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Obstructive sleep apnoea (OSA) occurs because of recurrent narrowing and occlusion of the velopharynx (VP) during sleep. The speci®c cause of OSA is unknown. Cephalometric radiography, ®breoptic nasopharyngoscopy, acoustic re¯ec-tion techniques, and computerized tomography have limitations (dynamic and tridimensional evaluation) in the mechanism of occlusion investigation. Static and dynamic examination of the soft tissue structures surrounding the upper airway during the respiratory cycle in wakefulness and sleep, can lead to a better understanding of the process.Ultrafast magnetic resonance imaging (one image per 0.8 s) was used to study the upper airway and surrounding soft tissue in 17 patients with OSA during wakefulness and sleep, and in eight healthy subjects whilst awake.The major ®ndings of this investigation in the 25 subjects were as follows: 1) the VP was smaller in apnoeic patients, only during part of the respiratory cycle; 2) the variation in VP area during the respiratory cycle was greater in apnoeic patients than in controls, particularly during sleep, suggesting an increased compliance of the VP in these patients; 3) VP narrowing was similar in the lateral and anterior-posterior dimensions, both in controls and apnoeic patients while awake; apnoeic patients during sleep have a more circular VP upon reaching the minimum area; 4) there was an inverse relationship between dimensions of the lateral pharyngeal walls and airway area, probably indicating that lateral walls are passively compressed or stretched as a result of changes in the airway calibre; and 5) soft palate and parapharyngeal fatpads were larger in apnoeic patients, although their role in the genesis of OSA is uncertain.It was concluded that changes in the velopharynx area and diameter during the respiratory cycle are greater in apnoeic patients than in normal subjects, particularly during sleep. This suggests that apnoeic patients have a more collapsible velopharynx, this being the main mechanism of obstruction. Eur Respir J 2001; 17: 79±86. Obstructive sleep apnoea (OSA) occurs because of recurrent narrowing and occlusion of the upper airway during sleep [1], and the site of obstruction is most commonly at the level of the velopharynx (VP). Unfortunately, the speci®c cause of this obstruction is unknown [2±4]. Cephalometric analysis [5,6], which provides information on the morphology of the upper airway, does not allow dynamic evaluation. Fibreoptic nasopharyngoscopy with the Mu È ller manoeuvre [4,7,8] allows a dynamic evaluation of the pharyngeal airway, but is usually performed with the patient awake, and the changes in pressure and shape during the manoeuvre are not necessarily representative of the physiological changes during quiet breathing. Acoustic re¯ection has been used to demonstrate increased effective compliance of the pharynx during wakefulness in OSA patients in response to changes in pharyngeal intraluminal pressure and lung volume [9,10]. A major limitation of the acoustic re¯ection technique is its inabi...

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The impact of blood eosinophilia in chronic obstructive pulmonary disease (COPD) remains controversial.To evaluate the prevalence and stability of a high level of blood eosinophils (≥300 cells·μL) and its relationship to outcomes, we determined blood eosinophils at baseline and over 2 years in 424 COPD patients (forced expiratory volume in 1 s (FEV) 60% predicted) and 67 smokers without COPD from the CHAIN cohort, and in 308 COPD patients (FEV 60% predicted) in the BODE cohort. We related eosinophil levels to exacerbations and survival using Cox hazard analysis.In COPD patients, 15.8% in the CHAIN cohort and 12.3% in the BODE cohort had persistently elevated blood eosinophils at all three visits. A significant proportion (43.8%) of patients had counts that oscillated above and below the cut-off points, while the rest had persistent eosinophil levels <300 cells·μL A similar eosinophil blood pattern was observed in controls. Exacerbation rates did not differ in patients with and without eosinophilia. All-cause mortality was lower in patients with high eosinophils compared with those with values <300 cells·μL (15.8% 33.7%; p=0.026).In patients with COPD, blood eosinophils ≥300 cells·μL persisting over 2 years was not a risk factor for COPD exacerbations. High eosinophil count was associated with better survival.

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The value and timing of multidimensional assessments in chronic obstructive pulmonary disease (COPD) remains unclear because there is little information about their variability and relationship to outcome. The aim of this study was to determine the progression of COPD using clinical and spirometric variability over time with mortality as the outcome.We determined the annual intra-individual variability of forced expiratory volume in 1 s (FEV1) and BODE (body mass index, airflow obstruction, dyspnoea, exercise capacity) index in 403 patients with at least five measurements. The pattern was defined as ''stable'' if the annual change remained constant in o66% of the observations and ''unstable'' if it did not meet that threshold. We explored the minimum number of yearly observations that related to mortality in the 704 patients of the cohort.The ''unstable'' pattern of FEV1 was seen in 53% and 40% of patients using a threshold of 40 mL?year -1 and 100 mL?year -1 , respectively. There was a slightly more ''stable'' pattern in the BODE index (62% for 1 point). A profile associated with mortality was defined by a baseline measurement followed by annual measurements for 2 years of the BODE index, but not its individual components, including FEV1 (p,0.001).Progression of COPD measured using FEV1 is inconsistent and relates poorly to outcome. Monitoring the more stable BODE index better assesses disease progression. @ERSpublications COPD patients have a high annual variability in FEV1. The BODE index is more stable and useful to assess COPD progression