title: Thrombin activatable fibrinolysis inhibitor activation peptide shows association with all major subtypes of ischemic stroke and with TAFI gene variation.
abstract: OBJECTIVE
  Thrombin activatable fibrinolysis inhibitor (TAFI) attenuates fibrinolysis. The aim of the present study was to investigate the possible association between TAFI and overall ischemic stroke and ischemic stroke subtypes.
  
  
  RESULTS
  The Sahlgrenska Academy Study on Ischemic Stroke (SAHLSIS) comprises 600 cases (18 to 69 years) and 600 matched population controls. Stroke subtype was defined by the Trial of Org 10172 in Acute Stroke Treatment (TOAST) classification. TAFI was investigated at the protein level, by analyzing plasma levels of intact TAFI and released activation peptide [AP], and at the genetic level, by genotyping a selection of eleven single nucleotide polymorphisms. After adjustment for traditional risk factors, both TAFI measurements showed association with overall ischemic stroke (AP: odds ratio, 2.22; 95% confidence interval, 1.89 to 2.61; intact TAFI: odds ratio, 1.21; 95% confidence interval, 1.06 to 1.38; for 1-SD increase in AP and intact TAFI, respectively). AP showed associations with all 4 major subtypes of ischemic stroke and intact TAFI to large vessel disease and cryptogenic stroke. TAFI genotypes and haplotypes showed significant associations with both TAFI measurements. In contrast, no association was observed between genetic variants and overall ischemic stroke.
  
  
  CONCLUSIONS
  TAFI levels show independent association with overall ischemic stroke. This association is stronger for released AP than for intact TAFI, and for released AP, it is present in all ischemic stroke subtypes.
authors.affiliation: Institute of Neuroscience and Physiology, Sahlgrenska Academy at Göteborg University, Guldhedsgatan 19, S-413 45 Göteborg, Sweden. claes.ladenvall@neuro.gu.se
authors.forename: Claes
authors.initials: C
authors.lastname: Ladenvall
authors.forename: Ann
authors.initials: A
authors.lastname: Gils
authors.forename: Katarina
authors.initials: K
authors.lastname: Jood
authors.forename: Christian
authors.initials: C
authors.lastname: Blomstrand
authors.forename: Paul J
authors.initials: PJ
authors.lastname: Declerck
authors.forename: Christina
authors.initials: C
authors.lastname: Jern
mesh_terms: D000328:Adult; D000368:Aged; D002545:Brain Ischemia / Q000150:complications*; D025901:Carboxypeptidase B2 / Q000097:blood* / Q000235:genetics*; D002544:Cerebral Infarction / Q000097:blood / Q000209:etiology / Q000401:mortality / Q000503:physiopathology; D002874:Chromosome Mapping; D014644:Genetic Variation; D006239:Haplotypes; D006801:Humans; D015810:Linkage Disequilibrium; D008875:Middle Aged; D020641:Polymorphism, Single Nucleotide; D012307:Risk Factors; D020521:Stroke / Q000097:blood* / Q000145:classification / Q000209:etiology / Q000235:genetics*; D013997:Time Factors
chemical_list: D025901:Carboxypeptidase B2