There is increasing evidence that intermittent hypoxia plays a role in the development of cardiovascular risk in obstructive sleep apnoea syndrome (OSAS) through the activation of inflammatory pathways. The development of translational models of intermittent hypoxia has allowed investigation of its role in the activation of inflammatory mechanisms and promotion of cardiovascular disease in OSAS. There are noticeable differences in the response to intermittent hypoxia between body tissues but the hypoxia-sensitive transcription factors hypoxia-inducible factor-1 and nuclear factor-kB appear to play a key role in mediating the inflammatory and cardiovascular consequences of OSAS. Expanding our understanding of these pathways, the cross-talk between them and the activation of inflammatory mechanisms by intermittent hypoxia in OSAS will provide new avenues of therapeutic opportunity for the disease.

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.

Cardiovascular disorders are common in patients with obstructive sleep apnoea syndrome (OSAS) but there is debate as to whether OSAS is an independent risk factor for their development, since OSAS may be associated with other disorders and risk factors that predispose to cardiovascular disease.In an effort to quantify the risk of OSAS patients for cardiovascular disease arising from these other factors, the authors assessed the future risk for cardiovascular disease among a group of 114 consecutive patients with established OSAS prior to nasal continuous positive airway pressure therapy, using an established method of risk prediction employed in the Framingham studies.Patients were 100 males, aged (meanSD) 529.0 yrs, and 14 females, aged 5110.4 yrs, with an apnoea/hypopnoea index of 4522 . h -1 . Based on either a prior diagnosis, or a mean of three resting blood pressure recordings >140 mmHg systolic and/or 90 diastolic, 68% of patients were hypertensive. Only 18% were current smokers, while 16% had either diabetes mellitus or impaired glucose tolerance, and 63% had elevated fasting cholesterol and/or triglyceride levels. The estimated 10-yr risk of a coronary heart disease (CHD) event in males was (meanSEM) 13.90.9%, 95% confidence interval (95% CI) 12.1±16.0, and for a stroke was 12.31.4%; 95% CI 9.4± 15.1, with a combined 10 yr risk for stroke and CHD events of 32.92.7%; 95% CI 27.8±38.5 in males aged >53 yrs.These findings indicate that obstructive sleep apnoea syndrome patients are at high risk of future cardiovascular disease from factors other than obstructive sleep apnoea syndrome, and may help explain the difficulties in identifying a potential independent risk from obstructive sleep apnoea syndrome.

Self-reported snoring is common in pregnancy, particularly in females with pre-eclampsia. The prevalence of inspiratory flow limitation during sleep in pre-eclamptic females was objectively assessed and compared with normal pregnant and nonpregnant females.Fifteen females with pre-eclampsia were compared to 15 females from each of the three trimesters of pregnancy, as well as to 15 matched nonpregnant control females (total study population, 75 subjects). All subjects had overnight monitoring of respiration, oxygen saturation, and blood pressure (BP).No group had evidence of a clinically significant sleep apnoea syndrome, but patients with pre-eclampsia spent substantially more time (31±8.4% of sleep period time, mean±sd) with evidence of inspiratory flow limitation compared to 15.5±2.3% in third trimester subjects and <5% in the other three groups (p=0.001). In the majority of pre-eclamptics, the pattern of flow limitation was of prolonged episodes lasting several minutes without associated oxygen desaturation. As expected, systolic and diastolic BPs were significantly higher in the pre-eclamptic group (p<0.001), but all groups showed a significant fall (p≤0.05) in BP during sleep.Inspiratory flow limitation is common during sleep in patients with pre-eclampsia, which may have implications for the pathophysiology and treatment of this disorder.

The increasing numbers of patients referred for evaluation of suspected obstructive sleep apnoea (OSA) places a growing burden on available sleep laboratory resources. A number of limited diagnostic systems have been developed in an effort to cope with this clinical problem. In this study, the diagnostic capabilities of one limited diagnostic system (ResCare Autoset) were compared with full polysomnography (PSG), using the Oxford SAC computerized system. Thirty six patients with suspected OSA had simultaneous studies performed both with the Autoset and Oxford PSG systems. The apnoea plus hypopnoea index (AHI) (events x h(-1)) scored by the Autoset system was compared with the AHI scored from the PSG raw tracings by an experienced sleep technician. There were highly significant correlations between the Autoset AHI and the AHI scored by the manual PSG scoring method (r=0.92; p<0.001). The positive predictive value for diagnosis of OSA for the Autoset was 86% when compared with manual PSG scoring, based on an AHI threshold for OSA of 15 events x h(-1). However, the agreement between Autoset and PSG was poor in severe cases of OSA, although not sufficiently so as to result in mistaken diagnosis in any of these cases. We conclude that the Autoset system is a sensitive and easy to use system, which facilitates screening for obstructive sleep apnoea with a reasonable degree of accuracy.

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.

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