title: Plasma beta-amyloid 1-40 is associated with the diffuse small vessel disease subtype.
abstract: OBJECTIVE
  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.
  
  
  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 Abeta levels.
  
  
  RESULTS
  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<0.001) and control subjects (P<0.001). No differences in Abeta(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 beta-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 beta-amyloid(1-40) levels are independently associated with the diffuse-SVD subtype. These results are consistent with the pathophysiological role of fraction Abeta(1-40) in disrupting endothelial vascular function.
authors.affiliation: Stroke Unit, Department of Neurociences, Hospital Universitari Germans Trias i Pujol (Badalona), Universitat Autònoma de Barcelona, Barcelona, Spain. mgomis.germanstrias@gencat.cat
authors.forename: Meritxell
authors.initials: M
authors.lastname: Gomis
authors.forename: Tomás
authors.initials: T
authors.lastname: Sobrino
authors.forename: Angel
authors.initials: A
authors.lastname: Ois
authors.forename: Mònica
authors.initials: M
authors.lastname: Millán
authors.forename: Ana
authors.initials: A
authors.lastname: Rodríguez-Campello
authors.forename: Natalia
authors.initials: N
authors.lastname: Pérez de la Ossa
authors.forename: Raquel
authors.initials: R
authors.lastname: Rodríguez-González
authors.forename: Jordi
authors.initials: J
authors.lastname: Jiménez-Conde
authors.forename: Elisa
authors.initials: E
authors.lastname: Cuadrado-Godia
authors.forename: Jaume
authors.initials: J
authors.lastname: Roquer
authors.forename: Antoni
authors.initials: A
authors.lastname: Dávalos
mesh_terms: D000208:Acute Disease; D000368:Aged; D016229:Amyloid beta-Peptides / Q000032:analysis / Q000097:blood*; D001160:Arterioles / Q000378:metabolism / Q000473:pathology; D020520:Brain Infarction / Q000097:blood* / Q000473:pathology* / Q000503:physiopathology; D015984:Causality; D002536:Cerebral Arteries / Q000378:metabolism* / Q000473:pathology* / Q000503:physiopathology; D015331:Cohort Studies; D015140:Dementia, Vascular / Q000097:blood / Q000473:pathology / Q000503:physiopathology; D042783:Endothelial Cells / Q000378:metabolism / Q000473:pathology; D005260:Female; D006801:Humans; D049292:Leukoaraiosis / Q000097:blood / Q000473:pathology / Q000503:physiopathology; D008297:Male; D008833:Microcirculation / Q000502:physiology; D008875:Middle Aged; D010446:Peptide Fragments / Q000032:analysis / Q000097:blood*; D011237:Predictive Value of Tests
chemical_list: D016229:Amyloid beta-Peptides; D010446:Peptide Fragments; C078592:amyloid beta-protein (1-40)