Search

Despite international efforts to identify biomarkers of depression, none has been transferred to clinical practice, neither for diagnosis, evolution, nor therapeutic response. This led us to build a French national cohort (through the clinical and research network named SoPsy within the French biological psychiatry society (AFPBN) and sleep society (SFRMS)), to better identify markers of sleep and biological rhythms and validate more homogeneous subgroups of patients, but also to specify the manifestations and pathogeneses of depressive disorders. Before inclusions, we sought to provide a predefined, standardized, and robust set of data to be collected in all centers.A Delphi process was performed to achieve consensus through the independent rating of invited experts, the SoPsy-depression co-investigators (n=34). The initial set open for vote included 94 questionnaires targeting adult and child psychiatry, sleep and addiction.Two questionnaire rounds were completed with 94% participation in the first round and 100% participation in the second round. The results of the Delphi survey incorporated the consensus opinion of the 32 members who completed both rounds. Nineteen of the 94 questionnaires achieved consensus at the first round and seventy of 75 at the second round. The five remaining questionnaires were submitted to three experts involved in the steering committee during a dedicated meeting. At the end, 24 questionnaires were retained in the mandatory and 26 in the optional questionnaire set.A validated data collection set of questionnaires is now available to assess psychiatry, addiction, sleep and chronobiology dimensions of depressive disorders.

Sleep health is a major public health concern because of its correlation with physical and mental health, and it may be particularly altered in medical students. This study aims: i) to examine the sleep characteristics of French medical students and their knowledge about basic sleep hygiene rules and; ii) to examine the correlations between sleep quality and academic performances, as well as between sleep quality and sleep knowledge.Students from 4th, 5th and 6th years of medicine, of the Faculty of Paris Diderot, voluntarily responded to an online questionnaire including PSQI and multiple-choice quizzes (MCQ) about basic sleep hygiene rules.From the 177 participants, 49.7% had a poor sleep (PSQI5). Regarding sleep latency, 44.6% needed30min to fall asleep at least once a week, 26.5% slept 6 hours or less by night, 42.4% of them qualified their sleep quality as bad or very bad. A serious lack of knowledge about basic sleep hygiene rules was observed, with an average score at the MCQ of 6.61/10, and only 31% of medical students were aware of basic good sleep habits. Significant correlations were observed between sleep efficiency and all academic mean scores (both regarding the morning, afternoon, and pooled mean scores), and between sleep disturbances and the morning mean score.French medical students have a poor sleep quality, correlating with academic performances, and present a poor knowledge of basic sleep rules. These findings are a call to improve medical training schedules and to develop prevention and training programs.

El ronquido es frecuente. Se relaciona con el colapso faringeo durante el sueno y, dependiendo de la intensidad del colapso, se observaran ronquidos simples, limitaciones del flujo inspiratorio, hipopneas y apneas. El sindrome de apnea-hipopnea obstructiva del sueno (SAHOS) se define como una cantidad de apneas y/o hipopneas mayores a cinco por hora, siendo el SAHOS grave si el indice de apnea-hipopnea (IAH) es superior a 30 por hora. Frente a los ronquidos, es importante descartar el SAHOS debido a sus importantes consecuencias para la salud: somnolencia con riesgo de accidentes, repercusion cardiovascular (hipertension arterial [HTA], trastornos del ritmo, etc.) y metabolica (diabetes, hepatitis esteatosica, etc.). El diagnostico se basa en los registros realizados durante el sueno: completos (polisomnografia) o con evaluacion solo de los parametros cardiorrespiratorios (poligrafia). El uso de una u otra de estas exploraciones tiene en cuenta los sintomas del paciente y la sospecha de patologias del sueno asociadas. Las posibilidades terapeuticas son multiples y dependen de la gravedad de la roncopatia: cirugia de reduccion tisular de tipo palatoplastia para ronquidos simples, ortesis de avance mandibular o ventilacion nocturna con presion positiva para SAHOS moderado o grave, etc. Las indicaciones deben discutirse de forma consensuada. Las medidas higienico-dieteticas siempre deben combinarse, asi como el tratamiento global del paciente, teniendo en cuenta el riesgo cardiovascular y metabolico.

Resume En plus de l’impact psychologique du confinement et de l’epidemie, il existe des repercussions sur le sommeil qu’il faut prendre en compte par la mise en place de strategies adaptees afin de maintenir un bon etat de sante mental et de sante general. Le confinement peut desorganiser le sommeil en impactant, d’une part, les rythmes circadiens par une diminution de l’intensite des synchroniseurs exterieurs et, d’autre part, peut favoriser l’insomnie dans cette periode de stress aigu. Enfin, le confinement peut etre source d’une privation de sommeil chez ceux qui sont en premiere ligne et qui gerent la crise. De plus, chez les enfants/adolescents le confinement peut egalement destructurer les journees et ainsi avoir un impact sur la sante en generale. Pour cela, il est important de mettre en place certaines strategies de preventions de ces perturbations de sommeil afin d’attenuer l’impact psychologique, infectieux et faire face de maniere optimale a cette situation que nous vivons tous.

Restless legs syndrome, also called Willis-Ekbom disease, is a frequent sensorimotor disease, more often encountered in women than men. It is characterized by an urge to move legs, during the evening or the beginning of the night, increased by rest and relieved by movement. Two forms are classically distinguished: primary restless legs syndrome occurring in young adults with family history and secondary forms occurring in older adults with comorbidities such as iron deficiency, chronic renal failure or neurological diseases (affecting central or peripheral nervous system). The clinical impact of the urge to move the legs may be major, including in particular sleep disorders which can profoundly alter the quality of life. Pathophysiology of restless legs syndrome still remains partially understood and probably relies on dopamine metabolism abnormality secondary to cerebral iron deficiency in genetically susceptible patients. That's why, besides nutritional and sleep hygiene advices, treatment of restless legs syndrome includes iron supplementation if there is an iron deficiency. Pharmacological treatment, for severe to very severe forms, includes use of dopamine agonists, antiepileptic drugs or opioids. These medications have numerous side effects and each prescription has to be individually customized for each patient.

