Role Of Autonomic Dysfunction Research Articles

Chasing the Perplexing Purple Butterfly through Biopsychosocial Model-based Precision Medicine: the Enigma of Fibromyalgia Unraveled Biopsychosocial perspectives in fibromyalgia care

A purple butterfly symbolizes the heightened sensitivity to even a gentle touch in fibromyalgia (FM), which is a common syndrome with persistent widespread pain and tenderness. The biopsychosocial model is currently the main framework used to appreciate different factors contributing to chronic pain in FM. Widespread pain in fibromyalgia is effected by multiple biopsychosocial factors (cognitive ability, depression, somatization, psychological trauma, anxiety, and social deprivation/isolation), which interact and contribute to chronic persistent pain. Interaction of influences such as gender, neuroendocrine milieu, and the hypothalamo–pituitary–adrenal axis also affect FM susceptibility and its clinical expression. Multiple neuroanatomic and neurochemical systems with many autonomic, cognitive & affective processes manifest as multisymptom illness in FM. While the etiology of FM is elusive, the associated symptoms indicate the role of autonomic dysfunction in its pathophysiology. Fatigue and widespread pain characterizing FM may be consequent to peripheral tissue ischemia caused by sympathetically mediated vasoconstriction. In light of some common denominators among FM patients, which include genetic variation, sympathetic hyper-activation, maladaptive thoughts, ineffective coping strategies, and nonrestorative sleep, an individualized care approach can help subgroup and phenotype these patients for specific diagnosis and management. A multidisciplinary approach involving person-centered approaches to biopsychosocial concepts in FM, incorporating relaxation therapy, physical activity, and psychotherapy targeting negative emotions that amplify pain, maladaptive coping strategies, and environmental stressors, can help manage FM's course, outcomes, and treatment.

Orthostatic Intolerance after COVID-19 Infection: Is Disturbed Microcirculation of the Vasa Vasorum of Capacitance Vessels the Primary Defect?

Following COVID-19 infection, a substantial proportion of patients suffer from persistent symptoms known as Long COVID. Among the main symptoms are fatigue, cognitive dysfunction, muscle weakness and orthostatic intolerance (OI). These symptoms also occur in myalgic encephalomyelitis/chronic fatigue (ME/CFS). OI is highly prevalent in ME/CFS and develops early during or after acute COVID-19 infection. The causes for OI are unknown and autonomic dysfunction is hypothetically assumed to be the primary cause, presumably as a consequence of neuroinflammation. Here, we propose an alternative, primary vascular mechanism as the underlying cause of OI in Long COVID. We assume that the capacitance vessel system, which plays a key role in physiologic orthostatic regulation, becomes dysfunctional due to a disturbance of the microvessels and the vasa vasorum, which supply large parts of the wall of those large vessels. We assume that the known microcirculatory disturbance found after COVID-19 infection, resulting from endothelial dysfunction, microthrombus formation and rheological disturbances of blood cells (altered deformability), also affects the vasa vasorum to impair the function of the capacitance vessels. In an attempt to compensate for the vascular deficit, sympathetic activity overshoots to further worsen OI, resulting in a vicious circle that maintains OI. The resulting orthostatic stress, in turn, plays a key role in autonomic dysfunction and the pathophysiology of ME/CFS.

Decreased Nighttime Heart Rate Variability and Progression of White Matter Hyperintensities of Presumed Vascular Origin. A Prospective Study in Community-Dwelling Older Adults

