May 22nd, 2012
Studies Probe Effect of CPAP and Sleep Apnea on Hypertension
Larry Husten, PHD
Two studies published in JAMA provide additional, but not surprising, information about the relationship between obstructive sleep apnea (OSA) and hypertension — and the role of continuous positive airway pressure (CPAP).
In the first study, Ferran Barbé and colleagues randomized 725 people with OSA but no daytime sleepiness to either CPAP or no active treatment. After a median follow-up of 4 years, there were fewer cases of systemic hypertension or cardiovascular events in the CPAP group than in the control group, but this difference did not reach statistical significance.
Incidence of hypertension or cardiovascular events:
- CPAP: 9.20 per 100 person-years (CI, 7.36-11.04)
- Control: 11.02 per 100 person-years (CI, 8.96-13.08)
The authors conclude that the study may have been underpowered to find a significant difference, though they also speculate that CPAP may be less effective in OSA patients without daytime sleepiness.
In the second study, José Marin and colleagues followed 1889 people without hypertension who had a sleep test. Over a median follow-up of 12 years, OSA was associated with an increased risk for developing hypertension, and treatment with CPAP was associated with a lower hypertension risk.
Adjusted hazard ratio for hypertension (compared with controls without OSA):
- OSA ineligible for CPAP: 1.33 (CI 1.01-1.75)
- Declined CPAP: 1.96 (CI 1.44-2.66)
- Nonadherent to CPAP: 1.78 (CI 1.23-2.58)
- CPAP therapy: 0.71 (95% CI 0.53-0.94)
The authors comment that their study is “clinically relevant considering that OSA, despite a high prevalence in Western populations, remains overwhelmingly unrecognized and untreated.” Although it was not a randomized study, the results strongly suggest “that OSA may be an independent modifiable risk factor for development of new-onset hypertension.”
In an accompanying comment, Vihesh Kapur and Edward Weaver discuss the limitations of the studies but write that the research contributes to the considerable body of evidence that “supports the role of identification and treatment of OSA to improve symptoms, quality of life, and cardiovascular end points.”