Association of the α-fibrinogen Thr312Ala polymorphism with poststroke mortality in subjects with atrial fibrillation

The alpha-fibrinogen Thr312Ala polymorphism occurs in close proximity to several sites important for factor XIIIa-dependent cross-linking, which raises the possibility that it affects fibrin clot stability. We determined the association of this polymorphism with ischemic stroke, stroke subtype, and...

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Bibliographic Details
Published in:Circulation (New York, N.Y.) N.Y.), 1999-05, Vol.99 (18), p.2423-2426
Main Authors: CARTER, A. M, CATTO, A. J, GRANT, P. J
Format: Article
Language:English
Subjects:
Amino Acid Substitution
Atrial Fibrillation - complications
Atrial Fibrillation - genetics
Biological and medical sciences
Brain Ischemia - etiology
Brain Ischemia - genetics
Brain Ischemia - mortality
Cardiac dysrhythmias
Cardiology. Vascular system
Comorbidity
Coronary Disease - epidemiology
Diabetes Mellitus - epidemiology
Female
Fibrinogen - genetics
Gene Frequency
Genetic Predisposition to Disease
Genotype
Heart
Humans
Hypertension - epidemiology
Male
Medical sciences
Point Mutation
Polymorphism, Genetic
Risk
Risk Factors
Smoking - epidemiology
Survival Analysis
Thromboembolism - epidemiology
Thrombophilia - genetics
Transglutaminases - physiology
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Summary:The alpha-fibrinogen Thr312Ala polymorphism occurs in close proximity to several sites important for factor XIIIa-dependent cross-linking, which raises the possibility that it affects fibrin clot stability. We determined the association of this polymorphism with ischemic stroke, stroke subtype, and poststroke mortality. There was no significant difference in the genotype distributions of patients with acute ischemic stroke (n=519) and healthy control subjects (n=423), nor was there any association of this polymorphism with stroke subtype. In a Cox regression model, a significant interaction between Thr312Ala and atrial fibrillation was identified in relation to poststroke mortality (P=0.002). In subjects in sinus rhythm (n=418), there was no difference according to genotype in the proportion of subjects who survived (approximately 60% in each group), whereas in subjects with atrial fibrillation (n=101), there was decreased survival in those possessing the A allele (TT=42.1%, TA=18%, AA=0%). The Thr312Ala polymorphism may give rise to an increased susceptibility for embolization of intra-atrial clot, and these findings could have important implications for identifying subjects most at risk of developing thromboembolic complications.
ISSN:0009-7322
1524-4539
DOI:10.1161/01.CIR.99.18.2423