ObjectivesEvidence on the role of autonomic dysfunction on white matter hyperintensities (WMH) progression is limited. This study aims to assess the impact of a low nighttime heart rate variability (HRV) on WMH progression in community-dwelling older adults. Materials and methodsFollowing a prospective longitudinal study design, all individuals aged ≥60 years enrolled in the Atahualpa Project Cohort from 2012 to 2019 were invited to receive baseline HRV determinations through 24-h Holter monitoring, together with clinical interviews and brain MRIs. These individuals were periodically followed by means of annual door-to-door surveys, and those who also received brain MRIs at the end of the study (May 2021) were included in the analysis. Poisson regression models, adjusted for relevant confounders, were fitted to assess the incidence rate ratio (IRR) of WMH progression according to nighttime standard deviation of normal-to-normal R-R intervals (SDNN). ResultsThis study included 254 individuals aged ≥60 years (mean age: 65.4 ± 5.9 years; 55% women). The mean nighttime SDNN was 116.8 ± 36.3 ms. Follow-up MRIs showed WMH progression in 103 (41%) individuals after a median follow-up of 6.5 years. In unadjusted analyses, nighttime SDNN was lower among participants who developed WMH progression than in those who did not (p < 0.001). A Poisson regression model, adjusted for relevant covariates, disclosed a significantly inverse association between nighttime SDNN and WMH progression (IRR: 0.99; 95% C.I.: 0.98–0.99; p = 0.014). ConclusionsStudy results show an inverse association between nighttime SDNN and WMH progression, and provide support for the role of sympathetic overactivity in this relationship.

New Insights Into the Role of Inflammation in the Brain in Heart Failure.

Heart failure is a growing medical problem. Although the underlying aetiology of heart failure differs according to the phenotype, there are some common characteristics observed in patients with heart failure. These include an increased sympathetic nerve activity, an activated renin–angiotensin system, and inflammation. The mechanisms mediating the increased sympathetic activity are not completely understood but the central nervous system plays a major role. Activation of the renin–angiotensin system plays an active role in the remodelling of the heart and in fluid and electrolyte imbalance. The presence of a central renin–angiotensin system means that locally produced angiotensin in the brain may also play a key role in autonomic dysfunction seen in heart failure. Markers of inflammation in the heart and in the circulation are observed in patients diagnosed with heart failure. Circulating pro-inflammatory cytokines can also influence cardiac function further afield than just locally in the heart including actions within the brain to activate the sympathetic nervous system. Preclinical evidence suggests that targeting the pro-inflammatory cytokines would be a useful therapy to treat heart failure. Most clinical studies have been disappointing. This mini-review suggests that pro-inflammatory cytokines in the brain play a key role and there is a problem associated with access of effective doses of the drugs to the site of action in the brain. The recent advances in nanotechnology delivery techniques may provide exciting future technology to investigate the role of specific pro-inflammatory mediators as novel targets within the brain in the treatment of heart failure.

Клинико-патогенетические аспекты хронического панкреатита в сочетании с вегетативной дисфункцией

Актуальность. В статье проанализированы особенности состояния вегетативной нервной системы у больных хроническим панкреатитом (ХП). Проведенные исследования показали, что наличие вегетативной дисфункции (ВД) осложняет течение хронического панкреатита. Все органы и системы нашего тела находятся под постоянным контролем вегетативной нервной системы. Проблема хронического панкреатита остается одной из наиболее актуальных проблем в современной гастроэнтерологии. Несмотря на внедрение новых методов, наблюдается низкая эффективность лечения ХП, что, вероятно, обусловлено недостаточностью знаний об определенных механизмах патогенеза, в частности о роли ВД в развитии и прогрессировании ХП. Итак, особенности состояния вегетативной нервной системы при хроническом панкреатите представляют значительный научный интерес. Цель исследования: изучить степень вегетативных нарушений и их клиническое течение у больных с хроническим панкреатитом. Материалы и методы. Обследовано 45 пациентов с ХП, проходивших лечение в дневном стационаре и гастроэнтерологическом отделении Тернопольской городской клинической больницы № 2. Диагноз «хронический панкреатит» выставляли на основе клинического протокола, принятого в соответствии с приказом № 638 МЗ Украины от 10.09.2014 г. Общеклинические и биохимические обследования проводили больным ХП в фазе обострения и нестойкой ремиссии (10–14 день пребывания в условиях дневного стационара). Результаты. По данным опросника Вейна, у 91,1 % (n = 41) больных ХП обнаружены признаки вегетативной дисфункции, которые сопровождались наиболее выраженными диспеп­тическим ((3,2 ± 1,0) балла) и болевым ((2,9 ± 1,3) балла) синдромами по данным гастроэнтерологического опросника (GSRS). Наличие вегетативной дисфункции у больных ХП сопровождалось повышением реактивной (среднее значение — (45,0 ± 5,7)) и личной (среднее значение — (43,0 ± 5,2)) тревожности, а также ростом нейротизма (среднее значение — (14,7 ± 2,4)) у 75,6 % больных. У больных ХП с ВД по индексу Кердо констатировано преобладание состояния ваготонии (56 %) над симпатикотонией (31 %) при уровне эйтонии 13 %. По результатам клиноортостатической пробы у 13 % пациентов с ХП установлена нормальная реакция гемодинамики на ее проведение, у 6,5 % — гиперсимпатикотонический и гипердиастолический варианты, у 74 % — асимпатикотонический, что указывает на истощение компенсаторных механизмов регуляции вегетативного тонуса. Выводы. По оценке данных исследования, установлено негативное влияние вегетативной дисфункции на течение хронического панкреатита.

