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Philippe Van De Borne - One of the best experts on this subject based on the ideXlab platform.
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increased Peripheral Chemoreceptors sensitivity and exercise ventilation in heart transplant recipients
Circulation, 2006Co-Authors: Agnieszka Ciarka, Nicolas Cuylits, Jeanluc Vachiery, Michel Lamotte, Jeanpaul Degaute, Robert Naeije, Philippe Van De BorneAbstract:Background—Heart failure is characterized by increased ventilation during exercise, which is positively related to increased Peripheral and central chemoreceptor sensitivity. Heart transplantation does not normalize the ventilatory response to exercise, and its effects on the chemoreflex control of ventilation remain unknown. We tested the hypothesis that chemoreceptor sensitivity is increased in heart transplant recipients (HTRs) and linked to exercise hyperpnea. Methods and Results—We determined the ventilatory, muscle sympathetic nerve activity (MSNA), and circulatory responses to isocapnic hypoxia and hyperoxic hypercapnia 71 years after transplantation in 19 HTRs with a normal left ventricular ejection fraction of 602%. Results were compared with those of 11 closely matched referent subjects. Sixteen patients and 10 referent subjects also underwent cycle ergometer exercise tests. HTRs compared with referent subjects presented higher MSNA (524 versus 343 bursts/min; P0.01) and heart rates (833 versus 683 bpm; P0.01) during room air breathing. The ventilatory response to hypoxia was higher in HTRs than in referent subjects (P0.01, ANOVA). The increase in MSNA also was more marked during hypoxia in the HTRs than in the referent group (P0.05, ANOVA). Responses to hyperoxic hypercapnia did not differ between the HTRs and the referent group. The ventilatory response to exercise, characterized by the regression slope relating minute ventilation to CO2 output, was steeper in HTRs than in referent subjects (382 versus 291 L/mm Hg; P0.01). Exercise ventilation in HTRs was related to the ventilatory response to isocapnic hypoxia (r0.57; n16; P0.05) and to the ventilatory response to hyperoxic hypercapnia (r0.50; n16; P0.05). Conclusions—Peripheral chemoreceptor sensitivity is increased in HTRs and is related to exercise hyperpnea after heart transplantation. (Circulation. 2006;113:252-257.)
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effects of Peripheral Chemoreceptors deactivation on sympathetic activity in heart transplant recipients
Hypertension, 2005Co-Authors: Agnieszka Ciarka, Nicolas Cuylits, Jeanpaul Degaute, Boutaina Najem, Marc Leeman, Olivier Xhaet, Krzysztof Narkiewicz, Martine Antoine, Philippe Van De BorneAbstract:Heart transplantation initially normalizes sympathetic hyperactivity directed at the muscle circulation. However, sympathetic activity increases with time after transplantation and the exact mechanisms responsible for sympathetic control in heart transplant recipients remain unclear. We examined the effects of Peripheral chemoreflex deactivation caused by breathing 100% oxygen on muscle sympathetic nerve activity (expressed as number of burst per minute and mean burst amplitude), heart rate, and mean blood pressure in 13 heart transplant recipients, 13 patients with essential hypertension, and 10 controls. Heart transplant recipients disclosed the highest sympathetic activity, whereas it did not differ between controls and patients with essential hypertension (5116 versus 3714 versus 3912 burst/min, respectively; P0.05). Breathing 100% oxygen, in comparison with 21% oxygen, reduced sympathetic activity (44 versus 12 burst/min, P0.01; 859 versus1018% of amplitude at baseline, P0.001) and mean blood pressure (45 versus 36 mm Hg; P0.05) in heart transplant recipients, decreased sympathetic activity (44 versus 03 burst/min, P0.05; 9016 versus1019% of amplitude at baseline, P0.05) in patients with essential hypertension, but did not reduce sympathetic activity (24 versus 33 burst/min, PNS; 9511 versus 9513% of amplitude at baseline, PNS) in control subjects. The sympathetic response to hyperoxia was more marked in heart transplant recipients than in controls (859 versus 9511% of baseline amplitude; P0.05). The decrease in sympathetic activity was most evident in patients with the longest time after heart transplantation (r0.75, P0.01). In conclusion, tonic chemoreflex activation increases resting muscle sympathetic nerve activity and favors blood pressure elevation after heart transplantation. (Hypertension. 2005;45:894-900.)
Curtis A Smith - One of the best experts on this subject based on the ideXlab platform.
