Alterations In Autonomic Control Research Articles

The surge in heart rate and blood pressure at respiratory event termination is dampened in children with down syndrome

BackgroundChildren with Down syndrome (DS) have a high prevalence of sleep disordered breathing (SDB) and altered cardiovascular autonomic control. We aimed to analyze the effect of DS on the surge in heart rate (HR) and pulse transit time (PTT, an inverse surrogate measure of blood pressure change) at respiratory event termination. Methods44 children (3–19 y) with DS and 44 typically developing (TD) children matched for SDB severity, age and sex underwent overnight polysomnography. Multilevel modelling determined the effect of DS on HR and PTT changes between a 10s pre-event to the latter half of each respiratory event (late-event) and 15s post-event during NREM and REM, accounting for SDB severity and event length. ResultsThe children with DS had a significantly smaller % change in HR late-event to post-event (NREM: DS 26.4 % ± 17.5 % (mean ± SD), TD 30.7 % ± 21.0 %; REM DS 16.9 % ± 15.3 %, TD 21.0 % ± 14.0 %; p < 0.05 for both) compared with TD children for obstructive events, and central events (13.2 % ± 17.0 %, TD 18.8 % ± 17.0 %; p < 0.01) during REM. %change in PTT was significantly smaller in the DS group during NREM and REM from pre-event and late-event to post-event compared with TD children for obstructive and central events. ConclusionThese results suggest children with DS have dampened HR and BP responses to respiratory events compared with TD children. Whether this is symptomatic of autonomic dysfunction or a protective factor for the cardiovascular system in children with DS remains to be elucidated.

Sympathetic Neural Overdrive and Diminished Exercise Capacity in Reduced Ejection Fraction Heart Failure Related to Anthracycline- Based Chemotherapy.

Cardiotoxicity is the most worrying cardiovascular alteration in patients treated with chemotherapy. To improve the understanding regarding the cardiotoxicity, we studied whether: 1) patients with cardiac dysfunction related to anthracycline-based chemotherapy have augmented sympathetic nerve activity and decreased exercise capacity and 2) these responses are similar to those observed in patients with heart failure caused by other etiologies. Sixteen patients with heart failure with reduced ejection fraction related to anthracycline-based chemotherapy with or without chest radiation (HFrEFCA), 10 patients with heart failure with reduced ejection not related to cancer therapy (HFrEF), and 16 age-and body mass index (BMI)-matched healthy controls were studied. Left ventricular ejection fraction (LFEF, Echocardiography), peak oxygen consumption (peak V̇O2, cardiopulmonary exercise test), muscle sympathetic nerve activity (MSNA, microneurography) and forearm blood flow (FBF, venous occlusion plethysmography) were measured. We found that peak oxygen consumption peak V̇O2 and LVEF were significantly reduced in patients with HFrEFCA compared to controls (P<0.0001) but similar to those found in HFrEFCA patients. The sympathetic nerve activity burst frequency and incidence were significantly higher in patients with HFrEFCA than in controls (P<0.0001). No differences were found between HFrEF and HFrEFCA patients. Peak V̇O2 was inversely associated with MSNA burst frequency (r=-0.53, P=0.002) and burst incidence (r=-0.38, P=0.01), and directly associated with LVEF (r=0.71, P<0.0001). Taken together, we conclude that patients who develop heart failure due to anthracycline-based chemotherapy have sympathetic neural overdrive and reduced exercise capacity. In addition, these physiological changes are similar to those observed in patients with HFrEF.

Attenuated cardiac autonomic function in humans with high-affinity hemoglobin and compensatory polycythemia.

