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OSA and Hypertension
Studies have consistently supported a role for obstructive sleep apnea (OSA) as a
risk factor for diurnal hypertension. A significant body of literature has now accu-
mulated in both cross-sectional and prospective population-based epidemiologic
studies to suggest a dose-response relationship between severity of OSA and likeli-
hood of incident HTN that is independent of the risk factors common to both disor-
ders such as obesity and metabolic syndrome [ 7 , 8 ]. Both US and European
guidelines for hypertension management recognize OSA as a frequent and modifi-
able contributor to systemic arterial hypertension [ 9 ].
Furthermore, in patients with preexisting hypertension as well as OSA, treatment of
OSA may confer improvements in blood pressure control. Despite increasing evidence
supporting that it is a major cause of refractory hypertension, OSA remains signifi-
cantly underdiagnosed, particularly among women and nonobese patients [ 10 ].
While early studies of hemodynamics in patients with OSA relied on invasive
blood pressure monitoring, more recent studies have employed ambulatory moni-
tors with frequent sampling (e.g., every 15–30 min) in order to examine circadian
variation in systolic and diastolic blood pressure. It is generally accepted that ambu-
latory blood pressure monitoring has greater prognostic value than office BP
measurements.
OSA and Incident Hypertension
The prevalence of hypertension in patients with OSA ranges from 35 to 80% across
studies [ 9 ], and the prevalence of resistant hypertension is expected to increase in
the coming years [ 11 ]. Although some of the association between OSA and hyper-
tension may be mediated by risk factors common to both disorders, such as obesity,
a large body of evidence now supports an independent role of OSA in the pathogen-
esis of hypertension [ 7 , 12 – 15 ].
The first prospective studies examined the relationship between OSA and the
development of future hypertension in patients who were normotensive at baseline
[ 7 ]. Early data came from the Wisconsin Sleep Cohort, an ongoing prospective lon-
gitudinal study of the causes and natural history of sleep disorders. Investigators
found a significant dose-response relationship between sleep-disordered breathing
at baseline and a diagnosis of new hypertension 4 years later, independent of poten-
tial confounding factors. Patients with even mild OSA were even at risk, with a
twofold greater risk of becoming hypertensive, whereas those with moderate OSA
had a threefold greater probability, compared with participants without OSA at
baseline (AHI <1 event per hour) [ 7 ]. Another observational study by Marin and
colleagues following nearly 2000 non-hypertensive subjects presenting to a sleep
clinic over 10 years found an increased incidence of hypertension in patients with
untreated OSA compared with controls [ 8 ].
L.A. Tobias and F. Roux