Il russamento e comune. E correlato al collasso faringeo durante il sonno e, a seconda dell’importanza di quest’ultimo, si osserveranno un russamento semplice, delle limitazioni del flusso inspiratorio e delle apnee. La sindrome da apnea-ipopnea ostruttiva del sonno (SAHOS) e definita da un numero di apnee e/o ipopnee superiori a 5 all’ora, con una SAHOS grave se l’indice di apnea-ipopnea (IAH) e superiore a 30 all’ora. Di fronte al russamento, e importante eliminare la SAHOS, a causa delle sue importanti conseguenze sulla salute: sonnolenza con rischio di incidente e ripercussione cardiovascolare (ipertensione arteriosa, disturbi del ritmo, ecc.) e metabolica (diabete, epatite steatosica, ecc.). La diagnosi si basa su registrazioni fatte durante il sonno: complete (polisonnografia) o registrando solo i parametri cardiorespiratori (poligrafia). L’uso di uno di questi due esami tiene conto dei sintomi del paziente e del sospetto di patologie del sonno associate. Le possibilita terapeutiche sono molteplici e dipendono dalla gravita della roncopatia: chirurgia di riduzione tissutale tipo palatoplastica per un russamento semplice, ortesi avanzata mandibolare o ventilazione notturna a pressione positiva per una SAHOS da moderata a grave e cosi via. Le indicazioni devono essere discusse collegialmente. Le misure sullo stile di vita devono sempre essere associate, cosi come la gestione complessiva del paziente, tenendo conto del rischio cardiovascolare e metabolico.

Restless legs syndrome, also called Willis-Ekbom disease, is a frequent sensorimotor disease, more often encountered in women than men. It is characterized by an urge to move legs, during the evening or the beginning of the night, increased by rest and relieved by movement. Two forms are classically distinguished: primary restless legs syndrome occurring in young adults with family history and secondary forms occurring in older adults with comorbidities such as iron deficiency, chronic renal failure or neurological diseases (affecting central or peripheral nervous system). The clinical impact of the urge to move the legs may be major, including in particular sleep disorders which can profoundly alter the quality of life. Pathophysiology of restless legs syndrome still remains partially understood and probably relies on dopamine metabolism abnormality secondary to cerebral iron deficiency in genetically susceptible patients. That's why, besides nutritional and sleep hygiene advices, treatment of restless legs syndrome includes iron supplementation if there is an iron deficiency. Pharmacological treatment, for severe to very severe forms, includes use of dopamine agonists, antiepileptic drugs or opioids. These medications have numerous side effects and each prescription has to be individually customized for each patient.

Introduction Le syndrome d’hypoventilation alveolaire centrale congenitale se manifeste par l’hypoventilation au cours du sommeil et la perte de la chemosensibilite au CO2. Il est cause par des mutations a expansion d’alanine du facteur de transcription Phox2b. In vitro, cette mutation provoque des agregats proteiques cytoplasmiques et une perte d’activite transcriptionnelle. Ces anomalies sont diminuees par un traitement des cellules par la geldanamycine, inhibiteur de HSP 90. Nous avons teste l’efficacite d’un de ses derives hydrosoluble (17-DMAG) chez la souris Phox2b27Ala/+ porteuse d’une mutation conditionnelle dont l’expression est limitee a la region du noyau retrotrapezoide (RTN), le principal chemorecepteur central. Ces souris presentent une perte des neurones du RTN (env. 70 %) et une abolition de la reponse au CO2. Methodes La ventilation basale (VE) et la reponse au CO2 (8 %) des souris mutantes et sauvages ont ete mesurees par plethysmographie entre 14 et 15 heures apres traitement au 17-DMAG (20 mg/kg) ou au PBS. Resultats Fig. 1 . Conclusion Le 17-DMAG augmente la reponse ventilatoire au CO2 chez le mutant conditionnel Phox2b27Ala/+. Nos donnees ne permettent pas de dissocier la reponse metabolique au CO2 des reactions comportementales liees a la perception du stimulus. Ce resultat suggere tout de meme qu’il est possible d’attenuer les effets toxiques de la mutation dans les neurones residuels du RTN et d’en restaurer partiellement la fonction.

We aimed to assess early electroencephalography findings in patients treated by venoarterial extracorporeal membrane oxygenation and their association with neurologic outcome.Single-center observational study.Medical ICU of a university hospital.An early standardized electroencephalography assessment, that is, standard electroencephalography followed by continuous electroencephalography, was performed in consecutive cardiogenic shock patients requiring venoarterial extracorporeal membrane oxygenation. Associations between electroencephalography findings and outcome, defined as a composite of acute brain injury or death at 14 days, were investigated.Twenty-two patients with a median Full Outline of Unresponsiveness score of 4 (interquartile range, 3-6) were studied. Pupillary light reflex, corneal reflex, and cough reflex were preserved in 20 (90%), 17 (77%), and 17 (77%) patients, respectively. Overall, standard electroencephalography findings consisted of diffuse slowing in 21 patients (95%) and severe background abnormalities in 13 patients (59%) (i.e., a discontinuous [n = 5; 23%] and/or an unreactive background [n = 9; 41%]). Severe background abnormalities on standard electroencephalography (poor outcome rate: 69% vs 22%; p = 0.03) and absence of sleep transients on continuous electroencephalography (poor outcome rate: 67% vs 14%; p = 0.02) were associated with a poor outcome, whereas neurologic findings and doses of sedation were not. Patients without sleep transients on continuous electroencephalography tended to have lower Full Outline of Unresponsiveness scores than patients with preserved sleep transients-appearing patterns.In patients treated by venoarterial extracorporeal membrane oxygenation, early severe background abnormalities on standard electroencephalography provide important information on neurologic outcome. The lack of sleep transients on continuous electroencephalography reflects the severity of brain dysfunction and might represent an additional prognostic marker.

Resume Les resultats preliminaires de l’etude SERVE-HF ont donne lieu a la diffusion d’une information de securite conduisant a la contre-indication de l’utilisation d’une ventilation auto-asservie (VAA) pour le traitement des apnees centrales chez les patients avec insuffisance cardiaque systolique symptomatique chronique avec fraction d’ejection du ventricule gauche (FEVG) ≤ 45 %. L’objectif de cet article est de faire le point sur ces resultats et d’apporter une argumentation reposant sur les donnees de la litterature en faveur de la poursuite de l’utilisation de cette ventilation dans des indications differentes telles que : insuffisance cardiaque a FEVG conservee, syndrome des apnees du sommeil (SAS) complexe, SAS central induit par les opiaces, SAS central idiopathique, SAS central consequence d’un accident vasculaire cerebral. Ces differents elements nous conduisent a proposer la mise en place de registres dedies aux patients desappareilles de leur VAA d’une part, et d’autre part dans le cadre des prochaines mises en place de ce type de ventilation dans ces indications specifiques afin d’assurer la securite des patients et permettre des decisions argumentees concernant l’utilisation de la VAA.