During hypoxic exposure, humans with high-affinity hemoglobin (and compensatory polycythemia) have blunted increases in heart rate compared with healthy humans with typical oxyhemoglobin dissociation curves. This response may be associated with altered autonomic control of heart rate. Our hypothesis-generating study aimed to investigate cardiac baroreflex sensitivity and heart rate variability among nine humans with high-affinity hemoglobin [6 females, O2 partial pressure at 50% [Formula: see text] (P50) = 16 ± 1 mmHg] compared with 12 humans with typical affinity hemoglobin (6 F, P50 = 26 ± 1 mmHg). Participants breathed normal room air for a 10-min baseline, followed by 20 min of isocapnic hypoxic exposure, designed to lower the arterial partial pressure O2 ([Formula: see text]) to ∼50 mmHg. Beat-by-beat heart rate and arterial blood pressure were recorded. Data were averaged in 5-min periods throughout the hypoxia exposure, beginning with the last 5 min of baseline in normoxia. Spontaneous cardiac baroreflex sensitivity and heart rate variability were determined using the sequence method and the time and frequency domain analyses, respectively. Cardiac baroreflex sensitivity was lower in humans with high-affinity hemoglobin than controls at baseline and during isocapnic hypoxic exposure (normoxia: 7 ± 4 vs. 16 ± 10 ms/mmHg, hypoxia minutes 15-20: 4 ± 3 vs. 14 ± 11 ms/mmHg; group effect: P = 0.02, high-affinity hemoglobin vs. control, respectively). Heart rate variability calculated in both the time (standard deviation of the N-N interval) and frequency (low frequency) domains was lower in humans with high-affinity hemoglobin than in controls (all P < 0.05). Our data suggest that humans with high-affinity hemoglobin may have attenuated cardiac autonomic function.

Heart rate surge at respiratory event termination in preterm and term born children with sleep disordered breathing

BackgroundRepetitive surges in heart rate (HR) at respiratory event termination underpin the altered autonomic HR control associated with sleep disordered breathing (SDB). As children born preterm are at greater risk of adverse cardiovascular outcomes, we aimed to determine whether the HR response to obstructive respiratory events was elevated compared to term-born children. MethodsFifty children (3–12 years) born preterm, were matched for SDB severity, age and gender with term born children. Multilevel modelling determined the effect of preterm birth and arousal on HR changes between a 10s baseline to the latter half of respiratory events and 15s post event during NREM and REM. Results1203 events were analysed (NREM: term 380; preterm 383; REM: term 207; preterm 233). During NREM fewer events terminated in arousal in the preterm compared with term group (preterm 68%; term 84%; χ2 = 27.2, p < 0.001). There were no differences in REM. During NREM, HR was lower in the preterm group at all event phases, with and without associated arousals (P < 0.01 for all). % change in HR from baseline to post event was higher in the preterm compared with term group (preterm: median 23% IQR (12%,34%); term: 18% (10%,29%); p < 0.01) and late event to post event (preterm: 30% (21%, 32%); term 28% (20%,39%); p < 0.01) in events associated with arousals. ConclusionThe greater magnitude of surges in HR following respiratory events terminating with arousal in preterm born children, although small, occur repeatedly throughout the night and may contribute to adverse cardiovascular outcomes, although further studies are required.

Respiratory Dysfunction in Parkinson's Disease: Relation with Dysautonomia.

Background:Parkinson's disease (PD) is a neurodegenerative disease perceived as a motor disorder. It is most commonly associated with autonomic dysfunction, affecting multiple systems. This altered autonomic control might be reflected by a parallel change in the airway caliber of these patients.Aim:To correlate the pulmonary impairment in patients with Parkinson's disease with the underlying dysautonomia.Materials and Methods:A total of 30 patients with Parkinson's disease participated in the study. Heart rate (HR) variability was recorded for 5 min to assess the autonomic dysfunction, followed by impulse oscillometry (IOS) and spirometry. IOS being an effort independent technique uses sound waves at different frequencies (5–25 Hz) to measure the airway impedance.Results:There was a significant decrease in SDSD (6.60 (10.18–6.01) vs. 12.22 (13.95–11.30); P = 0.04), RMSSD (6.59 (10.17–5.50) vs. 12.20 (13.93–11.28); P = 0.04), and total power (315.8 (506.3–120.7) vs. 771.3 (799.0–643.6); P = 0.04) in stage II as compared to stage I. Resistance at 20 Hz (R20) was found to be positively correlated with SDSD (r = 0.40, P = 0.04), RMSSD (r = 0.40, P = 0.04), and HF (r = 0.41, P = 0.03).Conclusion:Amongst the PD population, any changes in the parasympathetic component (responsible for bronchoconstriction) due to the underlying dysautonomia might be reflected as increased airway resistance in the pulmonary system.