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Peripheral Chemoreceptors determine the respiratory sensitivity of central Chemoreceptors to co2 role of carotid body co2
The Journal of Physiology, 2015Co-Authors: Curtis A Smith, Gregory M Blain, K S Henderson, Jerome A DempseyAbstract:We asked if the type of carotid body (CB) chemoreceptor stimulus influenced the ventilatory gain of the central Chemoreceptors to CO2. The effect of CB normoxic hypocapnia, normocapnia and hypercapnia (carotid body ≈ 22, 41 and 68 mmHg, respectively) on the ventilatory CO2 sensitivity of central Chemoreceptors was studied in seven awake dogs with vascularly-isolated and extracorporeally-perfused CBs. Chemosensitivity with one CB was similar to that in intact dogs. In four CB-denervated dogs, absence of hyper-/hypoventilatory responses to CB perfusion with of 19–75 mmHg confirmed separation of the perfused CB circulation from the brain. The group mean central CO2 response slopes were increased 303% for minute ventilation ()(P ≤ 0.01) and 251% for mean inspiratory flow rate (VT/TI) (P ≤ 0.05) when the CB was hypercapnic vs. hypocapnic; central CO2 response slopes for tidal volume (VT), breathing frequency (fb) and rate of rise of the diaphragm EMG increased in 6 of 7 animals but the group mean changes did not reach statistical significance. Group mean central CO2 response slopes were also increased 237% for (P ≤ 0.01) and 249% for VT/TI(P ≤ 0.05) when the CB was normocapnic vs. hypocapnic, but no significant differences in any of the central ventilatory response indices were found between CB normocapnia and hypercapnia. These hyperadditive effects of CB hyper-/hypocapnia agree with previous findings using CB hyper-/hypoxia.We propose that hyperaddition is the dominant form of chemoreceptor interaction in quiet wakefulness when the chemosensory control system is intact, response gains physiological, and carotid body Chemoreceptors are driven by a wide range of O2 and/or CO2. Key points The influence of specific carotid body (CB) normoxic hypocapnia, hypercapnia and normocapnia on the ventilatory sensitivity of central Chemoreceptors to systemic hypercapnia was assessed in seven awake dogs with extracorporeal perfusion of the vascularly isolated CB. Chemosensitivity in this preparation was similar to that in the intact animal. Separation of CB circulation from that of the brain was confirmed. When the isolated CB was hypercapnic vs. hypocapnic and when the isolated CB was normocapnic vs. hypocapnic, the group mean central CO2 response slopes of minute ventilation () (P ≤ 0.01) and mean inspiratory flow rate (VT/TI) (P ≤ 0.05) increased significantly. Tidal volume (VT), breathing frequency (fb)and rate of rise of diaphragm EMG were increased in 6 of 7 dogs but did not achieve statistical significance. We propose that hyperaddition is the dominant form of chemoreceptor interaction under conditions of quiet wakefulness in intact animals and over a wide range of CB and . Introduction Peripheral–central chemoreceptor interactive effects on control of breathing have been observed using animal models with isolated perfusion of the carotid body and/or central Chemoreceptors in such varied conditions as eupnoea, apnoea, hypercapnia, and hypoxia (Day & Wilson, 2007,2009; Smith et al. 2007,2010; Blain et al. 2009,2010; Dempsey et al. 2012; Fiamma et al. 2013). However, the exact nature of these chemoreceptor interactions are controversial with studies in a wide variety of experimental preparations and theoretical models claiming additive, hyperadditive, or hypoadditive effects on the control of breathing (Duffin, 1990; Duffin & Mateika, 2013; Teppema & Smith, 2013; Wilson & Day, 2013). Based on these divergent findings some investigators (Wilson & Day, 2013; Guyenet, 2014) have suggested a ‘hybrid’ model as a basis for Peripheral–central interaction, whereby variations in both the experimental models and in the prevailing physiological conditions and/or chemoreceptor stimuli may markedly alter the nature of the chemoreceptor interactions (also see Discussion). Accordingly, in the present study we have tested the nature of the Peripheral–central interaction under novel experimental conditions consisting of hypercapnic stimulation and hypocapnic inhibition at the level of the isolated CB chemoreceptor. This represents an important advance in addressing the interaction problem for several reasons. First, comparing normoxic hypercapnia/hypocapnia to