Resume La prevalence des syndromes d’apnees du sommeil (SAS) chez les patients insuffisants cardiaques (IC) est elevee, environ 60-70 %, tant dans l’IC systolique que dans l’IC a fonction ventriculaire preservee. Un large depistage est donc justifie, sachant que le point d’appel clinique que represente la somnolence est absent. Le SAS des patients IC peut prendre plusieurs formes : obstructif, central, ou mixte. Les deux dernieres formes sont provoquees par une instabilite des centres respiratoires. En termes de prise en charge, en dehors de l’optimisation des traitements de l’insuffisance cardiaque, la correction des troubles respiratoires nocturnes repose sur la pression positive, qu’elle soit en mode fixe pour les apnees obstructives, ou en mode servo-adapte pour les evenements centraux ou mixtes. Quel que soit le type de ventilation choisi, il est souhaitable de l’instaurer en milieu hospitalier. Malgre la contrainte que peut representer cette ventilation, sa prescription se legitime en raison des benefices qu’elle est susceptible d’apporter sur la fatigue, la qualite de vie, voire la fonction cardiaque. Les benefices sur la morbi-mortalite sont plus discutes, mais font l’objet de grandes etudes randomisees en cours de realisation.

Los ronquidos son frecuentes y pueden asociarse a episodios de apnea/hipopnea. Se relacionan con el colapso faringeo durante el sueno y, dependiendo de la relevancia de este, se observa un ronquido simple, limitaciones inspiratorias del flujo, hipopneas y apneas. El sindrome de apnea-hipopnea obstructiva del sueno (SAHOS) se define por un numero de apneas y/o hipopneas superior a 5/h. Se habla de SAHOS grave si el indice de apnea-hipopnea (IAH) es superior a 30/h. En un cuadro de ronquido, se debe descartar un SAHOS debido a las consecuencias significativas que tiene sobre la salud: somnolencia con riesgo de accidentes, repercusion cardiovascular (hipertension arterial, enfermedad coronaria, arritmias, etc.) y metabolica (diabetes, hepatitis esteatosica, etc.). El diagnostico se basa en los registros realizados durante el sueno, bien completos (polisomnografia) o bien con evaluacion solo de los parametros respiratorios (poligrafia). El uso de una u otra de estas exploraciones tiene en cuenta los sintomas del paciente y la sospecha de enfermedades del sueno asociadas. Existen multiples posibilidades terapeuticas y dependen de la gravedad de la roncopatia: cirugia de reduccion tisular de tipo palatoplastia para un ronquido simple, ortesis de avance mandibular para un SAHOS moderado con somnolencia, ventilacion nocturna con presion positiva para un SAHOS grave, etcetera. Las indicaciones deben plantearse de forma consensuada. Siempre se deben asociar medidas higienicodieteticas, asi como un tratamiento global del paciente, teniendo en cuenta los riesgos cardiovascular y metabolico.

I russamenti sono frequenti e possono essere associati a delle apnee/ipopnee. Essi sono legati al collasso faringeo durante il sonno e, secondo l’importanza di questo, si osservano un russamento semplice, delle limitazioni inspiratorie di flusso, delle ipopnee e delle apnee. La sindrome delle apnee-ipopnee ostruttive del sonno (SAIOS) e definita da un numero di apnee e/o di ipopnee superiore a 5/h e la SAIOS e grave se l’indice di apnee-ipopnee (IAI) e superiore a 30/h. Di fronte a un russamento, e importante escludere una SAIOS a causa delle sue conseguenze importanti sulla salute: sonnolenza con conseguente rischio di incidenti e ripercussione cardiovascolare (ipertensione arteriosa, malattia coronarica, disturbi del ritmo, ecc.) e metabolica (diabete, epatite steatosica, ecc.). La diagnosi si basa su registrazioni realizzate durante il sonno, o complete (polisonnografia) o valutando solo i parametri respiratori (poligrafia). Il ricorso all’uno o all’altro di questi due esami prende in considerazione i sintomi del paziente e il sospetto di patologie del sonno associate. Le possibilita terapeutiche sono molteplici e dipendono dalla gravita della roncopatia: chirurgia di riduzione tissutale tipo palatoplastica per un russamento semplice, ortesi di avanzamento mandibolare per una SAIOS moderata sonnolenta, ventilazione notturna in pressione positiva per una SAIOS grave e cosi via. Le indicazioni devono essere discusse collegialmente. Le misure igienico-dietetiche devono sempre essere associate, cosi come una gestione globale del paziente, tenendo in considerazione il rischio cardiovascolare e metabolico.

Introduction Les troubles respiratoires du sommeil sont associes a un mauvais pronostic chez les patients presentant une insuffisance cardiaque chronique. La cohorte prospective mutlicentrique FACE a pour objectif de fournir des donnees a long-terme « en vie reelle » sur une population d’ICC (a fraction d’ejection ventriculaire gauche alteree ou preservee) presentant des apnees centrales predominantes ou combinees a des apnees obstructives, eligibles a la VAA. Une analyse intermediaire des donnees a 2 ans de suivi est presentee ici. Methodes Les donnees de morbi-mortalite, la fonction cardiaque et la qualite de vie sont evaluees sur une periode de 2 ans en fonction de l’observance a la VAA (traite : > 3 h/nuit ou controle : Resultats Trois cent quatre-vingt-onze patients ICC avec un SAS central ou un SAS combine ont ete inclus dans l’analyse. Le suivi median etait de 21,6 mois. Caracteristiques des patients a la visite initiale : âge 70,7 ± 11 ans, 87,5 % d’homme, IMC 28,3 ± 5,2 kg/m2. La FEVG etait severement ( 50 %) chez respectivement 38,7 %, 22,1 % et 39,2 % des patients ICC. Au total, 55,2 % des patients presentaient une etiologie ischemique. Soixante-neuf pour cent avaient un SAS central predominant et 31 % un SAS combine. Soixante-seize pour cent des patients avaient un SAS severe. Soixante-six pour cent des patients suivis etaient observants a la VAA. Une hypoxemie severe etait associee a une forte augmentation de la mortalite (HR = 12) dans cette population. La morbi-mortalite etait amelioree sous VAA chez les patients presentant une hypoxemie severe (T90, IDO > mediane) a l’inclusion, en particulier ceux avec une FEVG moderement alteree ou preservee, ou une obesite. Aucun benefice n’etait observe chez les patients peu hypoxemiques. Par contre, la VAA etait associee a un plus mauvais pronostic chez les patients ischemiques en particulier ceux avec une FEVG alteree. Conclusion Les resultats a 2 ans de l’etude FACE suggerent que les patients insuffisants cardiaques chroniques presentant des apnees centrales avec une hypoxemie severe ou une etiologie non ischemique, en particulier ceux ayant une FEVG moderement alteree ou preservee, pourraient beneficier le plus d’une prise en charge par VAA.