Brain Cellular Senescence as a Potential Mediator of Angiotensin II‐Induced Hypertension

Hypertension affects 1 in 3 US adults and is a leading risk factor for heart attack and stroke. The peptide hormone angiotensin II (Ang II) is a well-recognized driver of hypertension, particularly through its sympathoexcitatory actions within the central nervous system (CNS). Although a number of pro-hypertensive CNS mechanisms (i.e. neurogenic hypertension) have been elucidated, including oxidative and endoplasmic reticulum stress, how these mechanisms translate into long-term alterations in CNS circuits remains unclear. Intriguingly, stress-associated pathways can culminate in cellular senescence and the senescence-associated secretory phenotype (SASP). Chronic senescence/SASP leads to marked changes in cell metabolism, macromolecule damage, and a pro-inflammatory environment. Based on this, we hypothesized that CNS cellular senescence may be a key contributor to neurogenic hypertension. We first performed a proof-of-principle experiment to determine if CNS cellular senescence is involved in blood pressure regulation. C57Bl/6J male mice were fitted with intracerebroventricular (ICV) cannulas and underwent implantation of radiotelemeters for conscious recording of cardiovascular parameters. Following surgical recovery, the senescence inducing agent doxorubicin (0.00125 mg) or vehicle control was administered daily over three days (n=3/group). Daily ICV administration of doxorubicin resulted in marked elevations in mean arterial blood pressure within 48 hours that were sustained throughout the study (72 hours: 107±1 vs. 123±1 mmHg; ICV vehicle vs. doxorubicin, p<0.05). Relative to controls, ganglionic blockade (i.p. chlorisondamine 12 mg/kg) elicited a greater fall in blood pressure in doxorubicin-treated animals (Δ-11±4 vs. Δ-56±6 mmHg; ICV vehicle vs. doxorubicin, p<0.05). Given these findings that CNS cellular senescence is associated with a hypertensive phenotype, likely through alterations in autonomic control of blood pressure, we next profiled cellular senescence in key cardioregulatory nuclei during hypertension development. Male C57Bl/6J mice were implanted with subcutaneous osmotic minipumps for chronic infusion of Ang II (600 ng/kg/min). Brains were collected at baseline and after 14 days of Ang II infusion (n=4-5/group) and micropunches of cardiovascular and autonomic nuclei including the organum vasculosum lamina terminalis (OVLT), subfornical organ (SFO), and paraventricular nucleus of the hypothalamus (PVN) were collected. Two-week infusion of Ang II resulted in a robust increase in the key senescent gene p16 (CDKN2A) in the SFO (6.1±0.8 fold baseline, p<0.05). Interestingly, Ang II-induced hypertension was not associated with changes in p16 in the OVLT (2.2±0.7 fold baseline, p=0.2) and PVN (1.5±0.4 fold baseline, p=0.4). Additionally, Ang II-induced senescence in the SFO was paralleled by the upregulation of SASP indicators (e.g. Interleukin-1α: 6.5±1.4 fold baseline, p<0.05). Together, these findings indicate that: 1) CNS cellular senescence is pro-hypertensive; and 2) Ang II elicits cellular senescence/SASP in the SFO. Collectively, our data may point to brain cellular senescence as a novel mediator of hypertension.

Autonomic Dysfunction Increases Cardiovascular Risk in the Presence of Sleep Apnea

The high prevalence of sleep apnea syndrome (SAS) and its direct relationship with an augmented risk of cardiovascular disease (CVD) have raised SAS as a primary public health problem. For this reason, extensive research aiming to understand the interaction between both conditions has been conducted. The advances in non-invasive autonomic nervous system (ANS) monitoring through heart rate variability (HRV) analysis have revealed an increased sympathetic dominance in subjects suffering from SAS when compared with controls. Similarly, HRV analysis of subjects with CVD suggests altered autonomic activity. In this work, we investigated the altered autonomic control in subjects suffering from SAS and CVD simultaneously when compared with SAS patients, as well as the possibility that ANS assessment may be useful for the early stage identification of cardiovascular risk in subjects with SAS. The analysis was performed over 199 subjects from two independent datasets during night-time, and the effects of the physiological response following an apneic episode, sleep stages, and respiration on HRV were taken into account. Results, as measured by HRV, suggest a decreased sympathetic dominance in those subjects suffering from both conditions, as well as in subjects with SAS that will develop CVDs, which was reflected in a significantly reduced sympathovagal balance (p < 0.05). In this way, ANS monitoring could contribute to improve screening and diagnosis, and eventually aid in the phenotyping of patients, as an altered response might have direct implications on cardiovascular health.