Association of lipoprotein levels with sleep apnea: role of autonomic dysfunction.

Objectives. Although multiple mechanisms, including autonomic dysfunction, seem to link sleep-disordered breathing (SDB) with dyslipidemia in animal studies, the data in clinical studies are limited. The aim of this study was to explore the association of lipoprotein levels with SDB measures in healthy habitual snorers. We supposed that autonomic dysfunction is the linking mechanism.Methods. We enrolled 110 previously healthy subjects with complaints of habitual snoring. To assess SDB, polysomnography was performed. Blood samples for the analysis of total cholesterol (TC), high-density lipoprotein (HDL), low-density lipoprotein cholesterol (LDL), and triglycerides (TG) were obtained in a fasting condition after the polysomnography. Baroreflex sensitivity (BRS) was used to assess the autonomic dysfunction.Results. In stepwise multiple linear regression analysis, minimal nocturnal blood oxygen saturation (beta=-0.240, p=0.020) and neck circumference (beta=0.224, p=0.03) were the only significant contributors in model predicting TG. SDB measures were not identified as significant contributors in models predicting TC, LDL, and HDL. We failed to find any significant difference in BRS in SDB subjects when compared according to the presence or absence of hypercholesterolemia/ hypertriglyceridemia. In SDB subjects, the area under the curve in a receiver operating curve to predict hypercholesterolemia and hypertriglyceridemia by BRS was 0.468 (95% CI: 0.328-0.608) and 0.425 (95% CI: 0.304-0.546), respectively.Conclusions. Our results suggest that minimal nocturnal blood oxygen saturation is significant contributor in model predicting TG. No significant decrease in BRS was found in SDB subjects with hypercholesterolemia and hypertriglyceridemia. In SDB subjects, the role of autonomic dys-function in the development of dyslipidemia remains controversial.

Ganglionic Acetylcholine Receptor Antibodies and Autonomic Dysfunction in Autoimmune Rheumatic Diseases.

Autonomic neuropathy has been reported in autoimmune rheumatic diseases (ARD) including Sjögren’s syndrome, systemic sclerosis, rheumatoid arthritis, and systemic lupus erythematosus. However, the pathophysiological mechanism underlying autonomic dysfunction remains unknown to researchers. On the other hand, autoimmune autonomic ganglionopathy (AAG) is an acquired immune-mediated disorder, which causes dysautonomia that is mediated by autoantibodies against ganglionic acetylcholine receptors (gAChRs). The purpose of this review was to describe the characteristics of autonomic disturbance through previous case reports and the functional tests used in these studies and address the importance of anti-gAChR antibodies. We have established luciferase immunoprecipitation systems to detect antibodies against gAChR in the past and determined the prevalence of gAChR antibodies in various autoimmune diseases including AAG and rheumatic diseases. Autonomic dysfunction, which affects lower parasympathetic and higher sympathetic activity, is usually observed in ARD. The anti-gAChR antibodies may play a crucial role in autonomic dysfunction observed in ARD. Further studies are necessary to determine whether anti-gAChR antibody levels are correlated with the severity of autonomic dysfunction in ARD.