results from our prior use of hypoxia/hyperoxia at the carotid body (Blain et al. 2010) provides a test of the equivalence of the observed hyperadditive interactive effect in the presence of both major Peripheral chemoreceptor stimuli, i.e. CO2 and O2. Second, perturbations in per se have widespread physiological significance in the control of breathing and breathing stability during wakefulness and sleep, which appear to depend critically upon Peripheral–central chemoreceptor interactions (Smith et al. 2007; Dempsey et al. 2012; Fiamma et al. 2013). Third, we tested these interactive effects in a unique awake canine preparation which incorporates two essential characteristics for quantifying the nature of these interactions, namely (a) that the preparation’s chemoresponsiveness is within the physiological range and close to that in the intact animal, and (b) that central and Peripheral Chemoreceptors are truly separated both anatomically and functionally. Fourth, although there is no direct evidence we are aware of that the carotid sinus nerve discharge pattern can encode information concerning the nature of the carotid body stimulus, there are some lines of evidence showing that carotid body hypercapnia might have quite different cardiorespiratory influences from carotid body hypoxaemia. For example, in the awake goat, carotid body hypoxia, even for very short periods beyond the acute phase, progressively increased the ventilatory response whereas specific carotid body hypercapnia did not (Bisgard et al. 1986). In anesthetized goats short periods of hypoxia sensitized output of the carotid body chemoreceptor (Nielsen et al. 1988), whereas hypercapnia did not (Engwall et al. 1988). In anaesthetized rats, carotid body denervation prevented the response of CO2 sensitive neurons in the retrotrapezoid nucleus to very brief exposures of reduced , but had no effect on their response to inhaled CO2(Mulkey et al. 2004). In anaesthetized rats conditioned by exposure to chronic intermittent hypoxia for 10 days, acute intermittent hypoxia elicited long-term facilitation of carotid sinus nerve output whereas acute intermittent hyperoxic hypercapnia did not (Peng et al. 2003). Further, in awake humans, acute periods of arterial isocapnic hypoxaemia or asphyxia elicited marked lingering after-effects on muscle sympathetic nerve activity once the stimulus was removed whereas similar periods of arterial normoxic hypercapnia did not (Morgan et al. 1995; Xie et al. 2000,2001). We found that, in the awake dog, specific carotid body stimulation/inhibition by means of hyper- or hypocapnia resulted in hyperadditive interaction when the central Chemoreceptors were stimulated by means of increased . The similarity of these hyperadditive interactions to those caused primarily by means of changes in carotid body suggest that short-term changes in and at the carotid body have equivalent effects on Peripheral–central interaction for a given change in baseline ventilation.
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Role of central/Peripheral Chemoreceptors and their interdependence in the pathophysiology of sleep apnea.
Advances in Experimental Medicine and Biology, 2012Co-Authors: Jerome A Dempsey, Curtis A Smith, Gregory M Blain, Yuansheng Gong, Mihaela TeodorescuAbstract:Unstable periodic breathing with intermittent ventilatory overshoots and undershoots commonly occurs in chronic heart failure, in hypoxia, with chronic opioid use and in certain types of obstructive sleep apnea. Sleep promotes breathing instability because it unmasks a highly sensitive dependence of the respiratory control system on chemoreceptor input, because transient cortical arousals promote ventilatory overshoots and also because upper airway dilator muscle tonicity is reduced and airway collapsibility enhanced. We will present data in support of the premise that carotid Chemoreceptors are essential in the pathogenesis of apnea and periodicity; however it is the hyperadditive influence of Peripheral chemoreceptor sensory input on central chemosensitivity that accounts for apnea and periodic breathing. This chemoreceptor interdependence also provides a significant portion of the normal drive to breathe in normoxia (i.e. eupnea) and in acute hypoxia. Finally, we discuss the effects of preventing transient hypocapnia (via selective increases in FICO2) on centrally mediated types of periodic breathing and even some varieties of cyclical obstructive sleep apnea.
