Lowering blood pressure with continuous positive airway pressure: a work in progress

Abundant evidence supports a role of obstructive sleep apnoea (OSA) in the pathophysiology of cardiovascular diseases (CVDs), including hypertension [1]. During sleep, patients with OSA experience repeated episodes of upper airway obstruction, which are associated with hypoxaemia, ventilatory changes and arousal that precipitate haemodynamic and autonomic responses leading to acute blood pressure (BP) surges. Recurrent exposure to apnoeas and hypopnoeas and related hypoxic perturbations are thought to induce chronic impairment in BP regulatory mechanisms, ultimately compromising BP control across the 24 h and predisposing to sustained hypertension. Accordingly, OSA and high BP frequently co-occur – hypertension affects about 50% of OSA patients and more than 30% of hypertensive patients have OSA [1]. OSA also confers more than a two-fold increased risk of incident hypertension [2, 3], and high BP partially accounts for the excess CVD and death risk observed in OSA [4, 5].