on August 20, 2009
Published online before print August 20, 2009, doi: 10.1161/STROKEAHA.109.559641
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Submitted on June 4, 2009
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. * To whom correspondence should be addressed. 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 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 A Results—Median [quartiles] A Conclusions—Plasma
Revised on July 9, 2009
Accepted on July 10, 2009
Plasma
Meritxell Gomis MD*; 
-Amyloid 1–40 Is Associated With the Diffuse Small Vessel Disease Subtype
-amyloid peptide (A) deposition has been associated with lacunar infarcts and leukoaraiosis, but its specific relationship with SVD subtypes is unknown. We hypothesized that plasma A levels can play a different role in SVD subtypes in patients with acute lacunar stroke. levels.1–40 levels (40.4 [35.1, 50.5] versus 55.1 [42.3, 69.6] pg/mL), but not A1–42 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 A1–40 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 -amyloid1–40 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.-amyloid1–40 levels are independently associated with the diffuse-SVD subtype. These results are consistent with the pathophysiological role of fraction A1–40 in disrupting endothelial vascular function.
Key words: acute stroke • beta-amyloid protein • leukoaraiosis • small vessel disease