CPAP treatment of sleep apnoea in the early phase of stroke: growing evidence of effectiveness.

S leep apnoea has been shown to be a cardiovascular risk factor [1, 2], presumably with a major role attributable to intermittent hypoxia [3, 4]. Early reports have suggested a relationship between sleep-disordered breathing and stroke [5–8]. The association between sleep apnoea and both prevalent and incident stroke has been further established in general population cohorts [9, 10]. Specifically, the Wisconsin Sleep Cohort provided prospective evidence that sleep-disordered breathing precedes stroke and may contribute to the development of stroke [9]. The prospective analysis of the Sleep Heart and Health Study also showed, in males ,70 yrs of age, a strong adjusted association between ischaemic stroke and apnoea–hypopnoea index (AHI) in mild-to-moderate sleep apnoea [10]. In this subgroup of middle-aged males, in the mild-to-moderate range of severity (AHI 5–25 events?h), each one-unit increase in AHI was estimated to increase stroke risk by 6%. It has also been shown that stroke and sleep apnoea are associated with increased mortality [8, 11]. However, in a recent meta-analysis of 2,343 ischaemic or haemorrhagic stroke and transient ischaemic attack (TIA) patients, obstructive sleep apnoea (OSA) was very common, irrespective of the type of stroke or timing after stroke [12]. Regardless of whether the studies were performed in acute stroke units or rehabilitation units, OSA was found in .50% of the stroke patients. Also, central events were limited to 7% of the total number of abnormal respiratory events during sleep. Consequently, as this association between sleep apnoea and stroke has been demonstrated, treating sleepdisordered breathing could be expected to be beneficial [13, 14]. The role of continuous positive airway pressure (CPAP) in stroke patients presenting with sleep apnoea is, however, still under discussion. It remains uncertain whether CPAP is feasible in these patients with a long-term acceptance that seems much lower than in other patient subgroups and requires caution with respect to haemodynamic tolerance [14–17]. Also, whether CPAP is able to significantly alter stroke outcomes remains to be established. Although there are positive data from recent studies [18, 19], there are also conflicting data with limited benefit and possible deleterious effects [20]. In this issue of the European Respiratory Journal, PARRA et al. [21] report on a randomised controlled trial (RCT) assessing the impact of CPAP in ischaemic stroke patients followed for 2 yrs. Stroke patients with an AHI o20 events?h were randomised either to early CPAP within the first 3–6 days after stroke or conventional treatment. CPAP led to an earlier improvement in neurological symptoms and a reduction in cardiovascular events, but there was no improvement in patients’ survival or quality of life [21]. This is the first study of early CPAP carried out in a homogeneous group of patients with acute, first-ever ischaemic stroke. Potential beneficial effects of CPAP being administered earlier (i.e. within the first 24 h) with the stroke in progress cannot be excluded. It is also possible that the studied population was not fully representative of usual stroke patients. Severe stroke patients were likely to be excluded because only first-ever stroke patients with unaltered level of consciousness were eligible. The sample size of this study is also an issue. The study is probably slightly underpowered, which may explain why the cardiovascular event-free survival after 24 months was similar in both groups and also why the cardiovascular mortality rate, although being 0% in the CPAP group and 4.3% in the control group, was also not statistically different. Finally, the study was analysed in a per protocol and not an intention-to-treat manner, as the patients who did not tolerate CPAP were excluded form the analysis. Nevertheless, this remains the first study of this nature and, as such, is an important step forward.