the next 20 years. This new paradigm provides compelling evidence for the modulation of the parasympathetic nervous system as a novel treatment strategy for Alzheimer's disease and other degenerative brain diseases, specifically targeting nasal turbinate lymphatic flow.

“Assessment Of Cardiac Autonomic Dysfunction In Children With Cerebral Palsy Using Heart Rate Variability”

Background: Cardiac autonomic imbalance in children with CP might be due to primary brain insult, vary with different levels of Gross Motor Functional Classification System or may alter with multimodal therapies in various types of cerebral palsy (1,2) . It is important to understand and to create awareness that autonomic impairment in children with CP is in part due to sedentary lifestyle (3).HRV(Heart Rate Variability) in cerebral palsy is recognized as an important tool for monitoring cardiovascular health, in which autonomic imbalance is characterized by reduced HRV (i.e. regarded as increased cardiac sympathetic activity and decreased vagal modulation) (4,5) . Of the research that does exist, each study discusses only very few parameters of the autonomic nervous system, thus providing opportunities for further research and hence the need for the study. Materials and Methods: This is a cross-sectional case control study of 51 children with Cerebral Palsy (CP) and 51 normal children, conducted at District Early Intervention Centre (DEIC) in the Department of Paediatrics, Vani Vilas hospital. These 51 cases were assessed and classified based on their demographic features, etiology, type of CP, GMFCS scale and with the objectives of assessing the heart rate variability (HRV) in children with cerebral palsy and compare it with controls in both supine position and after a stress test, and also to correlate the obtained parameters with GMFCS level, type of CP using a systematically designed proforma. Results: Results of the study showed that of the children with CP studied, 62% were male children, and majority of were between 6-8 years of age (58%), and it was found that the most common etiology for CP in our study was due to perinatal asphyxia (43%), and 80% of the children had history of NICU admission. Of the 51 cerebral palsy children studied 72% were in GMFCS levels 3 and 4, regarding the topographical classification majority had spastic quadriplegia (58.8%) followed by spastic diplegia (15.7%). Study revealed that cerebral palsy children had significantly lower HRV, higher sympathetic activity, autonomic response deficit to stress test, and higher autonomic dysfunction when compared to normal children. Among cases, HRV was lowest with spastic quadriplegia and triplegic CP, in functional classification HRV was lowest among GMFCS 4 and 3. Conclusion: Cerebral palsy children had significantly higher sympathetic activity and less cardiac vagal modulation compared to normal children in supine position and there was existence of autonomic response deficit in cerebral palsy children after stress test, higher the motor impairment, higher was the sympathetic activity

Autonomic Nervous System: A Therapeutic Target for Cardiac End-Organ Damage in Hypertension.

More than 1.5 billion people worldwide have arterial hypertension. Hypertension increases the risks of death and cardiovascular disease, such as atrial fibrillation and heart failure. The autonomic nervous system plays an essential role in hypertension development and disease progression. While lifestyle factors, such as obesity and obstructive sleep apnea, predispose to hypertension by increasing sympathetic activity, hypertension itself maintains the autonomic nervous imbalance, providing the substrate for atrial fibrillation and heart failure. Therefore, autonomic nervous system modulation either by direct targeting or indirect treatment of comorbidities has the potential to treat both hypertension and related atrial and ventricular end-organ damage. We discuss interventions for the modulation of the autonomic nervous system for hypertension and related cardiac end-organ damage, including pharmacological adrenergic beta-receptor blockade, renal denervation, carotid baroreceptor stimulation, low-level vagal stimulation, and ablation of ganglionated plexuses. In summary, the literature suggests that targeting the autonomic nervous system potentially represents a therapeutic approach to prevent atrial and ventricular end-organ damage in patients with hypertension. However, clinical trials specifically designed to test the effect of autonomic modulation on hypertension-mediated cardiac end-organ damage are scarce.

