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Sleep quality is often poor in patients with chronic obstructive pulmonary disease (COPD), but these night-time symptoms are frequently unnoticed by physicians and/or not reported by patients themselves. Therefore, the prevalence and clinical impact of sleep disturbances and night-time symptoms in COPD is not well understood and has not been a clinical focus to date. To address this gap, an expert panel meeting was convened in Barcelona, Spain, in March 2011 to discuss the aetiology, evolution, burden, long-term clinical consequences and optimal management of night-time symptoms in COPD. The term “night-time symptoms” in COPD has not been distinctly defined in an objective sense but epidemiological data suggests that the prevalence of nocturnal symptoms and symptomatic sleep disturbance may exceed 75% in patients with COPD. The panel concluded that night-time symptoms in COPD are prevalent and bothersome; that their cause(s) are multiple and include demographic factors, such as age and obesity, pharmacotherapy, disease-specific symptoms and the presence of comorbid sleep disorders, and other medical conditions; and that potential long-term consequences can include lung function changes, increased exacerbation frequency, emergence or worsening of cardiovascular disease, cognitive effects, depression, impaired quality of life and increased mortality. To date, few interventional studies have investigated them, but emerging data suggest that bronchodilator therapy can improve them if deployed appropriately. In summary, night-time symptoms in COPD warrant further clinical investigation with validated tools.

The objective of the present article was to explore the relationship between obstructive sleep apnoea (OSA) and hypertension (HT) and/or arterial vascular disease (VD), including stroke and ischaemic coronary disease. Epidemiological and interventional studies on these relationships provide compelling evidence that OSA is causally related to HT. The causal relationship between OSA and VD other than HT has not been firmly established. A number of pathophysiological mechanisms that could potentially provide a causal link between obstructive sleep apnoea and hypertension, as well as vascular disease, have been identified. Available data on such mechanisms include sustained daytime sympathetic activation, oxidative stress, promotion of vascular inflammation and endothelial dysfunction.