ANAHEIM, CALIF —A new study suggests that almost three quarters of patients with ischemic stroke may have obstructive sleep apnea, and that the presence of sleep apnea is associated with significantly worse functional outcomes after stroke compared to patients without this condition. If their continuing work shows this association to hold true in larger numbers, the researchers hope to begin an interventional study to establish whether treating sleep apnea could improve outcomes for these patients. The data were presented at the American Heart Association’s 2001 Scientific Sessions.

APNEA, HYPERTENSION, AND STROKE

Epidemiologic studies in more than 6,000 patients have shown an “unequivocal” relationship between obstructive sleep apnea and the development of hypertension, probably through chronic activation of the sympathetic nervous system caused by sleep apnea, said senior study author T. Douglas Bradley, MD. Dr. Bradley is Director of the Sleep Research Laboratory, Toronto Rehabilitation Institute, and the Centre for Sleep and Chronobiology, University of Toronto.

“Since hypertension is the number one risk factor for strokes, one would expect an excess number of patients with strokes who have sleep apnea,” Dr. Bradley explained in an interview with Neurology Reviews. Other epidemiologic evidence has shown a significant relationship between sleep apnea and stroke, although the relationship does not appear to be as strong as that with hypertension, he commented. However, the additional oxygen deprivation caused by sleep apnea could aggravate further the hypoxic insult of the stroke, resulting in worse functional outcome in stroke patients with sleep apnea.

Obstructive sleep apnea is associated with lower cardiac output and reduced cerebral blood flow, he added, both contributing to “further noxious stimuli” for a brain already damaged by stroke. In this setting, the stroke might potentially be extended, the brain become susceptible to further strokes, or the lack of oxygen might cause the generation of neural inhibitory peptides, which can impair brain function, he said. In addition, normal sleep is associated with lower platelet activation, but it has been shown that patients with obstructive sleep apnea do not have this normal reduction in platelet activity because of frequent waking, perhaps raising their risk of ischemic events.

EXPECTED AND UNEXPECTED RESULTS

To examine this relationship, the researchers carried out sleep studies in 40 patients admitted to their stroke rehabilitation unit. For the purposes of their study, obstructive sleep apnea was defined as an apnea-hypopnea index of greater than 10 events an hour. Patients also underwent functional and cognitive assessments, including the Functional Independence Measure and the Mini-Mental Status Examination.

“We found that 72% of patients had sleep apnea, which is more than 10 times higher than in the otherwise healthy population,” Dr. Bradley said. They also found a direct relationship between the severity of obstructive sleep apnea and functional impairment, but not with cognitive impairment, even after controlling for the patients’ age, weight, and the type and location of the stroke.

“The sleep apneics were spending 18 days more in hospital, and when they left the hospital they were still more impaired than the other group—the functional impairment was relatively refractory to therapy,” he said. Currently, assessment and treatment of sleep apnea is not part of standard therapy for stroke patients, he noted; when they presented the data to stroke unit personnel at their own hospital, most acknowledged that snoring and daytime fatigue were common among their patients, but sleep apnea was not considered. “Despite the recognition of these problems, until now, awareness of sleep apnea as a factor that might contribute to functional disability in patients with strokes was very low among personnel working in our stroke unit,” he said.

TOWARD UNOBSTRUCTED OUTCOMES

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