title: Risk factors and progression of small vessel disease-related cerebral abnormalities.
abstract: A three year follow-up of 273 participants (mean age 60 years) of the Austrian Stroke Prevention Study provides first information on the rate and clinical predictors of progression of small vessel disease related cerebral abnormalities including white matter changes and lacunes. White matter hyperintensity progression was found in 17.9% of individuals over the 3 year period. New lacunes occurred in 2.2% of subjects. The overall frequency of progression of small vessel disease related brain changes was 19%. Diastolic blood pressure and early confluent or confluent white matter hyperintensities at baseline predicted lesion progression. Genetic association studies in the setting of the Austrian Stroke Prevention Study described that polymorphisms in the renin angiotensin system (RAS) increase the susceptibility for progression of cerebral small vessel disease. Homozygosity for the T allele of the M235T polymorphism of the angiotensinogen gene was associated with a 3.19-fold increased risk for lesion progression independently of arterial hypertension. These data suggest that drugs influencing the RAS system may allow to intervene with an unfavorable course of cerebral small vessel disease.
authors.affiliation: Department of Neurology, Karl-Franzens University, Graz, Austria. reinhold.schmidt@kfunigraz.ac.at
authors.forename: R
authors.initials: R
authors.lastname: Schmidt
authors.forename: F
authors.initials: F
authors.lastname: Fazekas
authors.forename: C
authors.initials: C
authors.lastname: Enzinger
authors.forename: S
authors.initials: S
authors.lastname: Ropele
authors.forename: P
authors.initials: P
authors.lastname: Kapeller
authors.forename: H
authors.initials: H
authors.lastname: Schmidt
mesh_terms: D000368:Aged; D015140:Dementia, Vascular / Q000453:epidemiology* / Q000235:genetics / Q000473:pathology*; D018450:Disease Progression; D006801:Humans; D012307:Risk Factors; D020521:Stroke / Q000453:epidemiology* / Q000235:genetics / Q000473:pathology*