Cardiac Autonomic Function in Adults Born Preterm

To evaluate cardiac autonomic function in adults born preterm. We studied the association between prematurity and cardiac autonomic function using heart rate variability measurements in 600 adults (mean age of 23.3years) from a geographically based cohort in Northern Finland. There were 117 young adults born early preterm (<34weeks), 207 born late preterm (34-36weeks), and 276 born at term (≥37weeks, controls). Autonomic function was analyzed by calculating time and frequency domain heart rate variability measurements using linear regression. Compared with controls, the mean difference in root mean square of successive differences (indicating cardiac vagal activity) was -12.0% (95% CI -22.2%, -0.5%, adjusted for sex, age, source cohort, and season P=.04) for the early preterm group and -7.8% (-16.8%, 2.0%, P=.12) for the late preterm group. Mean differences with controls in low frequency power (indicating cardiac vagal activity, including some sympathetic- and baroreflex-mediated effects) were -13.6% (-26.7%, 1.8%, P=.08) for the early preterm group and -16.4% (-27.0%, -4.3%, P=.01) for the late preterm group. Mean differences in high frequency power (quantifying cardiac vagal modulation in respiratory frequency) were -19.2% (-36.6%, 2.9%, P=.09) for the early preterm group and -13.8% (-29.4%, 5.3%, P=.15) for the late preterm group. Differences were attenuated when controlled for body mass index and physical activity. Our results suggest altered autonomic regulatory control in adults born preterm, including those born late preterm. Altered autonomic regulatory control may contribute to increased cardiovascular risk in adults born preterm.

Sleep disordered breathing in children disrupts the maturation of autonomic control of heart rate and its association with cerebral oxygenation.

Sleep disordered breathing (SDB) affects 4-11% of children and is associated with adverse neurocognitive, behavioural and cardiovascular outcomes, including reduced autonomic control. The relationship between heart rate variability (HRV; a measure of autonomic control) and age found in non-snoring control children was absent during sleep in children with SDB. Age significantly predicted increasing cerebral oxygenation during wake in non-snoring control children, whereas during sleep, HRV significantly predicted decreasing cerebral oxygenation. Cerebral oxygenation was not associated with either age or HRV in children with SDB during both wake and sleep. SDB significantly disrupts the normal maturation of autonomic control and the positive association between autonomic control and cerebral oxygenation found in non-snoring children, and we speculate that the dampened autonomic control exhibited by children with SDB may have an attenuating effect on cerebral autoregulation via the moderating influence of HRV on cerebral blood flow. The repetitive episodes of hypoxia that are features of sleep disordered breathing (SDB) in children are associated with alterations in autonomic control of heart rate in an age-dependent manner. We aimed to relate heart rate variability (HRV) parameters to age and measures of cerebral oxygenation in children (3-12years old) with SDB and non-snoring controls. Children (SDB, n=117; controls, n=42; 3-12years) underwent overnight polysomnography. Total (TP), low- (LF) and high-frequency (HF) power, tissue oxygenation index (TOI) and fractional tissue oxygen extraction (FTOE) were analysed during wake and sleep. Pearson's correlations determined the association between age and HRV parameters, and multiple linear regressions between HRV, age and cerebral oxygenation parameters. During wake, age had a positive association with LF power, reflecting increased parasympathetic and sympathetic activity with increasing age for both control and SDB groups. This association was also evident during sleep in controls, but was absent in children with SDB. In controls, during wake TOI had a positive, and FTOE a negative association with age. During sleep, TP, LF and HF power were significant, negative determinants of TOI and positive determinants of FTOE. These associations were not seen in children with SDB during wake or sleep. SDB disrupts the normal maturation of the autonomic control of heart rate and the association between HRV and cerebral oxygenation exhibited by non-snoring control children of primary school age. These results highlight the impact SDB has on cardiovascular control and the potential impact on adverse cardiovascular outcomes.