Ogilvie syndrome with caecal perforation following cesarean section: a rare case report from Jordan

Introduction: Ogilvie syndrome is a rare condition characterized by acute colonic dilation. In 1948, H. Ogilvie first described it in medical literature. Its incidence is estimated at 100 cases per 100 000 per year in the US. Both abdominal distention and pain are considered major symptoms. Presentation of case: A 32-year-old woman, 36+1 weeks pregnant, experienced labour pain and was admitted to the hospital. Upon examination, she was in labour, but the foetus was in a breech position, necessitating a caesarean section. After 36 h later, she returned to the emergency department with severe, 1-day-old diffuse abdominal pain, accompanied by moderate bilious vomiting and significant abdominal distension. Abdominal CT with contrast revealed pneumoperitoneum, abdominal wall emphysema, and pneumatosis intestinalis involving the caecum and ascending colon, suggesting bowel necrosis. Emergency laparotomy revealed a caecal perforation, which was closed surgically without resection. Clinical discussion: Ogilvie syndrome is more common in males but can occur in females for several reasons, including pregnancy, caesarean section, pelvic surgeries, and trauma. Several factors contribute to the occurrence of this syndrome, such as pelvic fractures and cardiac events. Surgery may be required if there is suspicion of bowel perforation or ischaemia. Conclusion: OS is a rare condition in women, often seen after childbirth or pelvic surgery, with an unclear cause but believed to be related to autonomic nervous system imbalance. Patients with abdominal pain and distension, without evidence of obstruction, should be evaluated for pseudo-obstruction using abdominal pelvic CT, and treatment may involve conservative measures, medication, and colonoscopic decompression.

The role of autonomic imbalance in the pathogenesis of hypertension and the therapeutic effectiveness of renal denervation (literature review)

Arterial hypertension (AH) remains a global problem of modern healthcare, since, despite advances in clinical pharmacology and the use of modern antihypertensive drugs, it continues to be a major risk factor for cardiovascular complications. This necessitates a more in-depth study of the pathogenetic mechanisms of this disease and the development of new pathogenetically based methods of its treatment. Every year more and more studies are published, the results of which indicate the significant role of autonomic imbalance in the pathogenesis of the disease. The article presents the main modern data concerning the study of this problem. A detailed analysis of works devoted to the role of sympathetic hyperactivation in a sustained increase in blood pressure (BP) and the development of pharmacotherapy-resistant forms of hypertension (RAH) was carried out. Particular attention is paid to the influence of modern endovascular methods on changes in the severity of immunoinflammatory processes, through the activation of which the hypertensive effects of increased activity of the sympathetic nervous system are realized. Possible mechanisms of the therapeutic effectiveness of renal denervation and prospects for further clinical application of the method are described.

Association of cardiac autonomic nerve function with serum zinc, calcium and magnesium in female hypothyroid patients

Background: Hypothyroidism is related to impaired cardiac autonomic nerve activity with altered levels of serum Zinc (Zn), Calcium (Ca) ‍and Magnesium (Mg).Altered Serum Zn,Caand Mg levels are also associated with autonomic imbalance and may raise cardiovascular risk.Heart rate variability (HRV) is an important marker for assessing cardiac autonomic nerve function(CANF). Objectives: To evaluate the association of serum Zn, Cal and Mglevels withCANF in female hypothyroid patients. Methods: This analytical cross-sectional study was conducted on 40 female hypothyroid patients aged 18-45 years. Thirty apparently healthy women were control. Serum Zn, Ca and Mg levels were estimated by autoanalyzer and CANF was assessed by time domain analysis of HRV recorded by Power Lab 8/35 AD Instruments, Australia. Statistical analysis was done by Independent sample‘t’ test, One way ANOVA followed by post-hoc Bonferroni test and Pearson’s correlation coefficient test. Results: Among time domain parameters of HRV, standard deviation of the RR intervals (SDRR), coefficient variation of RR interval (CVRR), SD rate, standard deviation of the difference between successive RR intervals (SDSD), square root of mean squared differences of successive RR intervals (RMSSD), proportion of RR interval with duration >50 ms (pRR50%) were significantly lower (p<0.05) in all hypothyroid patients as compared to control. On correlation analysis, serum Zn, Ca and Mg were significantly positively correlated with SDSD(p<0.01, p<0.001,p<0.01) RMSSD(p<0.01, p<0.001, p<0.01), pRR50%(p<0.01, p<0.01, p<0.05)and serum Ca was also positively correlated with SDRR(p<0.05) in hypothyroid patients. Conclusion:Serum ZnCa and Mg were associated with cardiac autonomic dysfunction. in female hypothyroid patients. J Bangladesh Soc Physiol 2023;18(1): 27-34

Unraveling the Nexus Between Ambient Air Pollutants and Cardiovascular Morbidity: Mechanistic Insights and Therapeutic Horizons.

