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  • Title: Blood pressure evolution after acute ischemic stroke in patients with and without sleep apnea.
    Author: Selic C, Siccoli MM, Hermann DM, Bassetti CL.
    Journal: Stroke; 2005 Dec; 36(12):2614-8. PubMed ID: 16282549.
    Abstract:
    BACKGROUND AND PURPOSE: Sleep apnea (SA) is an independent risk factor for arterial hypertension and is present in 50% to 70% of patients with ischemic stroke. The effects of SA on blood pressure (BP) and stroke outcome in the acute stroke phase are essentially unknown. METHODS: We studied 41 consecutive patients admitted within 96 hours after stroke onset. Stroke severity on admission (National Institutes of Health Stroke Scale [NIHSS]) and stroke outcome at discharge (modified Rankin Disability Scale [mRS]) were assessed. Nocturnal breathing was assessed with an ambulatory device the first night after admission. SA was defined by an apnea-hypopnea-index (AHI) > or =10/hour, and moderate-severe SA (MSSA) was defined by an AHI >30/hour. BP monitoring was performed during the first 36 hours after admission. A nondipping status (NDS) was defined by a ratio >0.9 of mean systolic BP during nights 1 to 2/mean systolic BP during day 2. RESULTS: SA was found in 28 (68%) and MSSA in 11 (27%) of 41 patients. A correlation was found between AHI and both NIHSS (r=0.331; P=0.035) and mRS (r=0.341; P=0.031). Patients with MSSA had higher systolic and diastolic BP values during night 1 (P=0.003), day 2 (P=0.004), and night 2 (P=0.03). NDS was found in 26 (63%) patients. Nondippers had a similar AHI but higher NIHSS (P=0.004) and mRS (P=0.005) than dippers. AHI and NDS were confirmed to be independent predictors for both stroke severity and stroke outcome in a multiple stepwise linear regression model. CONCLUSIONS: SA severity is associated with high 24-hour BP values but only weakly with stroke severity and outcome. Conversely, NDS is linked with a more severe stroke and a poorer evolution but not with SA severity. These data suggest different, although overlapping, pathophysiological and clinical implications of circadian and nocturnal BP values in acute stroke.
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