Obstructive sleep apnoea as a cause of nocturnal non-dipping blood pressure:recent evidence regarding clinical importance and underlying mechanisms

These recent reports regarding the very high general prevalence of SDB and factors that influence the relationship with hypertension prompt a reassessment of the clinical relevance regarding the association between OSA and hypertension, especially nocturnal hypertension, and the underlying mechanisms that may contribute to the development of a non-dipping nocturnal blood pressure profile in OSA patients.

This topic is important in the context of the recent SAVE (Sleep Apnea Cardiovascular Endpoints) trial report involving 2717 patients with established cardiovascular disease and moderate or severe OSA associated with minimal sleepiness who were randomised to best usual care with or without added continuous positive airway pressure (CPAP) therapy and followed for up to 7 years. CPAP therapy was not associated with any improvement in cardiac or cerebrovascular outcome, although data on secondary and

other end-points in the report indicated a small but significant reduction in diastolic blood pressure. This finding is particularly relevant in the context that the average compliance with CPAP was only 3.3 h and a recent meta-analysis indicates that beneficial effects of CPAP on blood pressure in OSA patients with minimal sleepiness are largely confined to patients using CPAP for >4 h per night.

Hypertension is present in up to 50% of patients with OSA, which is close to double the prevalence of hypertension in general population studies. Blood pressure normally follows a diurnal pattern such that the average nocturnal systolic blood pressure is >10% lower than during day-time. Loss of this nocturnal dipping blood pressure pattern in both normotensive and hypertensive subjects is associated with a worse cardiovascular prognosis [10], which is particularly relevant in OSA because of the high likelihood of a nocturnal non-dipping profile. Data from the Wisconsin Sleep Cohort Study indicate a

dose–response increase in the development of non-dipping hypertension with severity of SDB at baseline when followed for 7 years, which was confirmed by a recent report demonstrating that in patients attending a cardiology clinic with known cardiovascular disease and moderate or severe OSA there is a 4% increase in the odds of having a non-dipping blood pressure profile per unit increase in AHI. Further recent data from the Wisconsin Cohort indicate that SDB during rapid eye movement sleep is particularly associated with a non-dipping nocturnal blood pressure pattern.

OSA as a cause of nocturnal nondipping BP .pdf

Download PDF • 280KB