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OSA and Resistant HTN
The prevalence of unsuspected OSA in patients with resistant hypertension is very
high, estimated at 83% in one study [ 28 , 29 ]. Refractory hypertension in patients
with OSA is primary systolic rather than diastolic and is especially pronounced at
night. This is particularly important given that systolic BP has stronger prognostic
value for cardiovascular outcomes than does diastolic pressure [ 30 ].
One study of 125 patients with resistant hypertension was systematically evalu-
ated for known secondary causes of hypertension including aortic coarctation,
Cushing’s syndrome, obstructive sleep apnea, drugs, pheochromocytoma, primary
aldosteronism, renal parenchymal disease, renovascular hypertension, and thyroid
disorders [ 31 ]. OSA (defined as an AHI of 15 or greater) emerged as by far the most
common condition associated with resistant hypertension, seen in 64% of patients.
Risk factors for the presence of OSA included age over 50 years, neck circumfer-
ence ≥41 cm for women and ≥43 cm for men, and the presence of snoring in this
population. Another smaller study evaluating patients with treatment-resistant
hypertension found that 83% had unsuspected sleep apnea based on an apnea-
hypopnea index ≥10 events/h [ 28 ].
There appears to be a dose-response relationship between the severity of OSA
and the risk of resistant hypertension. Walia et al. recruited nearly 300 patients at
high risk for cardiovascular disease despite medical management and found that
patients with severe OSA had a fourfold higher adjusted odds of resistant hyperten-
sion (OR 4.1, 95% CI: 1.7–10.2) [ 32 ]. In addition, resistant hypertension was sig-
nificantly more common in patients with untreated severe than moderate OSA (58%
vs. 29%, respectively, p = 0.01).
Current guidelines on the management of resistant hypertension from the
American Heart Association (2008) recommend screening for the presence of OSA
in patients with resistant hypertension [ 33 ], and the seventh report of the Joint
National Committee on Prevention, Detection, Evaluation, and Treatment of High
Blood Pressure recognizes OSA as an identifiable cause of hypertension [ 18 ]. Joint
recommendations from the European Respiratory Society and European Society of
Hypertension echoed this recommendation in 2013, citing OSA as a “novel, fre-
quent and modifiable cause of systemic arterial hypertension” [ 9 ].
Pathophysiologic Mechanisms Linking Hypertension
and Sleep Apnea
A constellation of factors may underlie the relationship between HTN and OSA,
including sympathetic activation, activation of the renin-angiotensin-aldosterone
system, intermittent hypoxemia, inflammation, oxidative stress, and endothelial
dysfunction. These are shown in Figs. 13.1, 13.2, and 13.3. Some of these mecha-
nisms may act in a bidirectional manner.
L.A. Tobias and F. Roux