title: Angiotensin converting enzyme insertion/deletion genotype is associated with leukoaraiosis in lacunar syndromes.
abstract: OBJECTIVE
  Pathological and clinical data suggest that patients presenting with ischaemic lacunar syndromes may be a heterogenous group. Those with isolated lacunar infarction are thought to have localised atherosclerosis whereas in those with coexisting leukoaraiois a distinct diffuse small vessel vasculopathy may be the predominant underlying pathology. The ACE insertion/deletion (I/D) polymorphism is an important candidate gene in ischaemic cerebrovascular disease but, where lacunar stroke specifically has been examined, there have been discrepant reports concerning a possible association. It was hypothesised that the influence of the ACE gene may be different among the two subgroups of ischaemic lacunar stroke reflecting the heterogeneity of the small vessel disease phenotype.
  
  
  METHODS
  Eighty four consecutive patients presenting with classic lacunar syndromes were studied. All had acute cranial CT to exclude primary intracerebral haemorrhage and these were subsequently assessed for the presence and extent of leukoaraiosis. All patients were genotyped for the ACE insertion/deletion polymorphism.
  
  
  RESULTS
  There was a significant difference in the distribution of ACE genotype with the DD genotype occurring more often in patients with leukoaraiosis and the II and ID genotypes occurring more often among those in whom this was absent (chi(2)=9.06, p=0.01). In a logistic regression model the ACE DD genotype remained as an independent predictor for the presence of leukoaraiosis (p=0.02) in patients presenting with classic lacunar syndromes.
  
  
  CONCLUSIONS
  This study supports the hypothesis that there may be different types of small vessel disease in patients with classic lacunar syndromes and that the influence of the ACE DD genotype may be relevant in mediating the diffuse form of vessel injury.
authors.affiliation: Department of Neurology, St James's University Hospital, Beckett Street, Leeds LS9 7TF, UK.
authors.forename: A
authors.initials: A
authors.lastname: Hassan
authors.forename: A
authors.initials: A
authors.lastname: Lansbury
authors.forename: A J
authors.initials: AJ
authors.lastname: Catto
authors.forename: A
authors.initials: A
authors.lastname: Guthrie
authors.forename: J
authors.initials: J
authors.lastname: Spencer
authors.forename: C
authors.initials: C
authors.lastname: Craven
authors.forename: P J
authors.initials: PJ
authors.lastname: Grant
authors.forename: J M
authors.initials: JM
authors.lastname: Bamford
mesh_terms: D000368:Aged; D020520:Brain Infarction / Q000000981:diagnostic imaging / Q000235:genetics*; D002539:Cerebral Arterial Diseases / Q000000981:diagnostic imaging / Q000235:genetics; D002872:Chromosome Deletion; D005260:Female; D015971:Gene Expression Regulation, Enzymologic / Q000502:physiology; D005838:Genotype; D006801:Humans; D008297:Male; D016254:Mutagenesis, Insertional; D007703:Peptidyl-Dipeptidase A / Q000235:genetics*; D011110:Polymorphism, Genetic / Q000235:genetics; D012306:Risk; D013577:Syndrome; D014057:Tomography, X-Ray Computed
chemical_list: D007703:Peptidyl-Dipeptidase A