Role of autonomic dysfunction in the regulation of myocardial blood flow in systemic sclerosis evaluated by cardiac magnetic resonance.

Autonomic dysfunction (AD) is an early feature of systemic sclerosis (SSc). A regular endothelial function is a prerequisite for normal response of the myocardial blood flow (MBF) to cold pressure test (CPT). The aim of the study was to evaluate the relation between MBF and AD at rest and after CPT in asymptomatic SSc patients. Twenty SSc patients and 10 age-, sex- and body mass index-matched healthy controls underwent cardiac magnetic resonance at rest and after CPT. All subjects underwent 24hours ambulatory 3-channel electrocardiogram Holter to evaluate AD by heart rate variability. We did not observe any significant difference in MBF (mL/g/min) at rest and after CPT between SSc patients and healthy controls. Delta of MBF (difference between MBF after CPT and rest MBF) was lower (P=0.039) in SSc patients than healthy controls (0.28 [0.04-0.40] vs 0.33 [0.24-0.54]). The low frequency/high frequency (LF/HF) was higher (P=0.002) in SSc patients than healthy controls (3 [1.7-6] vs 1.8 [1.1-2.8]). The high frequencies (HF), modulated mainly by paraympathetic system, was lower (P = 0.003) in SSc patients than healthy controls (30 [16-42] vs 36.5 [24-44]). Sympathetic hyperactivity, due to reduction of parasympathetic activity (HF), is present in SSc patients. A negative correlation was observed between Delta of MBF and LF/HF (r = -0.572, P = 0.0031). AD, characterized by sympathovagal imbalance due to a reduced parasympathetic tone with high LF/HF ratio, could be responsible for the reduced myocardial vasodilatory response after CPT.

Interictal electrocardiographic alternations in patients with drug-resistant epilepsy

PurposePrevious studies suggested the possible role of autonomic dysfunction in sudden unexpected death in epilepsy (SUDEP). The aim of this study is to assess the interictal ECG alternations especially heart rate variability (HRV), as a marker of autonomic dysfunction, in patients with drug-resistant epilepsy and determine the effect of epilepsy type and duration, seizure frequency and anti-epileptic drugs (AEDs) on ECG findings. MethodsIn this comparative cross-sectional study, the interictal ECG parameters of 64 consecutive patients with drug-resistant epilepsy and the same number of age and sex-matched controls were analyzed. Epilepsy type and duration, seizure frequency, MRI findings and patients’ anti-convulsive medications were determined. ResultsOur study showed significant longer mean PR interval, shorter mean QRS duration, shorter mean QTc interval and longer corrected QT interval dispersion (QTcd) in patients with epilepsy compared to healthy subjects. The analysis of RR intervals revealed reduced RR standard deviation (SDNN), which is a marker of reduced HRV. A positive linear correlation was found between QRS duration and epilepsy duration. No significant correlation was found between taking a certain kind of AED, and ECG alternations, except for mild QTcd prolongation in patients taking valproate. ConclusionOur study showed clinically important alternations in interictal ECG parameters in patients with drug-resistant epilepsy which could result in sudden cardiac death.

Paediatric breath‐holding spells are associated with autonomic dysfunction and iron deficiency may play a role

This study assessed cardiac performance and iron in subjects aged 12-36months with breath-holding spells (BHSs). We consecutively recruited 40 subjects (55% male) experiencing BHSs from the general paediatric outpatients department at the Children's Hospital, Ain Shams University, Egypt, from 2015 to 2016. The 20 matched comparisons were mainly healthy siblings. The workup included iron levels and electrocardiograms. The age at the onset of BHSs was 5-24months with a median monthly frequency of 13. Almost two-thirds of the patients had cyanotic spells, and one-third had pallid spells, lasting 25-90seconds. Lower serum iron levels and higher QT dispersion and T-wave dispersion were recorded in patients than the comparison group, and 4.8% had dysrhythmia and bradycardia. We observed higher durations of bradycardia during attacks and higher occurrences of dysrhythmia during cyanotic spells, which were more frequent in patients with prolonged or frequent BHSs. Our study of patients aged 12-13months supported the theory of autonomic dysfunction in BHSs. The ECG findings, especially in patients with prolonged or frequent spells, need to be studied further to evaluate the risk of life-threatening events. Iron deficiency may play a role in autonomic dysfunction in patients with BHSs.