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role of central Peripheral Chemoreceptors and their interdependence in the pathophysiology of sleep apnea
Advances in Experimental Medicine and Biology, 2012Co-Authors: Jerome A Dempsey, Curtis A Smith, Gregory M Blain, Yuansheng Gong, Mihaela TeodorescuAbstract:Unstable periodic breathing with intermittent ventilatory overshoots and undershoots commonly occurs in chronic heart failure, in hypoxia, with chronic opioid use and in certain types of obstructive sleep apnea. Sleep promotes breathing instability because it unmasks a highly sensitive dependence of the respiratory control system on chemoreceptor input, because transient cortical arousals promote ventilatory overshoots and also because upper airway dilator muscle tonicity is reduced and airway collapsibility enhanced. We will present data in support of the premise that carotid Chemoreceptors are essential in the pathogenesis of apnea and periodicity; however it is the hyperadditive influence of Peripheral chemoreceptor sensory input on central chemosensitivity that accounts for apnea and periodic breathing. This chemoreceptor interdependence also provides a significant portion of the normal drive to breathe in normoxia (i.e. eupnea) and in acute hypoxia. Finally, we discuss the effects of preventing transient hypocapnia (via selective increases in FICO2) on centrally mediated types of periodic breathing and even some varieties of cyclical obstructive sleep apnea.
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Peripheral Chemoreceptors determine the respiratory sensitivity of central Chemoreceptors to co2
The Journal of Physiology, 2010Co-Authors: Curtis A Smith, Gregory M Blain, K S Henderson, Jerome A DempseyAbstract:We assessed the contribution of carotid body Chemoreceptors to the ventilatory response to specific CNS hypercapnia in eight unanaesthetized, awake dogs. We denervated one carotid body (CB) and used extracorporeal blood perfusion of the reversibly isolated remaining CB to maintain normal CB blood gases (normoxic, normocapnic perfusate), to inhibit (hyperoxic, hypocapnic perfusate) or to stimulate (hypoxic, normocapnic perfusate) the CB chemoreflex, while the systemic circulation, and therefore the CNS and central Chemoreceptors, were exposed consecutively to four progressive levels of systemic arterial hypercapnia via increased fractional inspired CO2 for 7 min at each level. Neither unilateral CB denervation nor CB perfusion, per se, affected breathing. Relative to CB control conditions (normoxic, normocapnic perfusion), we found that CB chemoreflex inhibition decreased the slope of the ventilatory response to CNS hypercapnia in all dogs to an average of 19% of control values (range 0–38%; n= 6), whereas CB chemoreflex stimulation increased the slope of the ventilatory response to CNS hypercapnia in all dogs to an average of 223% of control values (range 204–235%; n= 4). We conclude that the gain of the CNS CO2/H+ Chemoreceptors in dogs is critically dependent on CB afferent activity and that CNS–CB interaction results in hyperadditive ventilatory responses to central hypercapnia.
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contributions of central and Peripheral Chemoreceptors to the ventilatory response to co2 h
Journal of Applied Physiology, 2010Co-Authors: H V Forster, Curtis A SmithAbstract:The major objective of this review is to evaluate existing information and reach conclusions regarding whether there is interaction between Pco2/H+ stimulation of carotid (Peripheral) and intracran...
Luigi Matturri - One of the best experts on this subject based on the ideXlab platform.
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Peripheral Chemoreceptors postnatal development and cytochemical findings in sudden infant death syndrome
Histology and Histopathology, 2008Co-Authors: Andrea Porzionato, Luigi Matturri, A Parenti, De Caro RAbstract:The aim of the present study is to give a review of the postnatal development of Peripheral Chemoreceptors - carotid body, paraganglia, and pulmonary neuroendocrine cells (PNEC) - with implications in Sudden Infant Death Syndrome (SIDS). In the postnatal period, the hypoxic chemosensitivity of the carotid body gradually develops. Changes include proliferation of type I and II cells, increased numbers of dense core vesicles and K+ channels, and modifications of neurotransmitter/neuromodulator and receptor expression. Chromaffin paraganglia show increased expression of nitric oxide synthase and neuropeptides, and increased innervation. Innervation of PNEC develops fully only in the first postnatal period, after which their density falls. The neuropeptides produced by PNEC also changes, with increased expression of calcitonin gene-related peptide and neuropeptide YY and reduced expression of calcitonin and gastrin-releasing peptide. Most of the findings in the carotid body of SIDS victims, i.e., decrease in type I cells and dense cytoplasmic granules, and increase in progenitor cells, indicates immaturity of the carotid body, which may play a role in SIDS in the form of underlying biologic vulnerability. Aorticopulmonary paraganglia hyperplasia and increase of PNEC are also found in SIDS, and may be epiphenomena of alterations of the respiratory function with a pathogenetical role in SIDS. A comprehensive view of the pathogenesis of SIDS should also arise from the integration of Peripheral Chemoreceptors findings with neuro- and cardiopathologic ones.
