title: C-reactive protein, carotid atherosclerosis, and cerebral small-vessel disease: results of the Austrian Stroke Prevention Study.
abstract: OBJECTIVE
  C-reactive protein (CRP) is an inflammatory marker known to be a risk factor for stroke. We examined the associations between CRP, carotid atherosclerosis, white matter lesions, and lacunes as manifestations of cerebral large- and small-vessel disease.
  
  
  METHODS
  In the community-based Austrian Stroke Prevention Study, CRP concentrations were measured by a highly sensitive assay in 700 participants at baseline. All underwent carotid duplex scanning, and a subset of 505 subjects underwent brain magnetic resonance imaging. Imaging was repeated after 3 and 6 years. We graded carotid atherosclerosis in both common and internal carotid arteries on a 5-point scale and calculated the sum of scores as an index of the severity of carotid atherosclerosis. The volume of white matter lesions and the number of lacunes were considered small vessel disease-related brain abnormalities.
  
  
  RESULTS
  After adjustment for vascular risk factors, the severity and progression of extracranial carotid atherosclerosis increased with increasing quintiles of CRP. Only study participants in the fourth and fifth quintile (>2.50 mg/L) had significantly more baseline atherosclerosis and greater progression when we used the first quintile (<0.80 mg/L) as a reference. No interactions were seen between CRP quintiles and vascular risk factors for carotid atherosclerosis. The associations between severity and progression of small vessel disease-related brain abnormalities and CRP were nonsignificant.
  
  
  CONCLUSIONS
  We found evidence for differential effects of CRP in different beds of the arterial brain supply. CRP was a marker for active carotid atherosclerosis but not for small vessel disease-related brain lesions.
authors.affiliation: Department of Neurology, Medical University of Graz, Auenbruggerplatz 22, 8036 Graz, Austria. reinhold.schmidt@meduni-graz.at
authors.forename: Reinhold
authors.initials: R
authors.lastname: Schmidt
authors.forename: Helena
authors.initials: H
authors.lastname: Schmidt
authors.forename: Martin
authors.initials: M
authors.lastname: Pichler
authors.forename: Christian
authors.initials: C
authors.lastname: Enzinger
authors.forename: Katja
authors.initials: K
authors.lastname: Petrovic
authors.forename: Kurt
authors.initials: K
authors.lastname: Niederkorn
authors.forename: Susanna
authors.initials: S
authors.lastname: Horner
authors.forename: Stefan
authors.initials: S
authors.lastname: Ropele
authors.forename: Norbert
authors.initials: N
authors.lastname: Watzinger
authors.forename: Martin
authors.initials: M
authors.lastname: Schumacher
authors.forename: Andrea
authors.initials: A
authors.lastname: Berghold
authors.forename: Gerhard M
authors.initials: GM
authors.lastname: Kostner
authors.forename: Franz
authors.initials: F
authors.lastname: Fazekas
mesh_terms: D000368:Aged; D001161:Arteriosclerosis / Q000097:blood* / Q000453:epidemiology*; D001317:Austria / Q000453:epidemiology; D002097:C-Reactive Protein / Q000378:metabolism*; D002340:Carotid Artery Diseases / Q000097:blood* / Q000453:epidemiology* / Q000503:physiopathology; D002560:Cerebrovascular Circulation / Q000502:physiology; D015331:Cohort Studies; D005260:Female; D006801:Humans; D008297:Male; D008833:Microcirculation / Q000378:metabolism; D008875:Middle Aged; D012720:Severity of Illness Index; D020521:Stroke / Q000097:blood / Q000453:epidemiology / Q000503:physiopathology
chemical_list: D002097:C-Reactive Protein