To the top

Page Manager: Webmaster
Last update: 9/11/2012 3:13 PM

Tell a friend about this page
Print version

Thrombin activatable fibr… - University of Gothenburg, Sweden Till startsida
To content Read more about how we use cookies on

Thrombin activatable fibrinolysis inhibitor activation peptide shows association with all major subtypes of ischemic stroke and with TAFI gene variation

Journal article
Authors Claes Ladenvall
Ann Gils
Katarina Jood
Christian Blomstrand
Paul J. Declerck
Christina Jern
Published in Arterioscler Thromb Vasc Biol
Volume 27
Issue 4
Pages 955-62
ISSN 10795642
Publication year 2007
Published at Institute of Neuroscience and Physiology, Department of Clinical Neuroscience and Rehabilitation
Pages 955-62
Language en
Keywords Adult, Aged, Brain Ischemia/*complications, Carboxypeptidase U/*blood/*genetics, Cerebral Infarction/blood/etiology/mortality/physiopathology, Cerebrovascular Accident/*blood/classification/etiology/*genetics, Chromosome Mapping, Haplotypes, Humans, Linkage Disequilibrium, Middle Aged, Polymorphism, Single Nucleotide, Risk Factors, Time Factors, *Variation (Genetics)
Subject categories Dermatology and Venereal Diseases


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. METHODS AND 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. CONCLUSION: 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.

Page Manager: Webmaster|Last update: 9/11/2012

The University of Gothenburg uses cookies to provide you with the best possible user experience. By continuing on this website, you approve of our use of cookies.  What are cookies?