Autonomic dysfunction is associated with cardiac remodelling in heart failure patients.

AimsOrthostatic hypotension (OH) is a cardinal sign of autonomic dysfunction and a common co‐morbidity in heart failure (HF). The role of autonomic dysfunction in the development of structural cardiac anomalies in HF patients has not been sufficiently explored. We aimed to assess relations between orthostatic blood pressure (BP) responses during active standing and echocardiographic changes in a series of patients admitted for HF.Methods and resultsOne hundred and forty‐nine patients hospitalized for HF [mean age: 74 years; 30% women; ejection fraction (LVEF) 40 ± 16%] were examined with conventional echocardiograms and active‐standing test. Associations of cardiac remodelling parameters with the difference between supine and standing (after 3 min) systolic/diastolic BP were examined. Systolic BP decreased (−1.1 ± 15 mmHg), whereas diastolic BP increased (+1.0 ± 9.5 mmHg) after 3 min of active standing. A total of 34 patients (23%) met conventional OH criteria; i.e. systolic/diastolic BP decreases by ≥20/10 mmHg. In the multivariable linear regression analysis, adjusted for traditional cardiovascular risk factors and LVEF, a decrease in systolic BP upon standing was associated with greater left atrial volume [β per −10 mmHg: 2.37, standard error (SE) = 1.16, P = 0.043], and greater left ventricular mass (β per −10 mmHg: 5.67, SE = 2.24, P = 0.012), but not with other echocardiographic parameters. No significant associations were observed between signs of cardiac remodelling and decrease in diastolic BP.ConclusionsOrthostatic decrease in systolic BP among older HF patients is associated with structural cardiac changes such as increased left atrial volume and left ventricular mass, independently of traditional risk factors and left ventricular dysfunction.

Autonomic dysfunction in chronic pancreatitis and associated diseases of the digestive system

The article analyzes the literature on the role of autonomic dysfunction and other psychosomatic disorders in causing and progression of pancreatitis and associated gastrointestinal states. The influence of deviations of autonomic nervous system balance regulation on the emergence of hemodynamic, morphological, metabolic, energy disorders in aforementioned pathological conditions is studied. Pathogenic aspects of treatment of autonomic disorders are considered.

The role of autonomic dysfunction in predicting 1-year mortality after liver transplantation.

Model for end-stage liver disease (MELD) score has been extensively used to prioritize patients for liver transplantation and determine their prognosis, but with limited predictive value. Autonomic dysfunction may correlate with increased mortality after liver transplant. In this study, two autonomic biomarkers, complexity and deceleration capacity, were added to the predicting model for 1-year mortality after liver transplantation. In all, 30 patients with end-stage liver diseases awaiting liver transplantation were included. Complexity and deceleration capacity were calculated by multi-scale entropy and phase-rectified signal averaging, respectively. Different combinations of autonomic factors and MELD score were used to predict mortality rate of liver transplant after 1-year follow-up. Receiver-operating characteristics curve analysis was performed to determine clinical predictability. Area under the receiver-operating characteristics curve represents the overall accuracy. The 1-year mortality rate was 16.7% (5/30). The overall accuracy of MELD score used for predicting mortality after liver transplantation was 0.752. By adding complexity and deceleration capacity into the predicting model, the accuracy increased to 0.912. Notably, the accuracy of the prediction using complexity and deceleration capacity alone was 0.912. Complexity and deceleration capacity, which represent different dynamical properties of a human autonomic system, are critical factors for predicting mortality rate of liver transplantation. We recommend that these pre-operative autonomic factors may be helpful as critical adjuncts to predicting model of mortality rate in prioritizing organ allocation.