Resume La relation entre les troubles du sommeil et l’addiction a Internet a fait l’objet de peu de travaux. Devant l’importance de ces troubles retrouves dans notre pratique clinique, il nous a semble opportun de realiser une synthese des donnees disponibles et d’etablir les liens de causalite ou d’imputabilite entre la dependance a Internet et l’apparition de troubles du sommeil. Une revue de litterature a alors ete effectuee. Nous avons selectionne les articles scientifiques de langue anglaise et francaise publies entre 1974 et 2010 en consultant les bases de donnees Medline, Embase, Psycinfo, et Google Scholar. Les mots utilises seuls ou en association sont les suivants : addiction, dependence, Internet, behavioral adddiction, sleep. La prevalence de troubles du sommeil est importante, avec dysomnie, syndrome de privation du sommeil et retard de phase. Les mecanismes sont multiples et intriques : excitation psychique, effet potentiel de la lumiere sur la secretion de melatonine, association a d’autres addictions et comorbidites psychiatriques. Leur prise en charge passe par celle de l’addiction, mais peu d’articles traitent de ce sujet.

Objectif La dysautonomie pure (DP) est une pathologie rare (ORPHA441), synucleopathie ne concernant que le systeme nerveux peripherique, caracterisee par une hypotension orthostatique invalidante. Frequents dans les autres synucleopathies (Parkinson, atrophie multisystematisee), les troubles du sommeil sont peu decrits dans la DP. Les buts de cette etude sont : – explorer les troubles du sommeil ; – decrire la variabilite de la frequence cardiaque (VFc) au cours du sommeil. Methodes Les patients adresses pour suspicion de DP sont inclus de facon prospective, consecutive. A l’issue de leur bilan, 2 groupes sont constitues : DP confirmee et non-DP. Le sommeil est evalue par questionnaires et videopolysomnographie. L’analyse spectrale de la VFc est menee sous Mathlab® (R2017a). Resultats Quinze patients ont ete adresses entre 09/16 et 06/17, 1 a ete exclu (Parkinson), 9 ont une DP confirmee. Chez les DP : – la somnolence (7/9), la prevalence des impatiences (6/9), du trouble du comportement en SP (6/9), des apnees (6/9) et de l’HTA nocturne (8/9) etaient significativement plus importantes ; – l’analyse spectrale de la VFc retrouvait des basses frequences, des hautes frequences plus faibles. L’analyse spectrale de VFc lors des differents stades de sommeil est en cours. Conclusion Nos resultats suggerent que les troubles du sommeil dans la DP sont frequents, la presence d’un TCSP ne doit pas remettre en cause le diagnostic de DP, l’exploration du sommeil doit faire partie du bilan d’un patient DP. L’analyse spectrale de VFc donnera des elements supplementaires d’analyse de l’atteinte sympathique et parasympathique.

Resume Le syndrome d’apnees-hypopnees obstructives du sommeil (SAHOS) est frequent et sa prevalence en est encore plus elevee chez les patients deja porteurs de maladies cardiovasculaires. Depuis plus de 15 ans, un faisceau d’arguments convergents plaide pour une morbimortalite cardiovasculaire specifiquement attachee au SAHOS. Ce point a longtemps fait debat mais est maintenant acquis. Cela appelle a une prise en charge des apnees qui va au-dela de la correction des anomalies ventilatoires nocturnes et implique l’evaluation et le suivi d’eventuelles complications cardiovasculaires dans une strategie de prevention primaire et secondaire. Ce bilan initial et le suivi qui en decoule vont dependre du contexte dans lequel le SAHOS est decouvert. Chez un patient deja suivi et evalue, pour une(des) maladie(s) cardiovasculaire(s) et/ou metabolique(s), un bilan redondant est inutile. En revanche, devant un SAHOS decouvert sans antecedent connu ni evaluation, un bilan minimum est requis, notamment en cas de SAHOS severe. Outre l’examen clinique soigneux, un bilan biologique a visee metabolique est necessaire. La mesure ambulatoire de la pression arterielle doit se discuter au cas par cas, de meme que l’ECG et l’echo-doppler des troncs supra-aortiques.

Background: MRD therapy may improve BP in OSA pts with arterial hypertension (HTN). Aims: ORCADES, a French prospective multicenter cohort study is evaluating the long-term effects of a custom-made MRD in OSA pts who refused or did not tolerate CPAP. Interim data are presented at 3-month follow-up. Methods: Clinical benefits and side effects are evaluated in OSA pts fitted with a CAD/CAM MRD (Narval CC™). Patient was hypertensive (HTN) if office systolic and/or diastolic BP were respectively ≥140 and ≥90 mmHg. Results: 77 HTN and 222 non-HTN pts treated with MRD were analysed. Sex ratio (75% male), age (53±11y) and AHI (29±15/h) were similar in both groups. In HTN group, body mass index was higher and nadir SpO2 was lower. Therapy success (AHI reduction ≥50%) was higher in non-HTN group (84% vs. 66%, p=0.0012). Improvement in oxygen saturation, sleepiness or quality of life was equivalent in both groups with no weight change. In HTN group, SBP and DBP were reduced significantly and BP was normalized in 59% of pts. SBP decrease was correlated with mean SpO2 improvement (ρ=-0.30, p=0.022). Only 8% of pts stopped MRD due to side effects and mean usage was similar in both groups (6.7 hours/night). View this table: Evolution of BP under MRD therapy Conclusion: Custom-made CAD/CAM MRD is effective in OSA pts noncompliant with CPAP with additional benefits on blood pressure.