Air pollution poses a significant threat to cardiovascular health, contributing to the development and progression of various heart diseases. This review delves into the intricate relationship between ambient air pollutants and cardiovascular morbidity, elucidating the underlying mechanisms and exploring potential therapeutic approaches. We discuss the major types of air pollutants, including particulate matter (PM), nitrogen dioxide (NO2), sulfur dioxide (SO2), ozone (O3), and carbon monoxide (CO), and their respective roles in exacerbating cardiovascular conditions. The review highlights the key mechanisms by which air pollutants adversely impact the cardiovascular system, including systemic inflammation, oxidative stress, endothelial dysfunction, autonomic nervous system imbalance, and dysregulation of blood coagulation and thrombosis. Vulnerable populations, including children, the elderly, and those with pre-existing health conditions, are disproportionately affected. Air quality regulations aim to mitigate these effects by reducing pollutant levels, with the overall goal of lowering cardiovascular morbidity and improving public health outcomes. Specifically, stringent regulations focus on curbing vehicular emissions and industrial pollutants and promoting cleaner energy sources. Recent data underscore the importance of addressing environmental and behavioral risk factorsto prevent the growing global burden of cardiovascular disease. This review synthesizes the mechanistic pathways through which pollutants contribute to cardiovascular damage and highlights the urgent need for early detection strategies and targeted therapies. Improving public health through stricter air quality control measures and raising awareness of the health risks associated with pollution is crucial for mitigating the long-term cardiovascular impacts of air pollution.

The Role of the Autonomic Nervous System in Vasovagal Syncope.

The mechanism of vasovagal syncope (VVS) is multifaceted and involves a delicate balance within the autonomic nervous system (ANS). This review delves into the complex interplay between the ANS and VVS, elucidating the pivotal role that autonomic imbalance plays in the pathophysiology of this condition. Through a comprehensive exploration of the sympathetic and parasympathetic branches of the ANS, this review provides insights into the mechanisms that underlie VVS. In addition, this article discusses established and emerging research on the management of VVS.

Evaluation of Antipsychotic-Induced Neuroleptic Malignant Syndrome Using a Self-Organizing Map.

Introduction In neuropsychiatric pharmacotherapy, neuroleptic malignant syndrome (NMS) is a potentially serious side effect of antipsychotics characterized primarily by fever, disorientation, extrapyramidal disorders, and autonomic nervous system imbalance, which can lead to death if left untreated. We visualized the NMS profile of antipsychotics using a self-organizing map (SOM). We combined it with decision tree analysis to discriminate between 31 antipsychotics in more detail than typical antipsychotic (TAP) and atypical antipsychotic (AAP) classifications. Method A total of 20 TAPs and 11 AAPs were analyzed. We analyzed NMS reports extracted from the Japanese Adverse Drug Event Report (JADER) database based on standardized Medical Dictionary for Regulatory Activities (MedDRA) queries (Standardized MedDRA Queries (SMQ) code: 20000044, including 68 preferred terms). The SOM was applied using the SOM package in R version 4.1.2 (RFoundation for Statistical Computing, Vienna, Austria). Results The Japanese Adverse Drug Event Report (JADER) database contained 887,704 reports published between April 2004 and March 2024. The numbers of cases of NMS (SMQ code: 20000044) reported for risperidone, aripiprazole, haloperidol, olanzapine, and quetiapine were 1691, 1294, 1132, 1056, and 986, respectively. After the antipsychotics were classified into six units using SOM, they were adapted for decision tree analysis. First, 31 antipsychotics branched off into groups with loss of consciousness, with one group (10 TAPs) consisting entirely of TAPs, and the other consisting of antipsychotics that were further separated into two groups with coma induced by TAPs and AAPs. Conclusion The results of this study provide a reference for healthcare providers when predicting the NMS characteristics induced by each drug in patients, thereby facilitating the effective treatment of schizophrenia.

