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(Stroke. 2009;40:3197.)
© 2009 American Heart Association, Inc.

Original Contributions

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

Meritxell Gomis, MD; Tomás Sobrino, PhD; Angel Ois, MD; Mònica Millán, MD; Ana Rodríguez-Campello, MD; Natalia Pérez de la Ossa, MD; Raquel Rodríguez-González, BSc; Jordi Jiménez-Conde, MD, PhD; Elisa Cuadrado-Godia, MD; Jaume Roquer, MD, PhD Antoni Dávalos, MD, PhD

From the Stroke Unit (M.G., M.M., N.P.d.l.O., A.D.), Department of Neurosciences, Hospital Universitari Germans Trias i Pujol (Badalona), Department de Medicina de la Universitat Autònoma de Barcelona, Barcelona, Spain; the Clinical Neurosciences Research Laboratory (T.S., R.R.-G.), Hospital Clínico Universitario, University of Santiago de Compostela La Coruña, Spain; and Unitat d'Ictus (A.O., A.R.-C., J.J.-C., E.C.-G., J.R.), Servei de Neurologia, Hospital del Mar, Departament de Medicina de la Universitat Autònoma de Barcelona, IMIM-Hospital del Mar, Barcelona, Spain.

Correspondence to Meritxell Gomis, MD, Stroke Unit, Neurociences Department, Hospital Universitari GermansTrias i Pujol, Carretera de Canyet s/n Badalona, Barcelona, Spain. E-mail mgomis.germanstrias{at}gencat.cat

Background and Purpose— The underlying mechanisms of small vessel disease (SVD) subtypes are diffuse arteriopathy (diffuse-SVD) or microatheroma (focal-SVD). Endothelial dysfunction by β-amyloid peptide (Aβ) deposition has been associated with lacunar infarcts and leukoaraiosis, but its specific relationship with SVD subtypes is unknown. We hypothesized that plasma Aβ levels can play a different role in SVD subtypes in patients with acute lacunar stroke.

Methods— 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 Aβ levels.

Results— Median [quartiles] Aβ_1-40 levels (40.4 [35.1, 50.5] versus 55.1 [42.3, 69.6] pg/mL), but not Aβ_1-42 levels, were significantly higher in the diffuse-SVD group than in focal-SVD group (P<0.001) and control subjects (P<0.001). No differences in Aβ_1-40 levels were found between focal-SVD and control subjects. Logistic regression analysis showed that age (OR, 1.06; 95% CI, 1.01 to 1.12), history of hypertension (OR, 3.5; 95% CI, 1.3 to 9.2), and plasma β-amyloid_1-40 levels over the median value (OR, 17.3; 95% CI, 3.0 to 99 for the third quartile and OR, 6.0; 95% CI, 1.6 to 23 for the fourth quartile) were independently associated with the diffuse-SVD subtype.

Conclusions— Plasma β-amyloid_1-40 levels are independently associated with the diffuse-SVD subtype. These results are consistent with the pathophysiological role of fraction Aβ_1-40 in disrupting endothelial vascular function.

Key Words: acute stroke • beta-amyloid protein • leukoaraiosis • small vessel disease