Sleep disordered breathing (SDB) is common in patients with heart failure with reduced ejection fraction (HFrEF). An increased apnea-hypopnea index (AHI) is associated with poor outcomes. We examined whether an analysis of nocturnal desaturations (NDs) can improve the risk stratification.Three-hundred seventy-six consecutive patients with stable chronic HFrEF and LVEF ≤ 45% were prospectively screened using polygraphy. Sleep apnea (SA) was defined as an AHI ≥ 15. The mean age was 59 ± 13 years, the mean LVEF was 30 ± 6%, and the median AHI was 18 [IQR: 9.33). The composite end-point of death, heart transplantation or LV assistance occurred in 98 patients (26%) within 3 years. Minimal oxygen saturation (MOS) during sleep, the number of desaturations90%/h and the time spent with oxygen saturation90% were significantly associated with adverse events (adjusted HR 1.25 [1.03-1.52], 1.25 [1.03-1.53], and 1.28 [1.04-1.59]), whereas the AHI was not (1.10 [0.86-1.39]). The best MOS cut-off value for poor outcomes was ≤ 88%. The patients with an MOS ≤ 88% had a significantly higher event rate (31.9%) than those with an MOS88% (15.6%; p0.01). The risk assessment using an MOS of ≤ 88% in addition to established prognostic markers yielded a net reclassification index (NRI) of nearly 6% and was particularly useful in the subgroup of patients with events (NRI: 8.4%).In HFrEF patients, ND ≤ 88% appears to be predictive of adverse events, independent of the presence of SA. This suggests that the risk assessment in HFrEF should also include ND in top of AHI.

Resume Les troubles respiratoires du sommeil sont frequents chez les patients insuffisants cardiaques, touchant pres de la moitie de ces patients. Cependant, ils sont insuffisamment depistes et traites. Le mecanisme de ces apnees du sommeil est soit obstructif par collapsus des voies aeriennes superieures, soit central, et le plus souvent associe a une respiration periodique de Cheyne-Stokes. Les fortes depressions intrapleurales (soit au moment des apnees obstructives, soit lors de l’hyperpnee dans le Cheyne-Stokes), les eveils et microeveils et les hypoxies-reoxygenations repetees entrainent une augmentation de la postcharge ventriculaire et une activation sympathique contribuant a l’aggravation de l’insuffisance cardiaque et de son pronostic. Le traitement des syndromes d’apnees du sommeil (SAS) obstructifs par ventilation en pression positive permet une amelioration des symptomes diurnes (fatigue, somnolence) ainsi qu’une amelioration de la fonction cardiaque. Pour les SAS centraux, la premiere mesure est l’optimisation du traitement pharmacologique de l’insuffisance cardiaque. La ventilation nocturne doit etre envisagee si le SAS persiste malgre cela, sous couvert de precautions lors de sa mise en oeuvre, en raison des risques hemodynamiques qui lui sont attaches. Cette ventilation nocturne sera au mieux une ventilation a deux niveaux de pression, servoadaptee, dont l’algorithme est specifiquement dedie au traitement du Cheyne-Stokes. Plusieurs etudes ont demontre l’interet de la correction du SAS central pour ameliorer la fatigue et la somnolence de ces patients ainsi que leur fonction cardiaque. Il est donc important d’effectuer un depistage systematique des syndromes d’apnees du sommeil chez les patients insuffisants cardiaques chroniques, afin d’ameliorer leur prise en charge.

Several types of primary disease may recur after lung transplantation, but recurrence of pulmonary emphysema has so far never been published. We report the case of a 49-year-old white male who underwent single lung transplantation for emphysema related to alpha-1 antitrypsin deficiency and to superimposed smoking. The postoperative course was complicated by several rejection episodes. Subsequently, the patient remained stable without evidence of graft dysfunction for more than 10 years, but he resumed light smoking at 8 years after transplant. At 11 years after transplant, although the patient was still asymptomatic and had a stable lung function, recurrence of emphysema on the grafted side was diagnosed on computerized tomography of the thorax. One year later, the patient began to experience a moderate decline in lung function. Two separate bronchoalveolar lavages performed after the onset of the recurrence disclosed a significant elastolytic activity related to neutrophil serine-elastase in lavage fluid. In summary, we describe a case of recurrence of pulmonary emphysema in a patient with alpha-1 antitrypsin deficiency. The resumption of smoking has probably played a central role in the presence of elastolytic activity in lavage fluid and in the recurrence of emphysema.

Recent years have witnessed important advances in our understanding of the pathophysiology of primary pulmonary hypertension (PPH). Both genetic and mechanistic studies have succeeded in identifying new molecular pathways relevant to the process of pulmonary vascular remodelling which underlies PPH. Mutations in the type II bone morphogenetic protein receptor (BMPRII) are now considered to be the genetic basis for familial PPH and about 30% of cases of sporadic PPH. Identification of the BMP pathway as relevant to the aetiology of PPH now raises many questions about the link between the BMPRII mutant genotype and the PPH phenotype. That PPH does not develop in all subjects with BMPRII mutations suggests a crucial role for environmental or associated genetic factors. Simultaneously, mechanistic studies investigating the biological processes that underlie the complex vascular changes associated with PPH have identified major molecular pathways involved in constriction and proliferation of pulmonary vascular smooth muscle cells (SMCs), dysfunction of endothelial cells, and remodelling of extracellular matrix. Such mechanisms may be involved either in initiating or in perpetuating the disease. The finding that genetic polymorphism of some of the candidate genes related to these processes is closely associated with PPH suggests a causal relationship between the expression, or function, of these genes and the PPH phenotype. The association between PPH and the L allelic variant of the serotonin transporter (5-HTT) gene indicates that 5-HTT, which controls smooth muscle hyperplasia, probably contributes to susceptibility to

Study objectives: In adults, arterial blood samples are usually drawn using plastic syringes. In contrast to glass syringes, plastic syringes let oxygen diffuse through their wall. This results in PO2 changes during storage, especially when PO2 is high. An alternative to glass syringes is the Microsampler (Roche Diagnostics; Schaffhausen, Switzerland), a commercially available device consisting of a heparinized glass capillary fitted with a 26-gauge needle and used to collect arterial blood in the same way as a plastic syringe fitted with a needle. Design: We evaluated the performance of the Roche Microsampler for storing arterial blood in view of PO2 measurement, comparatively with glass and plastic syringes. Five approximate initial PO2 levels (650, 400, 200, 130, and 80 mm Hg) and two storage temperatures (ambient temperature and 4°C) were studied. Settings: Bench study. Results: Plastic syringes allowed reliable measurement of PO2 values when initial PO2 was too low to ensure complete hemoglobin oxygen saturation, but were associated with time-dependent underestimation of PO2 at higher initial PO2 values. No such underestimation occurred with the Roche Microsampler stored at 4°C for up to 1 h for all PO2 levels studied. Conclusion: The Roche Microsamplers appeared to be reliable devices in preventing oxygen diffusion. (CHEST 2001; 120:1651–1654)

