title: Role of cerebral amyloid angiopathy in intracerebral hemorrhage in hypertensive patients.
abstract: OBJECTIVE
  To assess the interaction of cerebral amyloid angiopathy (CAA) and arterial hypertension as cofactors for intracerebral hemorrhage (ICH).
  
  
  METHODS
  The authors investigated 129 postmortem brains of hypertensive patients with and without ICH. Sixty-four patients had had deep (n = 40) or lobar (n = 24) ICH. Sixty-five patients without ICH served as controls. Established risk factors for ICH (age, gender, severity of hypertension, bleeding disorders, intake of anticoagulants, and chronic alcoholism) were identified from medical records. Four specimens per brain were stained with hematoxylin-eosin and Congo red. The entire ICH cohort and subgroups were compared with controls using single-factor and multiple logistic regression analyses.
  
  
  RESULTS
  CAA was found in 15 of 64 subjects (23%) with ICH and in five of 65 controls (8%; p = 0.026). In single-factor analysis, CAA was more prevalent in lobar ICH compared with controls (p = 0.007) but not in deep ICH. Poor control of hypertension was more prevalent in the entire ICH group (p = 0.01) and in deep ICH (p = 0.016) but not in lobar ICH. ICH was predictive of the presence of CAA (odds ratio: 5.6, 95% CI: 1.8 to 19.5, p = 0.003), and CAA was more likely to be found in lobar ICH in multivariable-adjusted analysis. After adjustment for conventional risk factors, there was a weak association between CAA and deep ICH.
  
  
  CONCLUSIONS
  Cerebral amyloid angiopathy plays a major role in the pathogenesis of intracerebral hemorrhage even in patients with more evident risk factors.
authors.affiliation: Department of Neurology, University of Münster, Münster, Germany. ritterm@uni-muenster.de
authors.forename: M A
authors.initials: MA
authors.lastname: Ritter
authors.forename: D W
authors.initials: DW
authors.lastname: Droste
authors.forename: K
authors.initials: K
authors.lastname: Hegedüs
authors.forename: R
authors.initials: R
authors.lastname: Szepesi
authors.forename: D G
authors.initials: DG
authors.lastname: Nabavi
authors.forename: L
authors.initials: L
authors.lastname: Csiba
authors.forename: E B
authors.initials: EB
authors.lastname: Ringelstein
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D016657:Cerebral Amyloid Angiopathy / Q000150:complications* / Q000473:pathology* / Q000503:physiopathology; D002536:Cerebral Arteries / Q000473:pathology / Q000503:physiopathology; D002540:Cerebral Cortex / Q000098:blood supply / Q000473:pathology / Q000503:physiopathology; D018450:Disease Progression; D005260:Female; D006801:Humans; D006973:Hypertension / Q000150:complications* / Q000473:pathology* / Q000503:physiopathology; D020299:Intracranial Hemorrhage, Hypertensive / Q000209:etiology* / Q000473:pathology* / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D058225:Plaque, Amyloid / Q000473:pathology; D011237:Predictive Value of Tests; D012307:Risk Factors