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J L Pépin

Publications and source records attributed to J L Pépin.

At least 19 recordsLinked to original sources
PubMed2006

Non-arteritic anterior ischaemic optic neuropathy is nearly systematically associated with obstructive sleep apnoea.

AIM: To evaluate newly diagnosed non-arteritic anterior ischaemic optic neuropathy (NAION) patients for the existence of an associated sleep apnoea syndrome. METHODS: Newly identified NAION patient underwent polysomnography. The prevalence of sleep apnoea in NAION patients was compared to the prevalence previously found in the general population. Hypertension, diabetes, hyperlipidaemia, and atheromatous lesions of carotid vessels as classic risk factors associated with NAION were also identified. RESULTS: 27 consecutive newly diagnosed NAION patients (18 men and nine women, mean age 65 (SD 8) years, body mass index 27.2 (3.8) kg/m2) were included in the study. 24 of these 27 NAION patients (89%) exhibited a sleep apnoea syndrome (respiratory disturbance index: 37.2/h (SD 18.3/h). Risk ratio for a NAION patient to have sleep apnoea was 4.9 compared to the general population (p < 0.001). Sleep apnoea was 1.5-2-fold more frequent than the rate of the other identified risk factors typically associated with NAION (hypertension, diabetes). CONCLUSIONS: Sleep apnoea is the most frequent disorder associated with NAION and should be screened in this population. At least a questionnaire related to obstructive sleep apnoea symptoms and assessment of sleepiness should be systematically proposed to patients with NAION.

Adult↗
PubMed2005

Awake flow limitation with negative expiratory pressure in sleep disordered breathing.

BACKGROUND AND PURPOSE: Although upper airway collapsibility (UAC) is theoretically useful to anticipate severity of sleep-disordered breathing (SDB), inspiratory UAC measurements are poorly correlated with obstructive sleep apnea (OSA) severity. PATIENTS AND METHODS: We investigated in 15 healthy and 35 SDB awake subjects whether negative expiratory pressure (NEP) could be a technique which would allow us to anticipate SDB severity. We characterized in these subjects, both in supine and sitting position, at -5 and -10 cm H(2)O, the flow-volume curves and a new NEP quantitative index (ratio of the 'areas under the curve' of NEP flow-volume loop vs. spontaneous flow-volume loop). RESULTS: Abnormal flow-volume curves were significantly more frequent in patients with SDB than in healthy subjects, for both negative pressures in sitting posture and -10 cm H(2)O in supine position. The quantitative index decreased with the severity of SDB, independently of confounding factors (age, body mass index (BMI) and expiratory reserve volume (ERV)). In the supine position, at -5 and -10 cm H(2)O, thresholds of less than 160 and 180% respectively identified in 96.6% of SDB, whereas thresholds of greater than 160 and 180% were adequately classified in 76.9% of controls. CONCLUSIONS: NEP flow-volume curves and quantitative index during wakefulness are useful methods to detect UAC. These results, however, should be confirmed by a prospective study in the general population.

Adult↗
PubMed2005

[Alveolar hypoventilation during sleep and domiciliary assisted ventilation].

INTRODUCTION: An alveolar hypoventilation physiologically occurs during sleep and more specifically during REM sleep. STATE OF THE ART: During obstructive chronic respiratory failures, increases in PaCO2 that are associated with REM sleep can participate to the severity of daytime hypercapnia and in a subgroup of patients lead to an indication of nocturnal non-invasive ventilation (NIV) in association with the long-term oxygen therapy. A REM sleep hypoventilation generally appears during the early course of restrictive chronic respiratory failures. This REM sleep hypoventilation represents one of the most frequent reasons for initiating NIV in restrictive respiratory insufficiencies. Obesity-hypoventilation syndrome (OHS) refers to a hypercapnic chronic respiratory failure in which REM sleep hypoventilation is one of the main determinants. In France, in 2004, OHS is the primary chronic respiratory failure leading to at home NIV. NIV on OHS aims to maintain upper airway patency as sleep apnoea is frequently associated and to allow sufficient alveolar ventilation during REM sleep. PERSPECTIVES: Thus, sleep alveolar hypoventilation should be systematically assessed in obese patients and during the time curse evolution of all the chronic respiratory failures. This can be done relatively easily by using nocturnal oximetry concurrently with a transcutaneous PCO2 measurement. CONCLUSION: The understanding of exact mechanisms underlying abnormal respiratory events occurring during sleep allows optimising adjustments in NIV parameters.

Chronic Disease↗
PubMed2002

Brain electrical activity during combined hypoxemia and hypoperfusion in anesthetized rats.

