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  • Επιστημονικές Δημοσιεύσεις Μελών ΠΘ (ΕΔΠΘ)
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  • Επιστημονικές Δημοσιεύσεις Μελών ΠΘ (ΕΔΠΘ)
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Blood pressure changes in acute ischemic stroke and outcome with respect to stroke etiology

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Autor
Ntaios, G.; Lambrou, D.; Michel, P.
Datum
2012
DOI
10.1212/WNL.0b013e31826d5ed6
Schlagwort
ANTIHYPERTENSIVE TREATMENT
SUBTYPE
HYPERTENSION
TRIAL
VARIABLES
TREAT
Clinical Neurology
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Zusammenfassung
Objective: Previous research suggested that proper blood pressure (BP) management in acute stroke may need to take into account the underlying etiology. Methods: All patients with acute ischemic stroke registered in the ASTRAL registry between 2003 and 2009 were analyzed. Unfavorable outcome was defined as modified Rankin Scale score >2. A local polynomial surface algorithm was used to assess the effect of baseline and 24-to 48-hour systolic BP (SBP) and mean arterial pressure (MAP) on outcome in patients with lacunar, atherosclerotic, and cardioembolic stroke. Results: A total of 791 patients were included in the analysis. For lacunar and atherosclerotic strokes, there was no difference in the predicted probability of unfavorable outcome between patients with an admission BP of <140 mm Hg, 140-160 mm Hg, or >160 mm Hg (15.3% vs 12.1% vs 20.8%, respectively, for lacunar, p = 015; 41.0% vs 41.5% vs 45.5%, respectively, for atherosclerotic, p = 075), or between patients with BP increase vs decrease at 24-48 hours (18.7% vs 18.0%, respectively, for lacunar, p = 0.84; 43.4% vs 43.6%, respectively, for atherosclerotic, p = 0.88). For cardioembolic strokes, increase of BP at 24-48 hours was associated with higher probability of unfavorable outcome compared to BP reduction (53.4% vs 42.2%, respectively, p = 0.037). Also, the predicted probability of unfavorable outcome was significantly different between patients with an admission BP of <140 mm Hg, 140-160 mm Hg, and >160 mm Hg (34.8% vs 42.3% vs 52.4%, respectively, p < 0.01). Conclusions: This study provides evidence to support that BP management in acute stroke may have to be tailored with respect to the underlying etiopathogenetic mechanism. Neurology (R) 2012;79:1440-1448
URI
http://hdl.handle.net/11615/31434
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