Key result
N-CPAP linked to borderline hypertension control in ~83% of patients with upper airway resistance syndrome.
Why the study?
The role of upper airway resistance syndrome (UARS) in nocturnal blood pressure changes and borderline hypertension was unclear.
Does N-CPAP treatment reduce blood pressure in patients with Upper Airway Resistance Syndrome and borderline hypertension?
Observational (n=110)
Does N-CPAP treatment reduce blood pressure in patients with Upper Airway Resistance Syndrome and borderline hypertension?
Treatment of Upper Airway Resistance Syndrome with N-CPAP can effectively control borderline hypertension, highlighting the role of abnormal upper airway resistance in the development of hypertension.
Repetitive nocturnal BP surges in UARS may promote hypertension; small observational data leaves open treatment effects on outcomes.
Upper airway resistance syndrome (UARS) is a sleep-disordered breathing syndrome characterized by complaints of daytime fatigue and/or sleepiness, increased upper airway resistance during sleep, frequent transient arousals, and no significant hypoxemia. Of a population of 110 subjects (58 men) diagnosed as having UARS, we investigated acute systolic and diastolic BP changes seen during sleep in two different samples. First, six patients from the original subject pool were found to have untreated chronic borderline high BP, and were subjected to 48 h of continuous ambulatory BP monitoring before treatment and another 48 h of BP monitoring 1 month after the start of nasal-continuous positive airway pressure (N-CPAP) treatment. Five of six subjects used their equipment on a regular basis and had their chronic borderline high BP completely controlled. No change in BP values was seen in the last subject, who discontinued N-CPAP after 3 days. A second protocol investigated seven normotensive subjects drawn from the initial subject pool. Continuous radial artery BP recording was performed during nocturnal sleep with simultaneous polygraphic recording of sleep/wake variables and respiration. BP changes were studied during periods of increased respiratory efforts and at the time of alpha EEG arousals. Increases in systolic and diastolic BP were noted during the breaths with the greatest inspiratory efforts without significant hypoxemia. A further increase in BP was noted in association with arousals. Three of these subjects also underwent echocardiography during sleep, which demonstrated a leftward shift of the interventricular septum with pulsus paradoxus in association with peak end-inspiratory esophageal pressure more negative than -35 cm H2O. Our study indicates that, in the absence of classic apneas, hypopneas, and repetitive significant drops in oxygen saturation (below 90%), repetitive increases in BP can occur as a result of increased airway resistance during sleep. It also shows that, in some patients with both UARS and borderline high BP, high BP can be controlled with treatment of UARS. We conclude that abnormal upper airway resistance during sleep, often associated with snoring, can play a role in the development of hypertension.
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Guilleminault et al. (1996) conducted an observational in Upper airway resistance syndrome (n=110). Nasal-continuous positive airway pressure (N-CPAP) vs. Baseline (pre-treatment) was evaluated on Acute systolic and diastolic blood pressure changes during sleep and control of borderline high blood pressure. In patients with upper airway resistance syndrome, repetitive increases in blood pressure occurred during sleep, and N-CPAP treatment completely controlled borderline hypertension in 5 of 6 patients.
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