Study objectives The aim of this study was to investigate whether presence of expiratory abdominal muscle activity (EAMA) in obstructive sleep apnea syndrome (OSAS) patients during nasal continuous positive airway pressure (nCPAP) is due to either nCPAP overprescription or nCPAP underprescription. Design Airflow, esophageal pressure (Pes), and gastric pressure (Pga) were routinely measured during polysomnography aimed at determining the optimal nCPAP level, and the magnitude of EAMA was evaluated in relation to the nCPAP level and to the conventional indexes of upper-airway obstruction used during nCPAP titration. Patients The study was performed 12 patients with OSAS. Results Six patients displayed sustained EAMA, ie , EAMA lasting > 3 min, and characterized by a decrease in abdominal diameter and a paradoxical rise in Pga during expiration. In all six patients, EAMA decreased gradually as nCPAP neared optimal levels, and then disappeared when the optimal nCPAP level was achieved. The decrease in EAMA as nCPAP increased was associated with an increase in minute ventilation, decreases in both inspiratory and expiratory resistance, a decrease in Pes swing, and the normalization of the inspiratory flow contour. Conclusions We conclude that the EAMA observed in some OSAS patients might be an indirect marker of upper-airway obstruction, and that the presence of EAMA during nCPAP titration might indicate a suboptimal nCPAP level rather than a deleterious effect of nCPAP.

We evaluated whether tumor necrosis factor (TNF)-α induces an increase in permeability of an alveolar epithelial monolayer via gelatinase secretion and basement membrane degradation. Gelatinase secretion and epithelial permeability to radiolabeled albumin under unstimulated and TNF-α-stimulated conditions of an A549 human epithelial cell line were evaluated in vitro. TNF-α induced both upregulation of a 92-kDa gelatinolytic activity (pro form in cell supernatant and activated form in extracellular matrix) and an increase in the epithelial permeability coefficient compared with the unstimulated condition (control: 1.34 ± 0.04 × 10−6cm/s; 1 μg/ml TNF-α: 1.47 ± 0.05 × 10−6cm/s, P < 0.05). The permeability increase in the TNF-α-stimulated condition involved both paracellular permeability, with gap formation visualized by actin cytoskeleton staining, and basement membrane permeability, with an increase in the basement membrane permeability coefficient (determined after cell removal; control: 2.58 ± 0.07 × 10−6cm/s; 1 μg/ml TNF-α: 2.82 ± 0.02.10−6× cm/s, P < 0.05). Because addition of gelatinase inhibitors [tissue inhibitor of metalloproteinase (TIMP)-1 or BB-3103] to cell supernatants failed to inhibit the permeability increase, the gelatinase-inhibitor balance in the cellular microenvironment was further evaluated by cell culture on a radiolabeled collagen matrix. In the unstimulated condition, spontaneous collagenolytic activity inhibited by addition to the matrix of 1 μg/ml TIMP-1 or 10−6M BB-3103 was found. TNF-α failed to increase this collagenolytic activity because it was associated with dose-dependent upregulation of TIMP-1 secretion by alveolar epithelial cells. In conclusion, induction by TNF-α of upregulation of both the 92-kDa gelatinase and its inhibitor TIMP-1 results in maintenance of the gelatinase-inhibitor balance, indicating that basement membrane degradation does not mediate the TNF-α-induced increase in alveolar epithelial monolayer permeability.

Nocturnal polysomnography is the standard diagnostic test for sleep apnea syndrome (SAS) but is both expensive and time-consuming. We developed a predictive index for SAS based on pulmonary function data, including respiratory resistance determined by the forced oscillation technique, from 168 obese snorers with suspected SAS. Our model used logistic regression to obtain case-by-case predictions of the probability of SAS, defined as an apnea-hypopnea index (AHI) > or = 15 during overnight polysomnography. We then tested our model in a prospective group of 101 similar patients. Specific respiratory conductance and daytime oxygen saturation contributed significantly to the model. Sensitivity, specificity, positive predictive value (PPV), and negative predictive value (NPV) of the index computed from these parameters were 98%, 86%, 90%, and 97%, respectively. In the prospective group, the model proved repeatable, with 100% sensitivity, 84% specificity, 86% PPV, and 100% NPV. The high NPV may help to identify obese snorers with a SAS risk that is so low as to make polysomnography unnecessary. Based on the 50% prevalence of SAS in our study and on the fact that polysomnography is required in all patients with daytime somnolence, we calculated that using our model would have obviated the need for polysomnography in 38% of our patients.

The aim of this study was to investigate whether nasal prongs, which have been proposed to assess nasal flow during sleep, affect nasal airflow resistance (NR).NR was estimated by posterior rhinomanometry at a 0.5 L/s flow, under eight conditions: in the basal state, and with seven different nasal prongs.The study was performed in 17 healthy supine subjects, 8 of whom had basal NR values within the normal range (or = 2 cm H(2)O.L(-1).s, group 1), and 9 had increased basal NR values (2.5 cm H(2)O.L(-1).s, group 2), because of nare narrowness and/or deviated nasal septum.NR increased significantly while breathing with nasal prongs (p0.0001 in both groups). The changes in NR (DeltaNR) induced by the different nasal prongs were characterized by large intersubject and intrasubject variability, with a maximum DeltaNR of 24.2 cm H(2)O.L(-1).s. Significant differences were found between the DeltaNR induced by the different nasal prongs (p0.001 in group 1, and p0.0003 in group 2), and for six of them, DeltaNR was significantly higher in group 1 than in group 2 (p0.02).This study demonstrates that nasal prongs can markedly increase NR in subjects presenting with nare narrowness and/or deviated nasal septum. Further investigations that would include nocturnal polysomnography are still required to evaluate the possible influence of nasal prongs on the diagnosis of obstructive sleep apnea syndrome and its severity.

Acute severe muscle ischaemia is characterized by significant remodelling of basement membranes of myofibres. It was hypothesized that peripheral artery insufficiency is accompanied by similar muscle extracellular matrix (ECM) changes involving matrix metalloproteinase gelatinases. Using a model of femoral artery ligation, both gelatinase activity and basement membrane component degradation were studied in hindlimb skeletal muscles. SDS-PAGE zymography of muscle homogenates showed that acute moderate ischaemia was followed by a significant transient increase in expression of 72- and 92-kDa gelatinases during 48 h; the latter probably originated from inflammatory cells. In situ zymography showed that this increase occurred chiefly at the periphery of myofibres. Immunolocalization demonstrated 72-kDa gelatinase in interspaces and at the periphery of myofibres, and suggested that this enzyme may explain the gelatinolytic activities found by in situ zymography. Type IV collagen and laminin staining showed that the gelatinase expression increase correlated with dramatic basement membrane component alterations. Our data show that even moderate ischaemia results in significant muscle basement membrane remodelling due to matrix degrading enzymes matrix metalloproteinases (MMP) gelatinases.

