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

Artikel i vetenskaplig tidskrift
Författare Claes Ladenvall
Ann Gils
Katarina Jood
Christian Blomstrand
Paul J. Declerck
Christina Jern
Publicerad i Arterioscler Thromb Vasc Biol
Volym 27
Nummer/häfte 4
Sidor 955-62
ISSN 10795642
Publiceringsår 2007
Publicerad vid Institutionen för neurovetenskap och fysiologi, sektionen för klinisk neurovetenskap och rehabilitering
Sidor 955-62
Språk en
Länkar atvb.ahajournals.org/cgi/content/fu...
Ämnesord 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)
Ämneskategorier Dermatologi och venereologi

Sammanfattning

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.

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