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Cardioembolic Stroke May Be Associated With Obstructive Sleep Apnea
2012;17(7):1B, 20.

Cardioembolic Stroke May Be Associated With Obstructive Sleep Apnea

Cardioembolic stroke is more common in patients with obstructive sleep apnea (OSA), compared with patients without OSA.

BOSTON—Cardioembolic (CE) stroke is more common in patients with obstructive sleep apnea (OSA) than in patients without OSA, according to study findings presented at the 26th Annual Meeting of the Associated Professional Sleep Societies, LLC. These results provide insight into the possible etiologies of stroke in patients with OSA, and could guide tailored strategies for the management of stroke risk in these patients.

“We don’t yet understand how exactly OSA exerts its influence as a risk factor for stroke,” said Melissa C. Lipford, MD, of the Center for Sleep Medicine at the Mayo Clinic, Rochester, Minnesota. “Is it through atrial fibrillation, or could it be through other mechanisms?”

Investigating Mechanisms of Stroke in OSA
Lipford and colleagues examined the relationships between OSA, atrial fibrillation, and ischemic stroke in a retrospective case-control study of 53 consecutive patients who had undergone polysomnography (PSG) at the Mayo Clinic between January 2000 and September 2011 and who had an ischemic stroke within one year following PSG. Thirty-two patients met criteria for OSA (apnea-hypopnea index [AHI] >10) and were identified as cases; they had a mean AHI of 32.6 and a mean age of 67.6 years. Twenty-one patients did not meet criteria for OSA and were classified as controls; these patients had a mean AHI of 5.6 and a mean age of 62.0 years.

The researchers found that 72% of patients with OSA had CE stroke, compared with 33% of patients without OSA, and the frequency of CE stroke increased with OSA severity. Both large artery atherosclerosis and small vessel occlusion were found to be more common in patients without OSA. While atrial fibrillation (AF) was more common in patients with OSA than in controls (47% vs 24%, respectively), about one-third of the patients with OSA who also had CE stroke did not have documented AF. After adjustment for AF, the association between CE stroke and OSA remained significant.

CE risk factors—including high-risk factors, such as mitral stenosis, bioprosthetic or mechanical valves, and dilated cardiomyopathy—occurred more frequently in patients with OSA than in controls. Among patients with OSA, 84% had at least one CE risk factor, compared with 52% of patients without OSA. The researchers also found that among patients with OSA, there was a significantly higher proportion of CE stroke, compared with all other mechanisms for stroke.

Lipford pointed out that patients were diagnosed with OSA before their strokes occurred, not after. Had the patients been diagnosed with OSA in the post-stroke period, it would have been unclear whether OSA was one of the risk factors that led to the stroke, or if the stroke itself caused OSA. Lipford also noted that the study only included patients who had a stroke within one year following PSG in order to limit any confounding effects from OSA treatment. The researchers considered accounting for positive airway pressure (PAP) therapy compliance, but this proved to be too difficult to assess retrospectively.

Management of Risk Factors for CE Stroke
The study results “indicate that a higher level of suspicion for cardioembolism is warranted when evaluating patients with OSA who have had a stroke,” Lipford said. Additional studies would be needed to determine whether the higher rate of CE stroke in patients with OSA was caused by occult AF or related to other OSA-specific factors.

“It may be that OSA leads to structural and physiologic changes in the heart that can predispose patients to CE via mechanisms other than AF,” she added. “We also have to remember that the higher rate of CE stroke could represent a greater proportion of undiagnosed paroxysmal AF in our OSA group.”

The potential relationship between CE stroke and OSA might guide clinicians to consider using transesophageal echocardiography to identify CE risk factors, holter monitoring, or extended monitoring to identify paroxysmal AF, Lipford said. She noted that the overall management of stroke in patients with OSA “must be multifaceted,” as OSA also is associated with other risk factors, such as large artery atherosclerosis and small vessel occlusion.

Lipford recommended that future prospective studies include an evaluation of stroke mechanisms to better understand the relationship between ischemic stroke and OSA, as well as investigate the impact of PAP therapy on stroke risk factor reduction (including CE stroke risk factors) and determine whether screening for and treating OSA in patients with transient ischemic stroke will reduce their risk of stroke.

—John Merriman

 

Suggested Reading
Joe BE, Seok HY, Yu SW, et al. Prevalence of sleep-disordered breathing in acute ischemic stroke as determined using a portable sleep apnea monitoring device in Korean subjects. Sleep Breath. 2011;15(1):77-82.
Johnson KG, Johnson DC. Frequency of sleep apnea in stroke and TIA patients: a meta-analysis. J Clin Sleep Med. 2010;6(2):131-137.
Rola R, Wierzbicka A, Wichniak A, et al. Sleep related breathing disorders in patients with ischemic stroke and transient ischemic attacks: respiratory and clinical correlations. J Physiol Pharmacol. 2007;58 Suppl 5(Pt 2):575-582.
Wierzbicka A, Rola R, Wichniak A, et al. The incidence of sleep apnea in patients with stroke or transient ischemic attack. J Physiol Pharmacol. 2006;57 Suppl 4:385-390.


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