Implication of altered autonomic control for orthostatic tolerance in SCI.

Neural output from the sympathetic and parasympathetic branches of the autonomic nervous system (ANS) are integrated to appropriately control cardiovascular responses during routine activities of daily living including orthostatic positioning. Sympathetic control of the upper extremity vasculature and the heart arises from the thoracic cord between T1 and T5, whereas splanchnic bed and lower extremity vasculature receive sympathetic neural input from the lower cord between segments T5 and L2. Although the vasculature is not directly innervated by the parasympathetic nervous system, the SA node is innervated by post-ganglionic vagal nerve fibers via cranial nerve X. Segmental differences in sympathetic cardiovascular innervation highlight the effect of lesion level on orthostatic cardiovascular control following spinal cord injury (SCI). Due to impaired sympathetic cardiovascular control, many individuals with SCI, particularly those with lesions above T6, are prone to orthostatic hypotension (OH) and orthostatic intolerance (OI). Symptomatic OH, which may result in OI, is a consequence of episodic reductions in cerebral perfusion pressure and the symptoms may include: dizziness, lightheadedness, nausea, blurred vision, ringing in the ears, headache and syncope. However, many, if not most, individuals with SCI who experience persistent and episodic hypotension and OH do not report symptoms of cerebral hypoperfusion and therefore do not raise clinical concern. This review will discuss the mechanism underlying OH and OI following SCI, and will review our knowledge to date regarding the prevalence, consequences and possible treatment options for these conditions in the SCI population.

Fractal analysis of heart rate variability reveals alterations of the integrative autonomic control of circulation in paraplegic individuals

The autonomic nervous system plays a major role in the integrative control of circulation, possibly contributing to the ‘complex’ dynamics responsible for fractal components in heart rate variability. Aim of this study is to evaluate whether an altered autonomic integrative control is identified by fractal analysis of heart rate variability. We enrolled 14 spinal cord injured individuals with complete lesion between the 5th and 11th thoracic vertebra (SCIH), 14 with complete lesion between 12th thoracic and 5th lumbar vertebra (SCIL), and 34 able-bodied controls (AB). These paraplegic subjects have an altered autonomic integrative regulation, but intact autonomic cardiac control and, as to SCIL individuals, intact autonomic splanchnic control. Power spectral and fractal analysis (temporal spectrum of scale coefficients) were performed on 10 min tachograms. AB and SCIL power spectra were similar, while the SCIL fractal spectrum had higher coefficients between 12 and 48 s. SCIH individuals had lower power than controls at 0.1 Hz; their fractal spectrum was morphologically different, diverging from that of controls at the largest scales (120 s). Therefore, when the lesion compromises the autonomic control of lower districts, fractal analysis reveals alterations undetected by power spectral analysis of heart rate variability.

Implications of altered autonomic control on sports performance in athletes with spinal cord injury.

It is well known that athletes with spinal cord injury (SCI) may experience altered autonomic physiology that impacts their exercise capacity and sports performance. This is particularly relevant given the ever-increasing number of individuals with SCI who are actively engaged in sports at all levels, from community-based adaptive sports to elite Paralympic competitions. As such, the purpose of this article is to review the present literature regarding the implications of altered autonomic control on the safety and performance of athletes with SCI. A particular emphasis will be placed on the autonomic aspects of cardiovascular and thermoregulatory control in the athlete population, as well as the implications of autonomic dysreflexia in enhancing sports performance. Further research is needed to understand the autonomic factors that influence athletes with SCI in order to ensure optimal and safe sports competition. Additionally, this information is crucially relevant to the coaches, sports administrators, and team medical staff who work closely with athletes with SCI.

Prenatal Exposure to Snus Alters Heart Rate Variability in the Infant.