ВЕГЕТАТИВНІ РОЗЛАДИ ПРИ ХРОНІЧНОМУ ПАНКРЕАТИТІ ТА ПОЄДНАНИХ ШЛУНКОВО-КИШКОВИХ СТАНАХ

У статті проаналізовано літературні джерела щодо ролі вегетативних дисфункцій та інших психосоматичних розладів у виникненні та перебігу панкреатиту і поєднаних шлунково-кишкових станів. Досліджується вплив відхилення балансу регуляції вегетативною нервовою системою на появу гемодинамічних, метаболічних, енергетичних порушень при вищевказаних патологічних станах.

The role of autonomic dysfunction in cirrhotic patients before and after liver transplantation. Review of the literature.

In patients affected by hepatic cirrhosis, autonomic dysfunction is a common finding; usually it is asymptomatic but it may correlate with increased mortality and morbidity before, during and after liver transplant, due to hemodynamic instability in the course of stressful events like sepsis, gastrointestinal bleeding and reperfusion after transplantation surgery. Hyperdynamic circulation and hepatic dysfunction seem to play a role in the pathogenesis of autonomic dysfunction, even if pathophysiological mechanisms are not completely known. We present a revision of previous literature about prevalence, pathophysiological mechanisms, clinical features, and mortality and morbidity of autonomic dysfunction secondary to hepatic cirrhosis.

Autonomic dysfunction in multiple sclerosis.

Autonomic dysfunction is a prevalent and significant cause of disability among patients with multiple sclerosis. Autonomic dysfunction in multiple sclerosis is usually explained by lesions within central nervous system regions responsible for autonomic regulation, but novel evidence suggests that other factors may be involved as well. Additionally, the interactions between the autonomic nervous system and the immune system have generated increased interest about the role of autonomic dysfunction in the pathogenesis of multiple sclerosis. In this paper we analyze systematically the most relevant signs and symptoms of autonomic dysfunction in MS, considering separately their potential causes and implications.

Role of Autonomic Dysfunction and Relation with Diastolic Dysfunction in Resistant Hypertensives

PP-017 There may be a role of autonomic dysfunction and sympathetic overactivity in the development of hypertension. The risks of cardiovascular events and target organ damage are much more in resistant hypertension. In recent years; renal denervation therapies have become more popular for drug-

Abstract 498: Increased Blood Pressure Variability and Baroreflex Impairment in Patients With End-stage Renal Disease Undergoing Hemodialysis

Background: Patients with end-stage renal disease (ESRD) undergoing hemodialysis are susceptible to the development of autonomic dysfunction, which is associated with an increased risk of sudden death. Experimental and clinical evidence suggest a crucial role of autonomic dysfunction for both, the progression of renal disease and for the high rate of cardiovascular events in these patients. In the present study, we evaluated the heart rate variability (HRV), the blood pressure variability (BPV) and the baroreflex sensitivity (BRS) in ESRD patients undergoing hemodialysis and normal controls. Methods: Nine ESRD patients undergoing hemodialysis (mean age 53.4±10.2 years, 4 male) and nine age-matched healthy controls (mean age 52.8±10.2 years, 4 male) were assessed. Non−invasive curves of blood pressure (BP) were recorded continuously (Finometer ®) for 10 minutes, at rest, in the supine position. The heart rate variability (HRV) and systolic blood pressure variability (BPV) were estimated in the time and frequency domain (spectral analysis). The BRS was quantified by alpha index. Statistical analyzes were performed by Student's t test and the results were expressed as mean ± standard deviation. Results: ESRD patients presented lower HRV in time domain than healthy controls (SDNN: 25.8±10.7 vs. 44.6±11.7 ms, p&lt;0.01; VAR NN: 768.3±607.4 vs. 2113.9±1261.6 ms 2 , p=0.01). All frequency domain analyzed indexes, i.e., total power (361.9±297.0 vs. 1227.2±696.3 ms 2 , p&lt;0.01), high-frequency (181.8±128.7 vs. 358.7±179.8 ms 2 , p=0.047), low-frequency (55.1±44.2 vs. 444.6±389.9 ms 2 , p=0.02) and very-low-frequency (72.5±75.1 vs. 279.2±119.5 ms 2 , p&lt;0.01) of HRV were lower in ESRD patients. The BPV was higher in ESRD patients when compared to controls (VAR PAS: 98.4±72.0 vs. 35.4±21.4 ms 2 , p=0.03) and BRS was lower in ESRD patients (alpha index: 4.34±3.05 vs. 7.56±2.50 ms/mmHg, p&lt;0.02). Conclusion: ESRD patients undergoing hemodialysis presents reduced HRV, increase in BPV and reduced baroreflex sensitivity. These impairments may be associated with mortality in ESRD.

