NEW YORK (Reuters Health) – A new study shows that continuous positive airway pressure (CPAP) for obstructive sleep apnea (OSA) helps prevent hypertension, although a second study found the effect did not reach statistical significance – at least in patients without daytime sleepiness.
The two papers, both from Spain, appeared online today in the Journal of the American Medical Association.
“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,” the authors of a related editorial conclude. “In nonsleepy patients with OSA, the effect of CPAP therapy prescription remains unclear.”
The first study, conducted by Dr. Jose M. Marin, at the Hospital Universitario Miguel Servet in Zaragoza, and colleagues, involved a prospective cohort of 1,889 individuals without hypertension referred for polysomnography and followed for a median of 12.2 year.
The crude incidence of hypertension per 100 person years was 2.19 in participants without OSA (controls). Among those with OSA, the incidence was 3.34 in those ineligible for CPAP, 5.84 in patients who declined CPAP, 5.12 among those nonadherent to CPAP therapy, and 3.06 for patients compliant with CPAP therapy, according to the report.
Among the four groups of patients with OSA, the adjusted hazard ratio for incident hypertension (compared to controls) was 1.33, 1.96, 1.78, and 0.71, respectively. In other words, the risk of hypertension in OSA patients treated with CPAP was lower than in controls without OSA.
The other study was a randomized trial comparing CPAP to usual care in 723 patients with OSA but without daytime sleepiness. The main outcome was the incidence of hypertension or cardiovascular events (nonfatal MI, nonfatal stroke, transient ischemic attack, hospitalization for unstable angina or arrhythmia, heart failure, or cardiovascular death) during a median follow-up of four years.
The incidence of new hypertension or cardiovascular events per 100 person-years was 9.20 in the CPAP group and 11.02 in the control group – a non significant difference, the researchers found.
“When assessed separately, CPAP did not show any statistically significant effect on the incidence of new cardiovascular events or on new-onset hypertension,” add Dr. Ferran Barbe, of the Institut de Recerca Biomedica in Lleida, and colleagues.
However, they believe the study may have been underpowered to detect a significant difference.
In their editorial, Dr. Vishesh K. Kapur and Dr. Edward M. Weaver of the University of Washington in Seattle, write: “Although these studies significantly advance the understanding of the positive relationship between OSA and incident hypertension and the benefit of CPAP therapy, many questions remain regarding OSA, hypertension, and treatment.”
Elaborating, they continue, “What are the susceptible and responsive subgroups (e.g., OSA severity subgroups, sleepy vs. nonsleepy, and demographic subgroups)? How much CPAP use is necessary for an important treatment effect? What are the effects of other OSA treatments?”
They conclude, “These questions will require randomized controlled trials when feasible, subgroup analyses within these trials, and well-controlled observational studies. Novel approaches are needed, such as treatment withdrawal protocols.”