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Clinical Trial
. 2002 Oct;122(4):1125-32.
doi: 10.1378/chest.122.4.1125.

The effect of correction of sleep-disordered breathing on BP in untreated hypertension

Affiliations
Clinical Trial

The effect of correction of sleep-disordered breathing on BP in untreated hypertension

K Mae Hla et al. Chest. 2002 Oct.

Abstract

Objectives: To compare BP response to 3 weeks of nasal continuous positive airway pressure (CPAP) in hypertensive patients with and without sleep-disordered breathing (SDB).

Design: A controlled, interventional trial of nasal CPAP in patients with and without SDB.

Participants and setting: Twenty-four men, aged 30 to 60 years, with mild to moderate untreated hypertension recruited from employee health and primary care clinics.

Methods: Based on in-laboratory polysomnography, 14 hypertensive patients had SDB, defined by five or more episodes of apnea and hypopnea per hour of sleep (apnea-hypopnea index [AHI], > or = 5), and 10 had no SDB (AHI, < 5). We performed 24-h ambulatory BP monitoring on all patients at baseline, during CPAP, and after CPAP treatment. In patients with an AHI > or = 5, nasal CPAP was titrated to reduce the AHI to < 5. Patients with an AHI < 5 received CPAP of 5 cm H(2)O to control for any potential effect of CPAP per se on BP. Both groups received CPAP for 3 weeks.

Results: After adjusting for age and body mass index, the mean nocturnal systolic and diastolic BP changes after CPAP treatment in the SDB group were significantly different from those in the no-SDB group: -7.8 vs +0.3 mm Hg (p = 0.02), and -5.3 vs -0.7 mm Hg (p = 0.03), respectively. There was a similar, although statistically insignificant, difference in the adjusted mean daytime systolic and diastolic BP changes after CPAP treatment between the two groups (-2.7 vs +0.4 mm Hg and -2.3 vs -1.7 mm Hg, respectively).

Conclusions: Three weeks of nasal CPAP treatment of SDB in hypertensive men caused the lowering of nocturnal systolic and diastolic BP values, suggesting that increased nocturnal BP in persons with hypertension was causally related to the apnea and hypopnea events of SDB.

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