May 23, 2012 — A pair of studies released this week confirm an association between obstructive sleep apnea (OSA) and hypertension, and hint that adherent continuous positive airway pressure (CPAP) therapy may reduce the risk for new-onset hypertension.
Vishesh K. Kapur, MD, MPH, and Edward M. Weaver, MD, MPH, both from the University of Washington in Seattle, add that treatment of OSA “may not only reduce blood pressure (although modestly on average), but if confirmed by future studies also may prevent hypertension in at-risk patients. Thus, OSA deserves attention in patients with or at risk of developing hypertension as a potentially treatable cause of hypertension as well as other clinically important outcomes.”
A Modifiable Risk Factor
In their paper, José M. Marin, MD, from the Hospital Universitario Miguel Servet in Zaragoza, Spain, and colleagues report results of an observational cohort study of 1889 adults without hypertension referred for polysomnography between January 1, 1994, and December 31, 2000.
Among the 1579 patients with OSA, 462 were ineligible for CPAP therapy according to national treatment guidelines, 195 were eligible but declined CPAP, 98 were eligible and started CPAP but were nonadherent, and 824 were eligible and adhered to CPAP.
During a median follow-up of 12.2 years, 705 patients (37.3%) developed hypertension. “Compared with participants without OSA, untreated OSA was associated with an increased risk of new-onset hypertension, whereas treatment with CPAP therapy was associated with a lower risk of new-onset hypertension,” Dr. Marin told Medscape Medical News.
Table. Risk for Hypertension With OSA
| Group | Adjusted Hazard Ratio (95% Confidence Interval) |
| Ineligible for CPAP | 1.33 (1.01 – 1.75) |
| Declined CPAP | 1.96 (1.44 – 2.66) |
| Nonadherent to CPAP | 1.78 (1.23 – 2.58) |
| CPAP therapy | 0.71 (0.53 – 0.94) |
“OSA appears to be a modifiable risk factor for new-onset hypertension. Such findings are clinically relevant considering that OSA, despite a high prevalence in Western populations, remains overwhelmingly unrecognized and untreated,” Dr. Marin said.
In a separate paper, Ferran Barbé, MD, from the Institut de Recerca Biomedica, Lleida, Spain, and colleagues report results of a randomized, controlled trial (RCT) testing the effects of CPAP on incident hypertension or cardiovascular events in 723 adults with OSA but without daytime sleepiness. There were 357 adults in the CPAP group and 366 in the control group (usual care).
During follow-up lasting a median of 4 years, there were 68 cases of new hypertension and 28 cardiovascular events in the CPAP group, compared with 79 cases of new hypertension and 31 cardiovascular events in the control group.
In the CPAP group, there was a trend toward a reduction in the incidence of hypertension and cardiovascular events that did not reach statistical significance. The incidence of new hypertension or cardiovascular event per 100 person-years was 9.20 (95% confidence interval [CI], 7.36 – 11.04) in the CPAP group vs 11.02 (95% CI, 8.96 – 13.08) in the control group (incidence density ratio, 0.83; 95% CI, 0.63 – 1.1; P = .20).
However, the investigators note that their study may have limited power to detect a significant difference, and that a larger study or longer follow-up might have been able to identify a significant association between treatment and outcome.
They point out that a post hoc analysis “suggested that CPAP treatment may reduce the incidence of hypertension or cardiovascular events in patients with CPAP adherence of 4 h/night or longer.”
“This is the first RCT to focus on the effects of CPAP treatment in the prevention of hypertension and cardiovascular events in patients with sleep apnea,” Dr. Barbé added in comments to Medscape Medical News. “Our results show that when the patients use CPAP for more than 4 hours per night there is a reduction in the incidence of hypertension and cardiovascular events.”
Dr. Barbé’s advice: “If you want to prevent cardiovascular events or the development of hypertension, push your patients to use CPAP treatment for more than 4 hours per night.”
Questions Remain
In their editorial, Dr. Kapur and Dr. Weaver write that, “Taken together, these studies augment the evidence that the presence of OSA poses a risk for incident hypertension and provide strong but not definitive evidence that CPAP therapy may reduce the risk. In nonsleepy patients with OSA, the effect of CPAP therapy prescription remains unclear.”
They also note that many questions remain regarding OSA, hypertension, and treatment, including:
- What are the susceptible and responsive subgroups (eg, OSA severity subgroups, sleepy vs nonsleepy patients, and demographic subgroups)?
- How much CPAP use is necessary for an important treatment effect?
- What are the effects of other OSA treatments?
These questions, Dr. Kapur and Dr. Weaver say, “will require RCTs when feasible, subgroup analyses within these trials, and well-controlled observational studies. Novel approaches are needed, such as treatment withdrawal protocols.”
Despite lingering questions, they conclude, “considerable evidence supports the role of identification and treatment of OSA to improve symptoms, quality of life, and cardiovascular end points.”
Both studies were supported by grants from the Instituto Carlos III, Ministry of Health, Madrid, and the Spanish Society of Respiratory Medicine. The study by Dr. Barbé was also supported by Resmed (Bella Vista, Australia), Air Products-Carburos Metalicos (Barcelona), Respironics (Murrysville, Pennsylvania) and Breas Medical (Madrid). The study authors have disclosed no relevant disclosures. Dr. Kapur reported having owned stock within the last 3 years in Merck, Johnson & Johnson, and Bristol-Myers Squibb. Dr. Weaver had disclosed no relevant financial relationships.
JAMA. 2012;307:2161-2168, 2169-2176, 2197-2198.
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