In order to investigate the effects of moderate hypoxemia on brain electrical activity and the consequences of an altered cerebro-vascular response to hypoxemia, we recorded changes in electrical activity of the brain in anesthetized rats following unilateral carotid artery ligation (UCAL). In these animals, on the clamped side, cerebral blood flow, whilst normal during normoxia, shows less augmentation during hypoxemia. Six anesthetized (Halothane) Sprague-Dawley rats with UCAL were studied during 20 min periods of baseline (FI(O(2))=30%), hypoxemia (FI(O(2))=9.5%) and recovery (FI(O(2))=30%): mean arterial pressure of oxygen (PA(O(2))) achieved was 177.0, 37.6 and 160.1 mmHg, respectively. A significant decrease in the frequencies of the ECoG was observed bilaterally during hypoxemia: centroid frequency (fc)=3.37+/-0.14 and 2.85+/-0.13 Hz on the intact and clamped hemisphere respectively during hypoxemia versus fc=4.09+/-0.20 Hz (mean+/-S.E.M.) during baseline, which was not reversed during recovery (3.27+/-0.11 Hz) (ANOVA, P<0.01). The total power of the signal (Pw) was unaffected on the intact hemisphere but diminished on the clamped side during hypoxemia. Our results show that a significant slowing of ECoG is observed during hypoxemia of moderate intensity (40 mmHg) even when cerebro-vascular response to hypoxemia is preserved and that total power of the ECoG signal is severely diminished when the cerebro-vascular response to hypoxemia is impaired.

Animals↗
PubMed2002

[Pathophysiology of cardiovascular risk in sleep apnea syndrome (SAS)].

Different pathophysiological mechanisms underlie the morbid associations observed between sleep apnea syndrome (SAS) and cardiovascular disease. Cardiovascular responses to apnea can be divided into acute cardiovascular modifications following each nocturnal respiratory event and chronic adaptations of the cardiovascular system. The same stimuli always trigger acute cardiovascular response: hypoxemia, hypercapnea, changes in the intra-thoracic pressure, micro-arousals. Each obstructive or central respiratory event is associated with a peak in blood pressure, changes in the heart rate, generally bradycardia at onset of apnea and tachycardia when respiration is renewed. Oxygen desaturation is the strongest stimulus explaining the observed acute cardiovascular responses. When these stimuli are repeated every night, the cardiovascular system adapts with a higher sympathetic tone and lower parasympathetic tone during the diurnal period. Baroreceptors also become less sensitive in apneic patients. Finally, endothelial function is altered in SAS patients with a desensitization of the alpha and beta-2 adrengeric receptors, altered NO-dependent vasodilatation, and hypersensitivity to vasoconstriction induced, for example, by angiotensin 2. The cardiovascular morbidity associated with SAS is currently thought to concern the development of diurnal hypertension (dose-effect response), left ventricular failure, higher risk of coronary or cerebral events. Very recently, epidemiological studies suggested that continuous positive pressure ventilation in SAS patients can reduce the cardiovascular risk.

Adrenergic alpha-Antagonists↗
PubMed2002

[Tools available for the diagnosis of obstructive sleep apnea syndrome. Measurements for the evaluation of therapeutic efficacy].

Obstructive sleep apnea syndrome (OSAS) is characterized by the development of repeated episodes of pharyngeal collapse. Respiratory movements attempt to reopen the closed pharynx leading to resumption of ventilation associated with micro-arousals. Three kinds of measurements are needed to establish the diagnosis of OSAS: airflow (reduction or complete interruption), respiratory effort in response to increased airway resistance, micro-arousals associated with the end of the respiratory event. Classically, polysomnography was used to establish sleep architecture using electroencephalography, electromyography and electro-oculography. Air flow was measured by thermistors, chest and abdominal movements and oximetry were monitored. Other more accessible methods can also be used to establish reliable diagnosis. Measuring pulse transit time using ECG and oximeter sensors provide a semi-quantitative measurement of respiratory effort. Likewise, cardiovascular markers (heart rate, blood pressure, pulse time) can be used instead of electroencephalography to establish the arousal pattern. Cardiovascular markers are as sensitive and probably as specific as EEG for identifying micro-arousals. Measuring nasal pressure provides a much less invasive quantitative assessment of airflow than pneumotachography. The shape of the inspiratory signal is also an indirect marker of respiratory effort. These new tools can be used to characterize the three elementary abnormalities observed in OSAS: variations in airflow, increased respiratory effort, fragmented sleep, using a very simplified setting compared with classical techniques. Therapeutic monitoring of OSAS patients, particularly after surgery, should not be limited to physical examination known to lack sufficient sensitivity. It should also include simplified methods or complete polysomnography to obtain a precise measurement of residual respiratory events and sleep pattern after treatment.

Air Pressure↗
PubMed2002

[Surgery and obstructive sleep apnea syndrome: indications and precautions].

Surgery has long been a therapeutic option for obstructive sleep apnea syndrome (OSAS). The first procedures targeted the soft palate but results of isolated uvulo-palatopharyngoplasty (UPPP) were inconstant. A better understanding of the mechanisms involved in pharyngeal collapse incited interest in the role of the tongue and the retropharyngeal space. Surgical procedures were then developed for this level of the upper airways. There are a large number of possibilities. Excepting tracheostomy which court-circuits the collapsed zone, all the other procedures are designed to widen more or less one or more of the upper airway levels. The target can be the nose, the soft palate or the tongue, alone or in combinations. In all cases, the surgical alternative should be balanced against a non-invasive option: continuous positive pressure ventilation. The objective is to minimize the operative risks and sequelae while assuring success equivalent to positive pressure ventilation. It is important to note that sufficiently effective and permanent results have not been proven for any surgical technique, excepting tracheostomy and to a lesser degree bimaxillary advancement osteotomy, due to the lack of objective long-term rigorous evaluation. A considerable effort must be made in this domain.