We studied eight heavy snorers with upper airway resistance syndrome to investigate potential effects of sleep on expiratory airway and lung resistance, intrinsic positive end-expiratory pressure, hyperinflation, and elastic inspiratory work of breathing (WOB). Wakefulness and non-rapid-eye-movement sleep with high- and with low-resistance inspiratory effort (H-RIE and L-RIE, respectively) were compared. No differences in breathing pattern were seen across the three conditions. In contrast, we found increases in expiratory airway and lung resistance during H-RIE compared with L-RIE and wakefulness (56 ± 24, 16 ± 4, and 11 ± 4 cmH2O ⋅ l−1 ⋅ s, respectively), with attendant increases in intrinsic positive end-expiratory pressure (5.4 ± 1.8, 1.4 ± 0.5, and 1.3 ± 1.3 cmH2O, respectively) and elastic WOB (6.1 ± 2.2, 3.7 ± 1.2, and 3.4 ± 0.7 J/min, respectively). The increase in WOB during H-RIE is partly caused by the effects of dynamic pulmonary hyperinflation produced by the increased expiratory resistance. Contrary to the Starling model, a multiple-element compliance model that takes into account the heterogeneity of the pharynx may explain flow limitation during expiration.

Type II pneumocytes are key cells of the alveolar epithelium. They lie on the alveolar basement membrane, which influences their phenotype and functions. We hypothesized that type II pneumocytes degrade basement membrane components by producing gelatinases, members of the matrix metalloproteinase family. To investigate this hypothesis, we used primary cultures of rat type II pneumocytes and cultures of the human A549 cell line. We found by zymography that 70-kDa gelatinase was present in media conditioned by these cells. This 70-kDa gelatinase was identified as gelatinase A by a Western blot, and the presence of its mRNA was demonstrated by reverse transcription-polymerase chain reaction. A 95-kDa gelatinase could be induced under certain conditions. Production of gelatinases may take place during the turnover of basement membranes, in physiological and in pathophysiological processes. This was suggested by the increase in production of both gelatinases that we observed after in vitro exposure to LPS or interleukin-1. The presence of tissue inhibitors of matrix metalloproteinase-1 and -2 was also demonstrated, suggesting that degradation of extracellular matrix by type II pneumocytes is tightly regulated.

To investigate the role of human bronchial epithelial cells (HBECs) in the maintenance and remodeling of the extracellular matrix, we evaluated the expression by HBECs of 72- and 92-kDa gelatinases under basal conditions and after exposure to bacterial lipopolysaccharides (LPS). Confluent HBECs from explants were cultured in plastic dishes coated with type I and III collagens. Gelatin zymography of HBEC-conditioned media showed constitutive major 92-kDa and minor 72-kDa gelatinases recognized by specific human antibodies and totally inhibited by the metalloproteinase inhibitor EDTA. The identification of the two matrix metalloproteinases was confirmed by quantitative reverse transcription-polymerase chain reaction. Identical patterns of gelatinase expression were observed with repetitive primary cultures issued from the same explants. Zymography showed that exposure of HBECs to LPS induced 2- and 20-fold increases in 92-kDa gelatinase production and activation, respectively, as well as a smaller increase in activated 68-kDa gelatinase. With [3H]gelatin substrate, elevated metallogelatinolytic activity (138 microgram of hydrolyzed gelatin/48 h/10(6) cells) was also observed, whereas no activity was detected in the absence of LPS. A human epithelial cell line (16HBE14o-) exhibited the same basal profile of gelatinase activity, but this profile remained unchanged after exposure to LPS. Quantitative reverse transcription-polymerase chain reaction demonstrated only minimal changes in 92-kDa mRNA levels in response to LPS, but the half-life of 92-kDa gelatinase mRNA was increased with exposure to LPS. In contrast, concomitant slight increases in 72-kDa gelatinase protein and mRNA were found, suggesting that the control mechanisms regulating the expression of 92- and 72-kDa gelatinases by HBECs in response to LPS are divergent. All these data allowed us to propose that HBECs may be actively involved in the physiological and physiopathological remodeling of the airway basement membrane.

Polymorphonuclear neutrophil (PMN) migration across basement membrane is thought to be dependent on the degradation of membrane constituents. PMN gelatinase B, a metalloproteinase able to degrade type IV collagen, may be involved in this phenomenon. PMN gelatinase B is released in the extracellular medium as a latent proform and then activated, mainly by PMN elastase. We investigated the role of gelatinase B in PMN migration across a Matrigel basement membrane matrix coated onto a filter, in a Boyden chamber. The effects of gelatinase and elastase inhibitors on PMN migration in this system were tested. Chemokinesis of PMN was tested in the same Boyden chamber across a filter free of basement membrane. The agarose method was used to test the same inhibitors for effects on PMN chemotaxis. In both systems, FMLP 10(-7)M was used as a chemoattractant. Addition of 10(-8)M TIMP-1 (the preferential gelatinase B inhibitor) inhibited trans-basement membrane PMN migration by 52 +/- 6% (P0.05), without affecting PMN chemokinesis, chemotaxis, or degranulation. Also, (Ala)(2) Pro Val chloromethyl ketone (AAPVCK) 100 micron, a specific elastase inhibitor, inhibited trans-basement membrane PMN migration by 51 +/- 8% (P0.05), without affecting PMN chemokinesis, chemotaxis, or degranulation. The AAPVCK-TIMP combination led to a decrease in migration across Matrigel basement membrane (46 +/- 2%, P,0.05)similar to that seen with TIMP alone. AAPVCK was responsible for inhibition of gelatinase B activation, leading to a decrease in activated gelatinase from 14% to 2% of total gelatinase release (P0.05). All these results strongly suggest that gelatinase B is a major factor of PMN migration across basement membrane and that elastase may contribute to this process by activating pro-gelatinase B.

