AbstractBackground and Purpose—
Sleep-disordered breathing is common among patients with stroke resulting in 4- to 6-fold higher prevalence of obstructive sleep apnea (OSA). We prospectively evaluated clinical characteristics and laboratory markers of inflammation and coagulability associated with OSA severity during the acute post stroke period.Methods—
Consecutive patients admitted to the department of Neurology after an acute ischemic stroke were evaluated during the first 48 hours of symptom onset using Watch peripheral arterial tonometry, a wrist-worn ambulatory sleep study device that utilizes peripheral arterial tonometry. Morning blood samples of the patient were tested for tumor necrosis factor, interleukin-6, and plasminogen activator inhibitor-1 levels.Results—
A total of 43 patients with acute stroke were admitted during the study period, 22 (51%) of which have been found to have moderate sleep apnea (apnea hypopnea index [AHI]≥15), AHI≥5 was found in 86% of the patients, and severe OSA (AHI≥30) in 32.5%. Patients with OSA (AHI≥15) did not differ from the rest in stroke severity or symptoms, yet they had higher prevalence of recurrent stroke and atrial fibrillation. All 3 biomarkers levels were higher among patients with AHI≥15: tumor necrosis factor (6.39 versus 3.57 pg/mL), interleukin-6 (6.64 versus 3.14 pg/mL), and plasminogen activator inhibitor-1 (176.64 versus 98.48 pg/mL). After the stratification of AHI into 3 groups (AHI<5, 5–14, and ≥15), the analysis showed that only the highest AHI group differed from the other 2 groups in biomarkers levels.Conclusions—
Use of bed-side somnography technology revealed that in an unselected sample of patients with acute ischemic stroke, almost 90% had sleep-disordered breathing with third having severe form of the disorder. Sleep-disordered breathing was associated with significantly increased levels of inflammatory biomarkers, providing possible pathophysiological explanation of OSA-associated stroke risk. These results warrant prospective screening of patients with stroke for the presence of sleep-disordered breathing and lay the rationale for an interventional trial.