The association between obstructive sleep apnea (OSA) and hypertension is well established, with putative mechanisms including hypoxia-induced sympathetic activation, as well as renin-angiotensin-aldosterone activation. One would hope, then, that if OSA is causing the elevation in blood pressure (BP) — rather than just being an innocent bystander, or for instance being associated through a common comorbidity such as obesity — treatment of OSA might reduce BP.
Fava et al performed a systematic review and meta-analysis of randomized, controlled trials that reported data on BP in patients treated by continuous positive airway pressure (CPAP) for OSA (n = 2566). Overall, when compared to no treatment, OSA treatment was associated with a statistically significant reduction in BP, which was particularly prominent during the night (3.8/1.8 mmHg reduction). Although at first blush this degree of BP lowering might not seem that important, CPAP treatment trials are characterized by three limitations: 1) they are short term — most are 3 months or less, 2) the fact that patients entered a CPAP trial does not guarantee full compliance with the CPAP, and 3) less than half of the patients had hypertension, so we would anticipate a very small change in BP in a non-hypertensive population. Indeed, in subgroup analysis it is demonstrated that trials with longer duration and among patients with better compliance, BP reductions were greater.
Recognition that OSA is associated with resistant hypertension, coupled with the knowledge that CPAP treatment of OSA improves BP, bolsters both the therapeutic rationale for CPAP and inclusion of OSA screening as a component of evaluation for patients with resistant hypertension.
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