The advantage of being a National Referral Centre for patients with suspected obstructive sleep apnoea (OSA) was used to seek clinical factors predictive of OSA, and thus determine if the number of polysomnography tests required could be reduced. Patients were mainly primary referrals, from an island population of 3.5 million.Two hundred and fifty consecutive patients underwent clinical assessment, full polysomnography, and a detailed self-administered questionnaire. This represents one of the largest European studies, so far, utilizing full polysomnography.Fifty four percent (n=134) had polysomnographic evidence of OSA (apnoea/hypopnoea index (AHI) ≥15 events·h -1 sleep). Patients with OSA were more likely to be male, and had a significantly greater prevalence of habitual snoring, sleeping supine, wakening with heartburn, and dozing whilst driving. Alcohol intake, age and body mass index (BMI) were significant independent correlates of AHI. After controlling for BMI and age, waist circumference correlated more closely with AHI than neck circumference among males, while the opposite was true among females.No single factor was usefully predictive of obstructive sleep apnoea. However, combining clinical features and oximetry data, where appropriate, approximately one third of patients could be confidently designated as having obstructive sleep apnoea or not. The remaining two thirds of patients would still require more detailed sleep studies, such as full polysomnography, to reach a confident diagnosis.

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H Ha ae em mo od dy yn na am mi ic c e ef ff fe ec ct ts s o of f n na as sa al l c co on nt ti in nu uo ou us s p po os si it ti iv ve e a ai ir rw wa ay y p pr re es ss su ur re e i in n s se ev ve er re e c co on ng ge es st ti iv ve e h he ea ar rt t f fa ai il lu ur re e R. Liston*, P.C. Deegan*, C. Right heart catheter studies were performed in seven awake males (aged 51-75 yrs) with stable CHF, before, during and after the application of 5 cmH 2 O NCPAP over 3 h. All patients had left ventricular ejection fractions ≤30% and baseline pulmonary capillary wedge pressures >12 mmHg, and six patients were in atrial fibrillation.Cardiac index fell from baseline in all patients whilst on NCPAP, with the greatest fall at 2 h (from 3.3±0.3 (mean±SEM) at baseline to 2.8±0.2 l·min -1 ·m -2 ) and rose back to baseline after NCPAP withdrawal. Systemic vascular resistance (SVR) increased during NCPAP application (1,268±108 to 1,560±82 dyn·s -1 ·cm 5 ), with baseline SVR showing a significant negative correlation vs percentage fall in cardiac index (CI) at 2 h on multiple linear regression analysis (r 2 =0.8).These data indicate that domiciliary nocturnal NCPAP should not be prescribed as part of the therapy in severe CHF without first determining the individual patient's cardiac response to such therapy.

Congenital central hypoventilation syndrome is a rare disorder characterised by chronic alveolar hypoventilation, which becomes more pronounced during sleep and may be associated with neurocristopathies, such as Hirchsprung's disease. A mutation in the PHOX2B gene has recently been identified.In a family of both parents and five offspring, detailed clinical assessment, pulmonary function testing, overnight sleep studies and ventilatory responsiveness to progressive hypercapnia (V9R,CO 2 ) were performed, in addition to analysis of known genetic loci for this condition.The father and four of the offspring demonstrated features of central hypoventilation with nonapnoeic oxygen desaturation during sleep and diminished V9R,CO 2 , despite normal pulmonary function. The lowest sleep saturation was median (range) 79% (67-83%) and V9R,CO 2 was 2. . An in-frame five amino acid polyalanine expansion of the PHOX2B gene was found in all affected subjects, while the mother and fifth child, who did not have features of central hypoventilation, had a normal PHOX2B gene. Magnetic resonance imaging of the brainstem in one severely affected child was normal.The present study of a unique family confirms that transmission of late-onset congenital central hypoventilation syndrome is autosomal dominant in nature.