The treatment for obstructive sleep apnoea (OSA) with continuous positive airway pressure (CPAP) or mandibular advancement devices (MADs) is associated with blood pressure (BP) reduction; however, the overall effect is modest. The aim of this systematic review and meta-analysis of randomised controlled trials (RCTs) comparing the effect of such treatments on BP was to identify subgroups of patients who respond best to treatment.The article search was performed in three different databases with specific search terms and selection criteria. From 2289 articles, we included 68 RCTs that compared CPAP or MADs with either passive or active treatment. When all the studies were pooled together, CPAP and MADs were associated with a mean BP reduction of −2.09 (95% CI −2.78– −1.40) mmHg for systolic BP and −1.92 (95% CI −2.40– −1.43) mmHg for diastolic BP and −1.27 (95% CI −2.34– −0.20) mmHg for systolic BP and −1.11 (95% CI −1.82– −0.41) mmHg for diastolic BP, respectively. The subgroups of patients who showed a greater response were those aged <60 years (systolic BP −2.93 mmHg), with uncontrolled BP at baseline (systolic BP −4.14 mmHg) and with severe oxygen desaturations (minimum arterial oxygen saturation measured by pulse oximetry <77%) at baseline (24-h systolic BP −7.57 mmHg).Although this meta-analysis shows that the expected reduction of BP by CPAP/MADs is modest, it identifies specific characteristics that may predict a pronounced benefit from CPAP in terms of BP control. These findings should be interpreted with caution; however, they are particularly important in identifying potential phenotypes associated with BP reduction in patients treated for OSA.

Awareness of the importance of sleep-related disorders in patients with cardiovascular diseases is growing. In particular, sleep-disordered breathing, short sleep time, and low sleep quality are frequently reported by patients with heart failure (HF). Sleep-disordered breathing, which includes obstructive sleep apnoea (OSA) and central sleep apnoea (CSA), is common in patients with HF and has been suggested to increase the morbidity and mortality in these patients. Both OSA and CSA are associated with increased sympathetic activation, vagal withdrawal, altered haemodynamic loading conditions, and hypoxaemia. Moreover, OSA is strongly associated with arterial hypertension, the most common risk factor for cardiac hypertrophy and failure. Intrathoracic pressure changes are also associated with OSA, contributing to haemodynamic alterations and potentially affecting overexpression of genes involved in ventricular remodelling. HF treatment can decrease the severity of both OSA and CSA. Indeed, furosemide and spironolactone administration, exercise training, cardiac resynchronization therapy, and eventually heart transplantation have shown a positive effect on OSA and CSA in patients with HF. At present, whether CSA should be treated and, if so, which is the optimal therapy is still debated. By contrast, more evidence is available on the beneficial effects of OSA treatment in patients with HF.

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This study demonstrated that patients with ALS have a significant poor quality of sleep, and this correlated with the severity of ALS and daytime somnolence. Increased awareness for sleep-wake problems in patients with ALS is important, as effective intervention could lead to a better management of these patients.