Humans↗
PubMed2001

Characterization of obstructive nonapneic respiratory events in moderate sleep apnea syndrome.

Obstructive nonapneic respiratory events (ONAREs, i.e., obstructive hypopneas [OHs] and respiratory effort related arousals [RERAs]) are clinically important as producing sleep fragmentation but are much more difficult to detect and classify than obstructive apneas. We characterized 1,061 ONAREs in 15 unselected patients with moderate sleep apnea-hypopnea syndrome (OSAHS) according to the 1999 American Academy of Sleep Medicine (AASM) Task Force recommendations concerning accurate skills for respiratory measurements (i.e., pneumotachograph and esophageal pressure [Pes]) and definitions of respiratory events. OHs were defined as > or = 50% decrease in flow or < 50% but > or = 30% decrease in flow associated with either a desaturation of > or = 3% or a cortical arousal. RERAs corresponded to a less than 30% decrease in flow associated with an arousal. OHs represented a large majority of the events (79.9%, n = 848). Among the events demonstrating a 30 to 50% reduction in flow (n = 392), the occurrence of a cortical arousal permitted the classification of 246 events as OHs (62.8%). RERAs represented only 5.3% of the events. Finally 14.8% of the events were classified as indeterminate owing to a < 50% and > or = 30% airflow decrease without arousal or desaturation or an airflow decrease less than 30% without arousal. The same level of DeltaPes was observed at the end of OHs and RERAs (21.9 +/- 5.5 versus 18.9 +/- 5.7 cm H(2)O respectively [NS]) whereas the reduction in flow was as expected, higher for OH (57.9 +/- 10.7 versus 21.3 +/- 4.9%). In a population of moderate OSAHS, OH represented the dominant type of ONAREs when RERAs should be considered as specific but relatively rare respiratory events. The occurrence and the recognition of a microarousal represented the key associated factor for classifying respiratory events as hypopneas. The high rate (15%) of unclassified events demonstrated some limitations in the AASM Task Force recommendations for definitions of respiratory events. Similar levels of DeltaPes found at the end of RERAs and OHs, although the reduction in flow was higher for OHs, suggest that different levels of collapsibility can exist throughout the night in a given patient.

Data Interpretation, Statistical↗
PubMed2001

Charcot-Marie-Tooth disease and sleep apnoea syndrome: a family study.

BACKGROUND: Charcot-Marie-Tooth (CMT) disease is a genetically heterogeneous group of hereditary motor and sensory polyneuropathies in which sleep apnoea has rarely been reported and no causal relation shown. We looked for an association between the most common subtype of CMT disease (CMT1A) and sleep apnoea syndrome. METHODS: Having diagnosed sleep apnoea and CMT in one family member (index case), we prospectively investigated 13 further members not previously suspected of having neuropathy or apnoeas. All had a neurological examination, electroneuromyography, polysomnography, and genetic testing for CMT disease. FINDINGS: 11 of the 14 family members had the autosomal dominant demyelinating form of CMT disease with PMP22 gene duplication on chromosome 17. Whatever their neurological disability, all 11 individuals had sleep apnoea syndrome with a mean (SD) apnoea-hypopnoea index of 46.6/h (28.5) of sleep (normal value <15/h). The remaining three family members were free from neuropathy and sleep apnoea syndrome. Sleep apnoea and neuropathy severity were highly correlated; the compound muscle action potential (CMAP) amplitude of the median nerve was inversely correlated with the apnoea-hypopnoea index (r=-0.69, p=0.029). The severity of neuropathy and sleep apnoea were higher in male CMT individuals and were correlated with age and body mass index. No wake or sleep diaphragmatic dysfunction was shown. INTERPRETATION: We think that sleep apnoea syndrome is related to a pharyngeal neuropathy. Upper airway dysfunction, previously described in the CMT2C subtype, might be a clinical expression of the CMT1A subtype, to which familial susceptibility could predispose.

Adolescent↗
PubMed2001

Sleep apnoea and Turner's syndrome.

A 32-yr-old female with Turner's syndrome and anatomical craniofacial abnormalities, presented with obstructive sleep apnoea syndrome. This was initially treated by nasal continuous positive airway pressure and secondarily cured by maxillomandibullar advancement osteotomy. Anatomical upper airway abnormalities and hormonal factors, which predispose Turner patients to develop obstructive sleep apnoea syndrome, are discussed. A systematic assessment and treatment of sleep-disordered breathing is probably of interest in these patients.

Adult↗
PubMed2001

[Imaging in obstructive sleep apnea syndrome].

Obstructive sleep apneas result from pharyngeal collapse during sleep. Upper airways may be investigated using either static or dynamic techniques during wakefulness or sleep. In OSAS patients, imaging has different goals: to describe the anatomy of the pharynx and the sequence of the pharyngeal collapse, to try to select patients that will benefit from surgery, and to analyze the results of different treatments.

Airway Resistance↗