CPAP wards off worsening BP in pre- and masked hypertensives with sleep apnea

February 02, 2011

São Paulo, Brazil - Patients with severe obstructive sleep apnea (OSA) who were treated with continuous positive airway pressure (CPAP) saw falls in blood pressure in a new study[1]. The patients either had masked hypertension or were considered to be prehypertensive, Dr Luciano F Drager (University of São Paulo Medical School, Brazil) and colleagues report in a study published online January 17, 2011 in Hypertension.

Drager explained to heartwire that OSA and high blood pressure are common conditions that frequently coexist, and it has already been shown that the treatment of OSA with CPAP is able to reduce BP in those afflicted by both conditions. However, this rarely normalizes the BP to the point that antihypertensive medications can be discontinued, he notes.

But targeting patients with OSA and prehypertension—considered a "precursor" to sustained hypertension—or masked hypertension—patients with normal office BPs but abnormal 24-hour, ambulatory BPs—with CPAP might mean that such patients could avoid antihypertensive therapy altogether, he says.

Consequently, he believes that anyone discovered to have severe OSA and prehypertension or masked hypertension should be treated with CPAP. "Despite the fact that our study was relatively small, our results regarding the reduction of the frequency of prehypertension and masked hypertension are convincing and reinforce the concept that CPAP therapy is helpful not only for alleviating sleep-related symptoms but also for avoiding the occurrence of hypertension and preventing the development of cardiovascular diseases in patients with OSA. So, treatment with CPAP may have a significant health and economic impact."

Reducing BP: An additional reason for using CPAP in severe OSA

In their study, Drager and colleagues randomized 36 male patients with untreated severe OSA with diagnostic criteria for prehypertension (BP 120-139/80-89 mm Hg) and/or masked hypertension to either CPAP for three months (n=18) or no treatment (control group, n=18).

There were no significant changes in BP in those randomized to the control group. In contrast, those randomized to CPAP had significant reductions in office systolic BP (from 126 to 121 mm Hg; p=0.001) and a trend toward a reduction in diastolic BP (from 75 to 73 mm Hg; p=0.08), as well as a significant decrease in daytime and nighttime systolic and diastolic BP (p<0.05 for each comparison).

There was also a significant reduction in the frequency of prehypertension (from 94% to 55%; p=0.02) and masked hypertension (from 39% to 5%; p=0.04), but only in the CPAP group.

"To the best of our knowledge, this is the first study that evaluated the impact of CPAP on prehypertension and masked hypertension in patients with OSA," say Drager et al.

The results suggest that OSA may be the main determinant of prehypertension and masked hypertension in a substantial proportion of patients, so screening of BP with 24-hour ambulatory blood-pressure monitoring is needed in those with OSA who are considered normotensive in the office, they say.

Drager adds that all patients with severe OSA should "ideally" be treated with CPAP, but access to treatment varies because of cost and adherence issues. "We believe that our results support an additional reason for indicating CPAP in this subset of patients."

The authors had no conflicts of interest.

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