Maternal use of smoked tobacco during pregnancy causes significant morbidity and mortality in the human infant including alterations in autonomic control with increased risk of sudden infant death syndrome. We hypothesized that maternal snus (smokeless tobacco) use during pregnancy affects autonomic cardiac regulation in the infant, as measured by heart rate variability (HRV) and the low frequency and high frequency ratio (LF/HF ratio). A prospective observational study of 56 infants of women who used snus (n = 23) or cigarettes (n = 13) during pregnancy versus tobacco- and nicotine-free controls (n = 19). The nicotine dose was estimated by questionnaires at 4 timepoints pre- and post-natally. The infants' urine cotinine concentration and HRV during 2 hours of sleep were studied 1-2 months after birth. LF/HF ratio was higher in snus (mean 3.31; 95% CI 2.78-3.83) and smoke (3.51;2.54-4.47) compared to controls (2.15; 1.76-2.54, p = .002). Early prenatal nicotine exposure "without" any further exposure increased the LF/HF ratio (3.19; 2.55-3.84, p = .02). Continuous prenatal nicotine exposure "without" postnatal exposure was also associated with a residual increase in LF/HF ratio (4.40; 3.38-5.42, p < .001). There was no difference between infants exposed to smokeless versus smoked tobacco, suggesting a common constituent (nicotine) altering autonomic cardiac regulation. Infants to mothers who used snus during pregnancy showed lower vagal activity with an increased LF/HF ratio compared to controls, and similar to infants of smokers. Even early prenatal exposure to snus has a lasting impact on autonomic cardiac regulation suggesting a fetal "re-programing" of the developing autonomic nervous system. The results indicate that smokeless tobacco (Swedish snus) affects the developing autonomic nervous system during gestation. Even if exposure is interrupted during the first or second trimester, effects in autonomic cardiac regulation are seen in the 1-2 month-old infant. This underlines the importance of abstaining from all types of tobacco use during the whole pregnancy. Our findings may also have more general relevance to other routes by which nicotine can be delivered to a fetus and newborn.

Alterations in cardiac autonomic control in spinal cord injury.

A spinal cord injury (SCI) interferes with the autonomic nervous system (ANS). The effect on the cardiovascular system will depend on the extent of damage to the spinal/central component of ANS. The cardiac changes are caused by loss of supraspinal sympathetic control and relatively increased parasympathetic cardiac control. Decreases in sympathetic activity result in heart rate and the arterial blood pressure changes, and may cause arrhythmias, in particular bradycardia, with the risk of cardiac arrest in those with cervical or high thoracic injuries. The objective of this review is to give an update of the current knowledge related to the alterations in cardiac autonomic control following SCI. With this purpose the review includes the following subheadings: 2. Neuro-anatomical plasticity and cardiac control 2.1 Autonomic nervous system and the heart 2.2 Alteration in autonomic control of the heart following spinal cord injury 3. Spinal shock and neurogenic shock 3.1 Pathophysiology of spinal shock 3.2 Pathophysiology of neurogenic shock 4. Autonomic dysreflexia 4.1 Pathophysiology of autonomic dysreflexia 4.2 Diagnosis of autonomic dysreflexia 5. Heart rate/electrocardiography following spinal cord injury 5.1 Acute phase 5.2 Chronic phase 6. Heart rate variability 6.1 Time domain analysis 6.2 Frequency domain analysis 6.3 QT-variability index 6.4 Nonlinear (fractal) indexes 7. Echocardiography 7.1 Changes in cardiac structure following spinal cord injury 7.2 Changes in cardiac function following spinal cord injury 8. International spinal cord injury cardiovascular basic data set and international standards to document the remaining autonomic function in spinal cord injury.

Influence of menopause on cardiovascular responses to behavioral stressors: A comparative study