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Peripheral Chemoreceptors and sudden infant death syndrome a wide open problem
Current Cardiology Reviews, 2005Co-Authors: Luigi Matturri, Giulia Ottaviani, Anna Maria Lavezzi, Simone G RamosAbstract:This review will focus on the basic mechanisms of the Peripheral Chemoreceptors elicited by studies on mature Chemoreceptors and on the alterations observed in these structures related to sudden infant death. The integrated response of the Peripheral Chemoreceptors consists of the transduction of alterations in the chemical milieu, regulating the temperature of their environment to alterations in cardiovascular and respiratory performance. Over the years, much has been written about the relative importance of the carotid and aortic bodies in the Peripheral chemoreceptor response, and it is therefore worthwhile to consider the current state-of-the-art on that issue. Several lines of evidence have suggested that abnormalities in chemoreception may play a role in central hypoventilation syndromes. The sudden infant death syndrome (SIDS) involves a failure of respiration and affects infants in their early postnatal months. Unstable respiratory activity during sleep, prolonged sleep apnea, and oropharyngeal/laryngeal dysfunction induced by liquid stimulation of the upper airways have been postulated to be implicated in its genesis. It has also been found that in comparison with normal infants, infants suffering from the “aborted syndrome” (near-miss infants) are hypoventilated during quiet sleep, and have an impaired ventilatory response to carbon dioxide breathing.
Andrea Porzionato - One of the best experts on this subject based on the ideXlab platform.
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central and Peripheral Chemoreceptors in sudden infant death syndrome
The Journal of Physiology, 2018Co-Authors: Andrea Porzionato, Veronica Macchi, Raffaele De CaroAbstract:: The pathogenesis of sudden infant death syndrome (SIDS) has been ascribed to an underlying biological vulnerability to stressors during a critical period of development. This paper reviews the main data in the literature supporting the role of central (e.g. retrotrapezoid nucleus, serotoninergic raphe nuclei, locus coeruleus, orexinergic neurons, ventral medullary surface, solitary tract nucleus) and Peripheral (e.g. carotid body) Chemoreceptors in the pathogenesis of SIDS. Clinical and experimental studies indicate that central and Peripheral Chemoreceptors undergo critical development during the initial postnatal period, consistent with the age range of SIDS (<1 year). Most of the risk factors for SIDS (gender, genetic factors, prematurity, hypoxic/hyperoxic stimuli, inflammation, perinatal exposure to cigarette smoke and/or substance abuse) may structurally and functionally affect the developmental plasticity of central and Peripheral Chemoreceptors, strongly suggesting the involvement of these structures in the pathogenesis of SIDS. Morphometric and neurochemical changes have been found in the carotid body and brainstem respiratory Chemoreceptors of SIDS victims, together with functional signs of chemoreception impairment in some clinical studies. However, the methodological problems of SIDS research will have to be addressed in the future, requiring large and highly standardized case series. Up-to-date autopsy protocols should be produced, involving substantial, and exhaustive sampling of all potentially involved structures (including Peripheral arterial Chemoreceptors). Morphometric approaches should include unbiased stereological methods with three-dimensional probes. Prospective clinical studies addressing functional tests and risk factors (including genetic traits) would probably be the gold standard, allowing markers of intrinsic or acquired vulnerability to be properly identified.
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Central and Peripheral Chemoreceptors in sudden infant death syndrome.
