Abstract
Background&Purpose: Although clinically silent infarcts (CSI) have been linked to an increased risk of stroke, only limited data exist regarding associated risk factors. Sleep apnea (SA), as an independent stroke risk factor itself, is associated with chronic microvascular changes (CMC), yet the relationship between SA and CSI remains unclear. We sought to determine the frequency and severity of SA in patients with CSI or CMC as well as how SA relates to outcomes in these patients. Subjects&Methods: Over an 18-month period, consecutive patients with acute cerebral ischemia prospectively underwent overnight in-hospital respiratory polygraphy within 5 days from symptom-onset. Sleep apnea was present when apnea-hypopnea-index (AHI) was ≥5/h. We collected demographics and clinical variables at baseline. All CTs and MRIs were independently reviewed by a neuroradiologist who was blinded to the sleep study findings and outcome. CSI was defined as any lesion consistent with a remote ischemic infarct without known history of a corresponding neurologic deficit. CMC was defined as diffuse white matter alterations not attributable to another neurologic condition. Modified Rankin Scale (mRS) was used to assess functional outcome at discharge and 180 days. Baseline demographics were analyzed using chi-square and Wilcoxon rank sum test. Correlations and logistic regression were used to predict CSI and CMC. Results: We evaluated a total of 56 patients for the presence of SA. Demographics, clinical variables and outcomes are shown in the Table . SA was present in 91% (n=51) of the study population. There was no correlation between AHI and the presence of CMC (p=0.75). After adjustment for gender, AHI was found to be a significant independent predictor of CSI (OR 1.04, 95%CI 1.0-1.08; p=0.03). In patients who had either CSI or CMC, the higher the AHI the less likely favorable functional outcome (mRS 0-2) was achieved at discharge (OR=0.94, 95%CI 0.89-0.99; p=0.02). AHI was not a significant independent predictor of functional outcome at 180 days (p=0.25). Conclusions: In our study population, SA was found to be frequent in both CMC and CSI with >1/3 of CMC patients and >1/2 of CSI patients having severe SA. Moreover, SA was found to be an independent predictor of clinically silent infarcts. The less favorable outcome in CSI and CMC patients with high AHI warrants further investigation in these at-risk populations, perhaps with early non-invasive ventilatory correction of sleep apnea.
Published Version
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