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Plasma β-Amyloid 1-40 Is Associated With the Diffuse Small Vessel Disease Subtype

The underlying mechanisms of small vessel disease (SVD) subtypes are diffuse arteriopathy (diffuse-SVD) or microatheroma (focal-SVD). Endothelial dysfunction by beta-amyloid peptide (Abeta) deposition has been associated with lacunar infarcts and leukoaraiosis, but its specific relationship with SVD...

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Published in:Stroke (1970) 2009-10, Vol.40 (10), p.3197-3201
Main Authors: GOMIS, Meritxell, SOBRINO, Tomas, DAVALOS, Antoni, OIS, Angel, MILLAN, Mònica, RODRIGUEZ-CAMPELLO, Ana, PEREZ DE LA OSSA, Natalia, RODRIGUEZ-GONZALEZ, Raquel, JIMENEZ-CONDE, Jordi, CUADRADO-GODIA, Elisa, ROQUER, Jaume
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Language:English
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Summary:The underlying mechanisms of small vessel disease (SVD) subtypes are diffuse arteriopathy (diffuse-SVD) or microatheroma (focal-SVD). Endothelial dysfunction by beta-amyloid peptide (Abeta) deposition has been associated with lacunar infarcts and leukoaraiosis, but its specific relationship with SVD subtypes is unknown. We hypothesized that plasma Abeta levels can play a different role in SVD subtypes in patients with acute lacunar stroke. We studied 149 patients with acute ischemic stroke of SVD etiology according to Trial Of Org 10172 In Acute Stroke Treatment criteria and 25 age-matched control subjects. Patients were classified into focal-SVD: 39 patients with isolated lacunar infarct without leukoaraiosis and diffuse-SVD: 110 patients with an isolated lacunar infarct with leukoaraiosis or with multiple lacunar infarcts with or without leukoaraiosis. Baseline data included vascular risk factors and extensive laboratory tests, including plasma Abeta levels. Median [quartiles] Abeta(1-40) levels (40.4 [35.1, 50.5] versus 55.1 [42.3, 69.6] pg/mL), but not Abeta(1-42) levels, were significantly higher in the diffuse-SVD group than in focal-SVD group (P
ISSN:0039-2499
1524-4628
DOI:10.1161/STROKEAHA.109.559641