Obstructive Sleep Apnea in Acute Stroke

Stroke, a leading cause of death and disability worldwide, requires effective therapeutic measures to ameliorate its clinical and socioeconomic burden. Increased knowledge of the pathogenetic mechanisms involved in cerebral ischemia demonstrates that therapies should be administered early and targeted at establishing reperfusion and inhibiting damage mediators. Sleep-disordered breathing (SDB) is a wide spectrum of sleep-related respiratory abnormalities including both central and obstructive forms. The most common form of SDB, obstructive sleep apnea (OSA), is an independent risk factor for stroke. The exact mechanism remains unknown, the primary reason described in the literature is: episodes of obstructive apnea can cause intermittent hypoxemia. This can lead to surges in blood pressure because of sympathetic activation and release of vasoconstrictive substances, such as endothelin. SDB is common among patients with stroke, who have a 4to 6-fold higher prevalence of OSA. In the acute post stroke period, patients with OSA have a greater functional impairment and higher mortality rates than patients without OSA. The use of continuous positive airway pressure treatment is associated with decreased mortality and better functional recovery after stroke. Recently, treatment of SDB during the acute post stroke period was suggested as an additional measure for improving stroke outcome. However, the mechanisms in which SDB affect stroke outcome are not clear, and SDB screening and treatment is not yet a routine practice. Early detection and treatment of OSA may benefit patient’s life, and this early management of OSA may lead to fewer cardiovascular events. In this prospective study, we evaluated clinical characteristics and laboratory markers of inflammation and coagulability Background and Purpose—Sleep-disordered breathing is common among patients with stroke resulting in 4to 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. Sleepdisordered 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. (Stroke. 2016;47:1207-1212. DOI: 10.1161/STROKEAHA.115.011749.)