Correspondence
We read with interest the article by McMillan and colleagues. 1 We commend the efforts of the group in doing this robust, real life, trial. Although the results of the trial are a practical solution to an unexplored problem, we mention here some relevant points. First, a large discrepancy exists between the overnight desaturation index (ODI) and Epworth sleepiness scores (ESS). A high ODI (mean 29·4 in the continuous positive airway pressure [CPAP] group) but an ESS of only 11·6 (mean in the CPAP group) poses the question as to whether the patients in this group were hypoxic right from the start, as the inclusion criteria did recruit patients with O2 of more than 90% on air. No blood gases were done at the time of recruitment despite the fact that the mean BMI in the CPAP group was 33·9 kg/m2. This discrepancy could also be due to the fact that the perception of sleepiness in the elderly might be different to that in the younger population, so they might have underscored in their ESS.2 Second, the mean usage of CPAP in the intervention group was less than 2 h (between 3 and 12 months usage), which is well below the time recommended (4–6 h) to get positive outcomes from this treatment. 3 Hence, whether the reduction in ESS was due to the treatment itself or part of the patient’s attitude towards sleep is not known. These findings become important for the funding of such treatment, which might cost the clinical commissioning group UK £1363 per patient per year. Third, the study failed to show any improvement in cognitive function with CPAP treatment but this could be because patients had high Mini–Mental State Examination scores (mean 29 in the CPAP group) already at the time of recruitment— therefore any effect would have been
coincidental. Declining cognition, particularly in this age group (mean age 70·9 years in CPAP group), with 30% of study participants having cardiovascular risk factors, is of growing interest.4 The study should have looked at answering this question to help further research in this interesting area.
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Sleep apnoea in the elderly
We declare no competing interests.
*Nawaid Ahmad, Koottalai Srinivasan, Thirumalai R Naicker, Harmesh Moudgil
[email protected] Princess Royal Hospital, Shrewsbury and Telford Hospitals NHS Trust, Apley Castle, Telford, Shropshire TF2 0DL, UK 1
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McMillan A, Bratton DJ, Faria R, et al., on behalf of the PREDICT Investigators. Continuous positive airway pressure in older people with obstructive sleep apnoea syndrome (PREDICT): a 12-month, multicentre, randomised trial. Lancet Respir Med 2014; 2: 804–12. Morrell M, Finn L, McMillian A, Peppard PE. Aging reduces the association between sleepiness and sleep disordered breathing. Eur Respir J 2012; 40: 386–93. Weaver TE, Maislin G, Dinges DF, et al. Relationship between hours of CPAP use and achieving normal levels of sleepiness and daily functioning. Sleep 2007; 30: 711–19. Yaffe K, Laffan AM, Harrison SL, et al. Sleepdisordered breathing, hypoxia, and risk of mild cognitive impairment and dementia in older women. JAMA 2011; 306: 613–19.
Authors’ reply We thank Dr Ahmad and colleagues for their comments about our article1 reporting the outcome of the PREDICT trial, a 12-month randomised controlled trial showing that continuous positive airway pressure (CPAP) reduces subjective sleepiness in older people with obstructive sleep apnoea syndrome at 3 months, with this beneficial effect maintained at 12 months. The first issue raised was that the severity of obstructive sleep apnoea, as measured by the overnight desaturation index (ODI), appeared disproportionately high compared with the symptoms of sleepiness measured by the Epworth sleepiness score (ESS). This relationship could have occurred if the recruited patients with obstructive sleep apnoea syndrome were hypoxic at baseline,
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producing an increased likelihood of desaturation during apnoea or hypopnoea, and a consequent high ODI. However, the correlation between ODI and ESS, and between ESS and the apnoea/hypopnoea index are known to be poor.2 Also, although arterial blood gases were not measured at baseline, the oxygen saturation (SpO2) on room air was recorded. Mean (SD) SpO2 on room air for the Best Supportive Care group (n=138) was 95·4% (2·0) versus 95·3% (1·8) for the CPAP group (n=140). Despite the low mean CPAP use in our trial, we found a therapeutic dose–response relation between treatment effect and CPAP use. The treatment effect was also consistent with previous studies, and the mean CPAP use was similar to a 6-month, randomised, controlled trial of CPAP in minimally symptomatic patients with obstructive sleep apnoea.3 We disagree that the reduction in ESS was due to the patient’s attitude to sleep because the study design controlled for factors such as sleep attitudes and clinic appointments. Lastly, the co-primary outcomes of our trial were an improvement in sleepiness, and cost-effectiveness over 12 months. We acknowledge that the effect of obstructive sleep apnoea syndrome on cognitive function in older people is an important issue, but this was not the primary outcome of this trial. The secondary analysis did not find any evidence that CPAP improved cognitive e21