Arterial hypertension and obstructive sleep apnoea syndrome: treatment resistance and the role of autonomic dysfunction

Aim. To study the role of obstructive sleep apnoea syndrome (OSAS) in the development of treatment resistance in patients with arterial hypertension (AH). To assess the effects of autonomic nervous system (ANS) dysfunction, as one of the potential pathophysiological mechanisms of inadequate blood pressure (BP) reduction in patients with AH and OSAS. Material and methods. The study included 365 ambulatory AH patients: 194 with OSAS and 161 with resistance to antihypertensive therapy after 6-15 months. The 24-hour BP monitoring (BPM) and 24-hour cardio-respiratory monitoring of electrocardiogram (ECG), with heart rate variability (HRV) analysis, were performed. Results. Among patients with AH and OSAS, most individuals had low antihypertensive therapy compliance. All parameters of 24-hour BPM in this group were lower than in OSAS-free hypertensives, and this difference was more pronounced in patients with lower treatment compliance, particularly for pulse BP and HR. HRV parameters correlated with apnoea-hypopnoea index (AHI) and BP levels during 24-hour BPM. However, in multivariate analyses, these correlations were observed only for HRV parameters and AHI. Conclusion. In AH patients, OSAS aggravates the clinical course of the disease. ANS dysfunction could be one of the mechanisms underlying the development of antihypertensive treatment resistance.

Impaired cerebral autoregulation in primary biliary cirrhosis: implications for the pathogenesis of cognitive decline

Cognitive impairment is recognised in the early stages of primary biliary cirrhosis (PBC). To determine the mechanisms that underlie the cognitive dysfunction that can occur in early-stage PBC, with a particular focus on the role of autonomic dysfunction and altered cerebral autoregulation. Early-stage PBC patients, and age- and sex-matched controls. Brain magnetic resonance imaging to determine the relationship between structural brain abnormalities (T(2)) and cerebral vasculature responsiveness assessed using the Valsalva manoeuvre. Dynamic assessment of cerebral vascular flow using transcranial Doppler was also performed in PBC subjects to derive the pulsatility index (a marker of cerebral resistance) and the autoregulatory slope index [ASI; ratio between the cerebral blood flow velocity and blood pressure (BP)]. Cerebral resistance was increased (P=0.04), and cerebral autoregulation in response to the Valsalva was significantly impaired in the PBC group with markedly lower mean ASI values compared with the controls (7.8+/-7.0 vs -8.5+/-8.4; P=0.002). All controls had normal cerebral autoregulation compared with only 20% of the PBC group. Indicators of sympathetic failure (BP change between Valsalva phases III-IV and low-frequency heart rate variability) correlated with increasing globus pallidus (GP) T(2) values (P<0.05), beyond the effect of age. This study demonstrates the presence of increased cerebral vascular resistance and abnormal cerebral autoregulation in PBC patients, and identifies a potentially important association between the degree of abnormality in structural changes in the GP. These findings suggest that organic brain injury in PBC is directly related to autonomic dysfunction.