Autonomic Imbalance and Elevated Inflammatory Cytokines in Long COVID: A Cross-Sectional Study.

Following an infection with SARS-CoV-2, the virus that causes coronavirus disease 2019 (COVID-19), many individuals fully recover. On the other hand, a few have symptoms that last for weeks, months, or even years after their initial diagnosis. Symptoms of COVID-19 persisting for four weeks and more are termed long COVID. To assess the long-term cardiovascular morbidity by battery of cardiac autonomic function tests as well as the persistence of inflammation in COVID-recovered patients three months after initial infection. Methodology: 150 patients were selected who had recovered from COVID-19 at least three months prior to the study. After obtaining informed written consent, a throat swab was tested for COVID-19, and those with negative reverse transcription polymerase chain reaction (RT-PCR) results were subjected to autonomic function testing. Serum interleukin-6 and C-reactive protein levels were determined by enzyme-linked immunosorbent assay (ELISA) test. Out of 150 subjects 36 were found to have autonomic dysfunction graded according to Ewing's criteria. Individuals with autonomic dysfunction also had significantly increased inflammatory biomarker levels. There was also significant correlation between inflammatory markers and autonomic function test and heart rate variability parameters. Even years after the COVID-19 pandemic was declared, new symptom patterns and syndromes such as 'long COVID' are appearing.A better understanding of the pathophysiological mechanisms of post-COVID manifestations that affect the autonomic nervous system, as well as customized therapeutic care, should help reduce COVID-19 sequelae, particularly if we act early in the disease.

Cellular and Molecular Mechanisms Underlying Altered Excitability of Cardiac Efferent Neurons in Cirrhotic Rats.

Patients with cirrhosis often exhibit cardiac autonomic dysfunction (CAD), characterized by enhanced cardiac sympathetic activity and diminished cardiac vagal tone, leading to increased morbidity and mortality. This study delineates the cellular and molecular mechanisms associated with altered neuronal activities causing cirrhosis-induced CAD. Biliary and nonbiliary cirrhotic rats were produced by common bile duct ligation (CBDL) and intraperitoneal injections of thioacetamide (TAA), respectively. Three weeks after CBDL or TAA injection, the assessment of heart rate variability revealed autonomic imbalance in cirrhotic rats. We observed increased excitability in stellate ganglion (SG) neurons and decreased excitability in intracardiac ganglion (ICG) neurons in cirrhotic rats compared to sham-operated controls. Additionally, threshold, rheobase, and action potential duration exhibited opposite alterations in SG and ICG neurons, along with changes in afterhyperpolarization duration. A- and M-type K⁺ channels were significantly downregulated in SG neurons, while M-type K⁺ channels were upregulated, with downregulation of the N- and L-type Ca2⁺ channels in the ICG neurons of cirrhotic rats, both in transcript expression and functional activity. Collectively, these findings suggest that cirrhosis induces an imbalance between cardiac sympathetic and parasympathetic neuronal activities via the differential regulation of K+ and Ca2+ channels. Thus, cirrhosis-induced CAD may be associated with impaired autonomic efferent functions within the homeostatic reflex arc that regulates cardiac functions.

Influence of shift work on sleep quality and circadian patterns of heart rate variability among nurses.

