Obstructive Sleep Apnea in Acute Stroke
Do stroke patients with obstructive sleep apnea (OSA) have different levels of inflammatory markers?
This was a single-center prospective observational study with consecutive stroke patients ages >18 years admitted within 24 hours of an acute ischemic stroke. Excluded were patients with prior sleep-disordered breathing or chronic pulmonary disease. To diagnose sleep apnea, all underwent a portable sleep test in the hospital within 48 hours of stroke, using a peripheral arterial tonometry (PAT) device. Blood samples were obtained the morning after stroke admission to measure tumor necrosis factor, interleukin-6, and plasminogen activator inhibitor-1 levels. Prevalence of sleep apnea was defined as an apnea-hypopnea index (AHI) ≥15 events/hour. Comparison of sleep apnea patients was made to those with an AHI <15 events/hour.
A total of 43 patients were admitted with acute stroke and 22 (51%) were found to have AHI ≥15 events/hour. Patients with AHI ≥15 had higher prevalence of recurrent stroke and atrial fibrillation (p = 0.05 and 0.08, respectively). Mean values for three inflammatory biomarkers were higher among patients with AHI ≥15 than the rest. Blood pressure in the hospital, stroke scores, and length of stay did NOT differ between the AHI ≥15 group and the rest.
The authors concluded that in a small cohort of stroke patients, nearly 90% had sleep breathing disorder, defined as AHI ≥5 events/hour. Sleep-disordered breathing is associated with elevated inflammatory markers and may provide a possible mechanism for OSA-associated stroke risk.
OSA is associated with stroke, and CPAP therapy improves mortality and functional status after stroke. However, these mechanisms are not clear. The bedside nocturnal respiratory device, Watch PAT, indirectly detects apneas by measuring peripheral arterial volume changes using a finger mounted plethysmograph. These sleep breathing events have been correlated with those measured by standard in-laboratory polysomnography (Yalamachali S, et al. JAMA Otolaryngol Head Neck Surg 2013;139:1343-50). Study findings need to be repeated in a larger scale intervention trial to further the hypothesis that OSA is a major risk for stroke and its devastating disability. It may be that elevated inflammatory cytokines are one of the pathophysiologic links between sleep apnea, atrial fibrillation, and stroke. The hope is that more broad screening of risk populations for OSA and effective treatment may lead to fewer cardiovascular events.
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