Background: There is increased cardiovascular morbidity and mortality in post-menopausal women as compared to pre‑menopausal women. There is an altered autonomic control with a shift toward sympathetic hyperactivity in menopause. Abnormal autonomic activity, behavioral stressors, and estrogen deficiency are related with increased cardiovascular risk. However, the underlying cardiovascular mechanisms in menopause still remain unclear. Aims and Objectives: The aim of this study is to determine and compare the following parameters indicating cardiovascular sympathetic function status in pre-menopausal and post-menopausal women subjected to three behavioral stress tests: (i) Blood pressure (BP) response to sustained isometric handgrip test, (ii) BP response to cold pressor test, and (iii) BP response to standing from supine position (orthostasis). Materials and Methods: This was a cross-sectional study for which 150 pre-menopausal and 150 post-menopausal women were selected. They underwent three behavioral stress tests of sustained isometric handgrip test, cold pressor test, and orthostatic test. The parameters indicating cardiovascular sympathetic function status were determined. Statistical analysis was performed using Z-test. Results: Diastolic BP (DBP) response to sustained isometric handgrip and systolic BP (SBP) and DBP response to the cold pressor test showed statistically highly significant (P 0.05) greater fall in post-menopausal women. Conclusion: Sympathetic hyperactivity in response to behavioral stressors seen in post-menopausal women as compared to pre-menopausal women, suggests that the cardiovascular changes related to estrogen deficiency occurring in menopause may trigger adverse cardiovascular events.

Difficulties in diagnosis and treatment of severe secondary Raynaud’s phenomenon in a Cameroonian woman: a case report

BackgroundRaynaud’s phenomenon is a microvascular disorder that results in exaggerated vasoconstriction over vasodilatation secondary to an alteration in autonomic control. Though benign, it can result in severe ulceration and ultimately gangrene associated with disfiguration and permanent deformity. We present a case of severe secondary Raynaud’s phenomenon in a black-African patient from a resource-limited setting, with focus on the difficulties encountered in the diagnosis and treatment.Case presentationA 43-year-old female Cameroonian farmer with a 7-year history of episodic paresthesia in her fingers and toes (when exposed to cold) presented to our emergency department with severe pain, ulceration, and “darkening” of her fingertips over a period of 2 days. An examination revealed bilateral ulceration and dry gangrene of her fingers and toes, based on which a diagnosis of secondary Raynaud’s phenomenon due to a connective tissue disease was proposed. Results of paraclinical investigations were normal. Lifestyle modification along with a calcium channel blocker and phosphodiesterase type 5 inhibitor provided significant relief.ConclusionsAn early diagnosis and knowledge on appropriate treatment of Raynaud’s phenomenon is of vital importance to prevent permanent tissue damage and disability. Relying on biphasic color change for the diagnosis of Raynaud’s phenomenon in black Africans can be potentially misleading.

Alterations in autonomic cardiac modulation in response to normobaric hypoxia

Purpose: The present study aimed to determine if autonomic cardiac modulation was influenced by acute exposure to normobaric hypoxia. Method: Ten healthy male lowland dwellers completed five block-randomised single-blinded, crossed-over acute exposures to a normobaric hypoxic environment, each separated by 24 hours’ recovery (20.3%, 17.4%, 14.5%, 12.0% and 9.8% FIO2). Supine recordings were made of arterial oxygen saturation and electrocardiogram (ECG). RR intervals from the ECG trace were analysed for time (SDNN, lnrMSSD), frequency (lnVLF, lnLF, lnHF, lnTP, LFnu, and HFnu), and nonlinear (DFA-α1 and SampEn) heart rate variability components. Results: A significant reduction in arterial SaO2 occurred with reduced FIO2, along with a rise in heart rate (Cohen’s d = 1.16, 95% Confidence Interval [2.64–6.46]), significant at 9.8% FIO2. A decrease in autonomic cardiac modulation was also found as shown by a statistically significant (at 9.8% FIO2) decrease in lnTP (d = 1.84 [1.74–1.94]), and SampEn (d = 0.98 [0.83–1.12]) and an increase in DFA-α1 (d = 0.72 [0.60–0.84]) from normoxia at 9.8% FIO2. Conclusion: The decrease in variability indicated a reduction in autonomic cardiac modulation. There appears to be a threshold ∼9.8% FIO2 (∼6000 m equiv.), below which significant alterations in autonomic control occur.