Shift work implementation is essential for providing continuous patient care in hospitals. However, working in shifts on a routine basis may disrupt the circadian pattern and alter the sleep-wakefulness cycle in nurses. Stress due to shift work can influence the adaptability of the cardiovascular system, produce psychophysiological strain and deteriorate work performance in female nurses. This study investigated the effect of morning and night shift work on sleep quality and circadian patterns governing heart rate variability (HRV) in female nurses working in a tertiary care hospital. Thirty-eight healthy female nurses were recruited. Frequency and time domain parameters of HRV were recorded as markers of cardiac autonomic function. A student t-test was used to investigate differences in HRV between morning and night shift workers. Mann-Whitney non-parametric test was applied for the difference between Pittsburgh Sleep Quality Index (PSQI) scores in the two groups. Standard deviation of the normal-to-normal interval (SDNN) (msec), total power (ms2) and high-frequency (HF) band power (ms2) were significantly reduced in night shift nurses than in morning shift nurses. The low-frequency (LF)/HF ratio was significantly increased in night shift nurses. The differences in standard deviation of the averages of NN intervals (SDaNN) (msec), root mean square of successive differences between adjacent NN intervals (RMSSD), mean NN, very low-frequency (VLF) band power (ms2) and LF band power (ms2) were not statistically significant. The global PSQI score was significantly higher among night shift workers than in morning shifts. Inadequate sleep can disrupt the body's ability to regulate heart rhythm and increase the risk of cardiovascular diseases and mortality. The research suggests a propensity for autonomic imbalance in night shift workers when compared to their counterparts on morning shifts.

Improving Lower Limb Function and Frailty in Frail Older Patients with Acute Myocardial Infarction After Percutaneous Coronary Intervention: A Randomized Controlled Study of Neuromuscular Electrical Stimulation.

A global public health problem, frailty is closely associated with poor prognosis after percutaneous coronary intervention (PCI) in older patients with acute myocardial infarction (AMI). Although exercise intervention is the most commonly used method to reverse and alleviate frailty, its application is restricted in patients with acute myocardial infarction following PCI due to cardiovascular instability and autonomic imbalance. Consequently, there is a need for a new practical intervention to address frailty syndrome in these patients. This study aimed to investigate the effect of neuromuscular electrical stimulation in frail older AMI patients post-PCI. A single-blind, randomized controlled trial was carried out in the Department of Cardiovascular Medicine from March to October 2023. A total of 100 eligible participants were randomly divided into two groups: experimental (n=50) and control (n=50) groups, respectively. Both groups received usual care. The experimental group underwent neuromuscular electrical stimulation (NMES) on bilateral quadriceps and gastrocnemius muscles for 30 minutes daily from day 1 to day 7 after surgery. The primary outcomes measured included the frailty score, lower limb muscle strength, and lower limb muscle quality. Secondary outcomes included the activities of daily living score, inflammatory markers, and length of hospital stay. All participants were included in an intention-to-treat analysis after the study ended. The frailty scores of the two groups exhibited a gradual decrease over time, and the scores of the experimental group were lower than those of the control group at 4 and 7 days after surgery (P<0.001). Concurrently, the lower limb muscle strength showed an increasing trend over the time in the experimental group and a decreasing trend in the control group, and the scores of the experimental group surpassed those of the control group (p<0.001). Moreover, a statistical difference was observed in the lower limb muscle mass across the groups after 7 days postoperatively compared with baseline on both sides (p<0.05). Neuromuscular electrical stimulation has the potential to enhance lower limb function and alleviate frailty in elderly patients with acute myocardial infarction after PCI. These findings introduce a novel intervention approach for frailty management in the elderly population.

Impact of Obstructive Sleep Apnea and Sympathetic Nervous System on Cardiac Health: A Comprehensive Review.

A prevalent condition linked to an elevated risk of cardiovascular disease is sleep apnea. This review examines the connections between cardiac risk, the sympathetic nervous system, and sleep apnea. The increased risk of hypertension, arrhythmias, myocardial infarction, and heart failure was highlighted in the pathophysiology of sleep apnea and its effect on sympathetic activation. It is also important to consider potential processes such as oxidative stress, inflammation, endothelial dysfunction, and autonomic imbalance that may relate sleep apnea-induced sympathetic activation to cardiac risk. With implications for creating innovative diagnostic and treatment approaches to lessen the cardiovascular effects of sleep apnea, the goal of this investigation is to improve the understanding of the intricate link between sympathetic activity, cardiac risk, and sleep apnea. This study aimed to clarify the complex relationship between cardiovascular health and sleep apnea by synthesizing the available research and highlighting the crucial role played by the sympathetic nervous system in moderating this relationship. Our thorough investigation may have important therapeutic ramifications that will direct the creation of focused therapies to enhance cardiovascular outcomes in sleep apnea sufferers.