The Journal of Physiology, 2018Co-Authors: Andrea Porzionato, Veronica Macchi, Raffaele De CaroAbstract:: The pathogenesis of sudden infant death syndrome (SIDS) has been ascribed to an underlying biological vulnerability to stressors during a critical period of development. This paper reviews the main data in the literature supporting the role of central (e.g. retrotrapezoid nucleus, serotoninergic raphe nuclei, locus coeruleus, orexinergic neurons, ventral medullary surface, solitary tract nucleus) and Peripheral (e.g. carotid body) Chemoreceptors in the pathogenesis of SIDS. Clinical and experimental studies indicate that central and Peripheral Chemoreceptors undergo critical development during the initial postnatal period, consistent with the age range of SIDS (
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Peripheral Chemoreceptors postnatal development and cytochemical findings in sudden infant death syndrome
Histology and Histopathology, 2008Co-Authors: Andrea Porzionato, Luigi Matturri, A Parenti, De Caro RAbstract:The aim of the present study is to give a review of the postnatal development of Peripheral Chemoreceptors - carotid body, paraganglia, and pulmonary neuroendocrine cells (PNEC) - with implications in Sudden Infant Death Syndrome (SIDS). In the postnatal period, the hypoxic chemosensitivity of the carotid body gradually develops. Changes include proliferation of type I and II cells, increased numbers of dense core vesicles and K+ channels, and modifications of neurotransmitter/neuromodulator and receptor expression. Chromaffin paraganglia show increased expression of nitric oxide synthase and neuropeptides, and increased innervation. Innervation of PNEC develops fully only in the first postnatal period, after which their density falls. The neuropeptides produced by PNEC also changes, with increased expression of calcitonin gene-related peptide and neuropeptide YY and reduced expression of calcitonin and gastrin-releasing peptide. Most of the findings in the carotid body of SIDS victims, i.e., decrease in type I cells and dense cytoplasmic granules, and increase in progenitor cells, indicates immaturity of the carotid body, which may play a role in SIDS in the form of underlying biologic vulnerability. Aorticopulmonary paraganglia hyperplasia and increase of PNEC are also found in SIDS, and may be epiphenomena of alterations of the respiratory function with a pathogenetical role in SIDS. A comprehensive view of the pathogenesis of SIDS should also arise from the integration of Peripheral Chemoreceptors findings with neuro- and cardiopathologic ones.
Piotr Niewinski - One of the best experts on this subject based on the ideXlab platform.
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carotid body modulation in systolic heart failure from the clinical perspective
The Journal of Physiology, 2017Co-Authors: Piotr NiewinskiAbstract:Augmented sensitivity of Peripheral Chemoreceptors (PChS) is a common finding in systolic heart failure (HF). It is related to lower left ventricle systolic function, higher plasma concentrations of natriuretic peptides, worse exercise tolerance and greater prevalence of atrial fibrillation compared to patients with normal PChS. The magnitude of ventilatory response to the activation of Peripheral Chemoreceptors is proportional to the level of heart rate (tachycardia) and blood pressure (hypertension) responses. All these responses can be measured non-invasively in a safe and reproducible fashion using different methods employing either hypoxia or hypercapnia. Current interventions aimed at modulation of Peripheral Chemoreceptors in HF are focused on carotid bodies (CBs). There is a clear link between afferent signalling from CBs and sympathetic overactivity, which remains the priority target of modern HF treatment. However, CB modulation therapies may face several potential obstacles: (1) As evidenced by HF trials, an excessive inhibition of sympathetic system may be harmful. (2) Proximity of critical anatomical structures (important vessels and nerves) makes surgical and transcutaneous interventions on CB technically demanding. (3) Co-existence of atherosclerosis in the area of carotid artery bifurcation increases the risk of central embolic events related to CB modulation. (4) The relative contribution of CBs vs. aortic bodies to sympathetic activation in HF patients is unclear. (5) Choosing optimal candidates for CB modulation from the population of HF patients may be problematic. (6) There is a risk of nocturnal hypoxia following CB ablation - mostly after bilateral procedures and in patients with concomitant obstructive sleep apnoea.
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carotid body removal for treatment of chronic systolic heart failure
International Journal of Cardiology, 2013Co-Authors: Piotr Niewinski, Ewa A Jankowska, Dariusz Janczak, A Rucinski, Przemyslaw Jazwiec, Paul A Sobotka, Zoar J Engelman, Marat Fudim, Stanislaw Tubek, Waldemar BanasiakAbstract:Abstract Background Augmented reflex response from Peripheral Chemoreceptors characterises chronic heart failure (CHF), contributes to autonomic imbalance and exercise intolerance and predicts poor outcome. Methods and results We present a case of a 56-year-old male patient with ischaemic CHF, who underwent surgical, unilateral carotid body resection to reduce Peripheral chemosensitivity. At 2-month and 6-month follow-ups, we document a persistent decrease in Peripheral chemosensitivity accompanied by an improvement in exercise capacity, sleep disordered breathing and quality of life. Autonomic balance was favourably affected as evidenced by improved heart rate variability and augmented cardiac baroreflex sensitivity. There were no procedure-related adverse events. Conclusions Denervation of a carotid body may offer a clinical strategy to restore autonomic balance and improve morbidity in heart failure (NCT01653821).