Introduction La ventilation non invasive (VNI) est le traitement usuel du syndrome d’apnees du sommeil (SAS) a composante centrale. Chez les insuffisants cardiaques (ICC) a FEVG alteree (aFVEG), son instauration peut s’accompagner de baisse de la pression arterielle (PA). Aucune donnee a ce jour n’a rapporte le meme effet chez les ICC dont la FEVG est preservee (pFEVG). Notre objectif etait d’etudier la tolerance hemodynamique de l’instauration de la VNI, tous modes de ventilation confondus, dans le SAS a composante centrale chez des ICC a pFEVG ( Fig. 1 ). Methodes Etude retrospective, observationnelle, transversale, monocentrique chez l’adulte (≥ 18 ans) presentant un SAS a composante centrale (au moins 30 % d’apnees centrales) diagnostique par un enregistrement poly(somno)graphique ; codage des stades du sommeil et des evenements respiratoires selon les recommandations internationales (AASM 2012 [1] ). Les chiffres de pression arterielle systolique (PAS), pression arterielle diastolique (PAD), pression arterielle moyenne (PAM) et frequence cardiaque (FC) sont exprimes en mediane [25 ; 75 percentiles]. Les valeurs avant et apres VNI ont ete comparees par le test de Wilcoxon, risque α = 5 % (logiciel GraphPad Prism 7). Resultats Vingt-six patients (22 hommes et 4 femmes, âge moyen = 72,7 ans [67,5 ;79], IMC moyen = 28,4 kg/m 2 [25,4 ; 29,7], FEVG = 64 % [56,2 ; 65]) presentant un SAS a composante centrale modere a severe ont ete inclus. Trois patients avaient un IAH compris entre 15 et 30 et 23 un IAH superieur a 30. Il n’y a pas eu de modification significative des PAS, PAD et PAM apres ventilation ( Fig. 1 ). Un seul patient (3,8 %) a diminue sa PAS d’au moins 20 % et un seul autre patient (3,8 %) a diminue sa PAD d’au moins 20 % par rapport au chiffre de base, sans retentissement clinique ni necessite d’interrompre la ventilation. La baisse de la FC est statistiquement significative mais sans portee clinique. Conclusion Notre etude montre que l’introduction de la VNI n’entraine pas de variation tensionnelle significative chez les ICC avec pFEVG presentant un SAS a composante centrale.

International audience

A growing body of evidence suggests that neutrophil-derived proteinases play a major role in lung tissue damage in cystic fibrosis (CF). Most previous studies have focused on serine proteinases such as neutrophil elastase, providing no information on the extent to which metalloproteinases participate in proteolytic processes in CF. To address this issue, we evaluated the contribution of one of the major neutrophil metalloproteinases, i.e., 95 kDa gelatinase (type IV collagenase), to the total gelatinolytic activity measured in sputum specimens from 27 patients with CF. Compared with asthmatic children (n = 9), CF patients had a 6.7 times greater level of total gelatinase activity in sputum revealed by zymography. The 95 kDa gelatinase was increased 3.7-fold in the CF subjects (2,441 +/- 411 [SEM] arbitrary units [AU] x 10(6) per ml of sputum versus 665 +/- 201 in asthmatics) and the 88-kDa active form 23.2-fold (2,272 +/- 372 AU x 10(6) per ml of sputum versus 98 +/- 43, respectively). Using radiolabeled 3H-gelatin as the substrate, we demonstrated uninhibited gelatinolytic activity in all CF patients; this activity was significantly correlated to disease severity as assessed by pulmonary function tests. Western blotting using anti-tissue inhibitor of metalloproteinase (anti-TIMP) and anti-95/88-kDa gelatinase antibodies demonstrated a more than 10-fold excess of 95/88 kDa gelatinase over TIMP. Bacterial proteinases from Pseudomonas aeruginosa were shown to contribute little to the gelatinolytic activity measured in sputum supernatants from patients with CF, although culture supernatants from various P. aeruginosa strains expressed gelatinolytic activity in vitro. Finally, lung damage, as assessed by increased type IV collagen degradation products in sputum, was significantly correlated to concentrations of active 88 kDa gelatinase. These data argue for a significant role of 95/88 kDa gelatinase in airway damage in CF.

The functional immaturity of neonatal alveolar macrophages (AM) may contribute to the increased susceptibility of neonates to lung injury. Because the secretion of proteinases by neonatal AMs may be involved in normal postnatal lung development and in repair after lung injury, we evaluated the capacity of neonatal AMs to secrete 92 kD Type IV collagenase. AMs were obtained by bronchoalveolar lavage from newborn rats at different postnatal ages. Total gelatinase activity was measured by zymography in AM-conditioned media. Spontaneous secretion of gelatinase from AMs varied significantly with age, the highest levels being found immediately after birth. Stimulation of AMs by PMA induced a four- to fivefold greater increase in total gelatinase activity during the first 10 d of postnatal life compared with adulthood. Using [3H]gelatin as the substrate, we found high free gelatinase activity only within 24 h after birth; data obtained after exposing cells to natural surfactant suggested that surfactant may account in part for this increase in free gelatinase activity. No secretion of tissue inhibitor of metalloproteinases (TIMP) by AMs was detectable in newborns within 24 h after birth. We conclude that AMs from newborn rats are able to secrete more gelatinase than AMs from adults, and this enzyme production profile during the neonatal period may contribute to the fact that newborns with lung injury are at high risk for extracellular matrix degradation.

Aims To determine whether severity patterns or nocturnal ventilation to treat sleep-disordered breathing (SDB) during chronic heart failure (CHF) is associated with adverse outcomes. Although SDB is frequent during CHF, the relationships between SDB and CHF outcomes are unknown. Methods and results A total of 384 CHF patients (82% men, mean age 59 ± 13 years) with a left ventricular ejection fraction (LVEF) of ≤45% (mean LVEF 29 ± 9%) were assessed by polygraphy in our clinic between 2001 and 2009. Nocturnal ventilation was started according to the severity of SDB. Combined endpoints were death, heart transplant, and implant of a ventricular assist device. The prevalence of obstructive sleep apnoea (OSA), central sleep apnoea (CSA), and Cheyne–Stokes respiration (CSR) was 62, 26, and 29%, respectively. A primary endpoint occurred in 31%. Mean follow-up for survivors was 47 ± 25 months. Those with moderate [apnoea–hypopnoea index (AHI) ≤5–20/h] and severe SDB (AHI ≥20/h), and OSA and CSA, had poor prognoses compared with patients without SDB (P = 0.036, P = 0.003, respectively). A total of 31% of SDB patients were treated with nocturnal ventilation. Treated SDB had a better outcome than untreated severe SDB after adjustment for confounding factors [P = 0.031; hazard ratio (HR) 0.56; 95% confidence interval (CI) 0.33–0.95]. Subgroup analysis that included only OSA showed a similar result after adjustment (P = 0.017; HR 0.40; 95% CI 0.19–0.95). Conclusions In CHF, SDB is associated with a poor prognosis whatever the SDB pattern, and nocturnal ventilation is associated with a better outcome.