Autonomic Cardiac Changes in Temporal Lobe Epilepsy

Background: epileptic patients suffer from many autonomic symptoms either during the seizure or in between seizures. Interictal autonomic cardiac changes may cause arrhythmia which may be life threatening. Aim of the work: to recognize the presence of cardiac autonomic changes in patients with temporal lobe epilepsy and to find the relation between autonomic cardiac changes and different variables. Patients and methods: Twenty patients with well controlled TLE and twenty patients with uncontrolled TLE were subjected to standard 12-lead ECG and 24 hour holter ECG. Results: QTc was significantly shorter in patients with uncontrolled TLE than in patients with well controlled TLE. Patients with uncontrolled TLE had a faster heart rate than patients with well controlled TLE. Patients with uncontrolled TLE showed significant less SDNN, rMSSD and PNN50 than those with well controlled seizures.On the other hand, LF and LF/HF ratio was significantly more in uncontrolled group than the controlled group. Conclusion: There is an interictal alteration in autonomic control of the heart in TLE. This alteration is corrected with proper control of seizures

Respiratory muscle strength effect on linear and nonlinear heart rate variability parameters in COPD patients.

IntroductionChronic obstructive pulmonary disease (COPD) is recognized as a multisystemic inflammatory disease associated with extrapulmonary comorbidities, including respiratory muscle weakness and cardiovascular and cardiac autonomic regulation disorders. We investigated whether alterations in respiratory muscle strength (RMS) would affect cardiac autonomic modulation in COPD patients.MethodsThis study was a cross-sectional study done in ten COPD patients affected by moderate to very severe disease. The heart rate variability (HRV) signal was recorded using a Polar cardiofrequencimeter at rest in the sitting position (10 minutes) and during a respiratory sinus arrhythmia maneuver (RSA-M; 4 minutes). Linear analysis in the time and frequency domains and nonlinear analysis were performed on the recorded signals. RMS was assessed using a digital manometer, which provided the maximum inspiratory pressure (PImax) and the maximum expiratory pressure (PEmax).ResultsDuring the RSA-M, patients presented an HRV power increase in the low-frequency band (LFnu) (46.9±23.7 vs 75.8±27.2; P=0.01) and a decrease in the high-frequency band (HFnu) (52.8±23.5 vs 24.0±27.0; P=0.01) when compared to the resting condition. Significant associations were found between RMS and HRV spectral indices: PImax and LFnu (r=−0.74; P=0.01); PImax and HFnu (r=0.74; P=0.01); PEmax and LFnu (r=−0.66; P=0.01); PEmax and HFnu (r=0.66; P=0.03); between PEmax and sample entropy (r=0.83; P<0.01) and between PEmax and approximate entropy (r=0.74; P=0.01). Using a linear regression model, we found that PImax explained 44% of LFnu behavior during the RSA-M.ConclusionCOPD patients with impaired RMS presented altered cardiac autonomic control, characterized by marked sympathetic modulation and a reduced parasympathetic response; reduced HRV complexity was observed during the RSA-M.

Increased vascular sympathetic modulation in mice with Mas receptor deficiency

Introduction:The angiotensin-converting enzyme 2 (ACE2)/angiotensin (Ang)-(1–7)/Mas axis could modulate the heart rate (HR) and blood pressure variabilities (BPV) which are important predictors of cardiovascular risk and provide information about the autonomic modulation of the cardiovascular system. Therefore we investigated the effect of Mas deficiency on autonomic modulation in wild type and Mas-knockout (KO) mice.Methods:Blood pressure was recorded at high sample rate (4000 Hz). Stationary sequences of 200–250 beats were randomly chosen. Frequency domain analysis of HR and BPV was performed with an autoregressive algorithm on the pulse interval sequences and on respective systolic sequences.Results:The KO group presented an increase of systolic arterial pressure (SAP; 127.26±11.20 vs 135.07±6.98 mmHg), BPV (3.54±1.54 vs 5.87±2.12 mmHg2), and low-frequency component of systolic BPV (0.12±0.11 vs 0.47±0.34 mmHg2).Conclusions:The deletion of Mas receptor is associated with an increase of SAP and with an increased BPV, indicating alterations in autonomic control. Increase of sympathetic vascular modulation in absence of Mas evidences the important role of Ang-(1–7)/Mas on cardiovascular regulation. Moreover, the absence of significant changes in HR and HRV can indicate an adaptation of autonomic cardiac balance. Our results suggest that the Ang-(1–7)/Mas axis seems more important in autonomic modulation of arterial pressure than HR.