A sleeping beast: Obstructive sleep apnea and stroke

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Release date: June 1, 2019
Expiration date: May 31, 2020
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Up to two-thirds of patients who have had a stroke have obstructive sleep apnea (OSA) afterward. These patients have worse outcomes than those without OSA in terms of short-term morbidity, functional and cognitive recovery, and mortality rates over the long term. Following a stroke, identifying OSA and treating it with positive airway pressure, if possible, are important clinical goals.


  • A low threshold for evaluating for OSA after a stroke is warranted: the prevalence is high in this population, and risk factors for OSA and its typical clinical picture may not be present.
  • Questionnaires can help screen for the likelihood of OSA and the need for more definitive assessment with polysomnography or home sleep apnea testing, tests that pose additional challenges after stroke.
  • Positive airway pressure (PAP) therapy remains the first-line treatment for OSA after stroke; it may improve recovery and reduce long-term sequelae of untreated OSA.
  • Acceptance of and adherence to PAP therapy can be especially problematic in this population, and alternatives should be considered if needed.



Obstructive sleep apnea (OSA) is an independent risk factor for ischemic stroke and may also, infrequently, be a consequence of stroke. It is significantly underdiagnosed in the general population and is highly prevalent in patients who have had a stroke. Many patients likely had their stroke because of this chronic untreated condition.

This review focuses on OSA and its prevalence, consequences, and treatment in patients after a stroke.


OSA is the most common type of sleep-disordered breathing.1,2 It involves repeated narrowing or complete collapse of the upper airway despite ongoing respiratory effort.3,4 Apneic episodes are terminated by arousals from hypoxemia or efforts to breathe.5 In contrast, central sleep apnea is characterized by a patent airway but lack of airflow due to absent respiratory effort.5

In OSA, the number of episodes of apnea (absent airflow) and hypopnea (reduced airflow) are added together and divided by hours of sleep to calculate the apnea-hypopnea index (AHI). OSA is diagnosed by either of the following3,4:

  • AHI of 5 or higher, with clinical symptoms related to OSA (described below)
  • AHI of 15 or higher, regardless of symptoms.

The AHI also defines OSA severity, as follows3:

  • Mild: AHI 5 to 15
  • Moderate: AHI 15 to 30
  • Severe: AHI greater than 30.

Diagnostic criteria (eg, definition of hypopnea, testing methods, and AHI thresholds) have varied over time, an important consideration when reviewing the literature.


In the most methodologically sound and generalizable study of this topic to date, the Wisconsin Sleep Cohort Study6 reported in 2013 that about 14% of men and 5% of women ages 30 to 70 have an AHI greater than 5 (using 4% desaturation to score hypopneic episodes) with daytime sleepiness. Other studies suggest that 80% to 90% of people with OSA are undiagnosed and untreated.1,7

The prevalence of OSA in patients who have had a stroke is much higher, ranging from 30% to 96% depending on the study methods and population.1,8–12 A 2010 meta-analysis11 of 29 studies reported that 72% of patients who had a stroke had an AHI greater than 5, and 29% had severe OSA. In this analysis, 7% of those with sleep-disordered breathing had central sleep apnea; still, these data indicate that the prevalence of OSA in these patients is about 5 times higher than in the general population.


Several risk factors for OSA have been identified.

Obesity is one of the strongest risk factors, with increasing body mass index (BMI) associated with increased OSA prevalence.4,6,13 However, obesity appears to be a less significant risk factor in patients who have had a stroke than in the general population. In the 2010 meta-analysis11 of OSA after stroke, the average BMI was only 26.4 kg/m2 (with obesity defined as a BMI > 30.0 kg/m2), and increasing BMI was not associated with increasing AHI.

Male sex and advanced age are also OSA risk factors.4,5 They remain significant in patients after a stroke; about 65% of poststroke patients who have OSA are men, and the older the patient, the more likely the AHI is greater than 10.11

Ethnicity and genetics may also play important roles in OSA risk, with roughly 25% of OSA prevalence estimated to have a genetic basis.14,15 Some risk factors for OSA such as craniofacial shape, upper airway anatomy, upper airway muscle dysfunction, increased respiratory chemosensitivity, and poor arousal threshold during sleep are likely determined by genetics and ethnicity.14,15 Compared with people of European origin, Asians have a similar prevalence of OSA, but at a much lower average BMI, suggesting that other factors are significant.14 Possible genetically determined anatomic risk factors have not been specifically studied in the poststroke population, but it can be assumed they remain relevant.

Several studies have tried to find an association between OSA and type, location, etiology, or pattern of stroke.10,11,16–19 Although some suggest links between cardioembolic stroke and OSA,16,20 or thrombolysis and OSA,10 most have found no association between OSA and stroke features.11,12,21,22


Untreated severe OSA is associated with increased cardiovascular mortality,21,22 and OSA is an independent risk factor for incident stroke.23 A number of mechanisms may explain these relationships.

Intermittent hypoxemia and recurrent sympathetic arousals resulting from OSA are thought to lead to many of the comorbid conditions with which it is associated: hypertension, coronary artery disease, heart failure, arrhythmias, pulmonary hypertension, and stroke. Repetitive decreases in ventilation lead to oxygen desaturations that result in cycles of increased sympathetic outflow and eventual sustained nocturnal hypertension and daytime chronic hypertension.1,5,9,13 Also implicated are various changes in vasodilator and vasoconstrictor substances due to endothelial dysfunction and inflammation, which are thought to play a role in the atherogenic and prothrombotic states induced by OSA.1,5,13

Cerebral circulation is altered primarily by the changes in partial pressure of carbon dioxide (Pco2). During apnea, the Pco2 rises, causing vasodilation and increased blood flow. After the apnea resolves, there is hyperpnea with resultant decreased Pco2, and vasoconstriction. In a patient who already has vascular disease, the enhanced vasoconstriction could lead to ischemia.1,5

Changes in intrathoracic pressure result in distortion of cardiac architecture. When the patient tries to breathe against an occluded airway, the intrathoracic pressure becomes more and more negative, increasing preload and afterload. When this happens repeatedly every night for years, it leads to remodeling of the heart such as left and right ventricular hypertrophy, with reduced stroke volume, myocardial ischemia, and increased risk of arrhythmia.1,5,13

Untreated OSA is believed to predispose patients to develop atrial fibrillation through sympathetic overactivity, vascular inflammation, heart rate variability, and cardiac remodeling.24 As atrial fibrillation is a major risk factor for stroke, particularly cardioembolic stroke, it may be another pathway of increased stroke risk in OSA.16,20,25

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