• Sleep Apnoea

Hypertension affects about 25% of the adult population worldwide. It ranks as the leading chronic risk factor for mortality, accounting for 13.5% of all deaths. Half of all strokes and ischaemic heart disease events are attributable to high blood pressure (BP).1 ,2

Obstructive sleep apnoea (OSA) is now recognised as a risk factor for the development of hypertension in European and the US International Guidelines. OSA and hypertension are linked in a dose-response fashion. This is true even when the usual confounding factors such as age, alcohol, tobacco consumption and Body Mass Index are taken into account.3 In a large prospective observational cohort followed for more than 12 years, it has been shown that compared with controls, the adjusted HRs for incident hypertension were twofold greater among patients with severe OSA who declined continuous positive airway pressure (CPAP) therapy.4

At least four meta-analyses derived from 32 randomised controlled trials (RCTs) have demonstrated that CPAP, the first-line therapy for moderate to severe OSA syndrome, reduces 24 h mean BP by approximately −2 mm Hg (pooled estimated effect).5–8 In these meta-analyses, heterogeneity is a clear concern with some of the analysed studies excluding hypertensive patients, while others only included hypertensive patients. Furthermore, the presence and/or the description of antihypertensive classes of medications are poorly reported. The first strength of the study by Bratton et al 9 is to restrict the investigation to a homogeneous group with minimally symptomatic OSA. Whereas CPAP treatment is clearly indicated in sleepy symptomatic OSA, CPAP prescription with the aim of reducing cardio-metabolic risk in minimally symptomatic patients remains a frequent clinical practice. This should be argued because CPAP effects on hypertension appear to be limited mainly to the more severe and symptomatic patients, with little benefit observed in patients who did not feel sleepy during …