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Factor XIII Val34Leu polymorphism modulates the prothrombotic and inflammatory state associated with atrial fibrillation

Atrial fibrillation (AF) has been shown to confer a prothrombotic or hypercoagulable state, which could be related to inflammation. Factor XIII (FXIII) catalyses the cross-linking of fibrin monomers, increasing clot resistance; specifically, a common polymorphism, Val34Leu, in the FXIII-A subunit ge...

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Bibliographic Details
Published in:Journal of molecular and cellular cardiology 2004-09, Vol.37 (3), p.699-704
Main Authors: Marín, Francisco, Corral, Javier, Roldán, Vanessa, González-Conejero, Rocío, del Rey, María Luz, Sogorb, Francisco, Lip, Gregory Y.H., Vicente, Vicente
Format: Article
Language:English
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Summary:Atrial fibrillation (AF) has been shown to confer a prothrombotic or hypercoagulable state, which could be related to inflammation. Factor XIII (FXIII) catalyses the cross-linking of fibrin monomers, increasing clot resistance; specifically, a common polymorphism, Val34Leu, in the FXIII-A subunit gene has been associated with more rapid FXIII activation. We hypothesised a role for this polymorphism in the prothrombotic state and inflammation in AF, and tested this hypothesis by measurement of indices of coagulation (tissue factor (TF) and fibrinogen), inflammation (interleukin-6 (IL6)) and platelet activation (soluble P selectin (sPsel)). Methods. – We studied 90 stable outpatients (73 ± 8 years) with persistent AF. The FXIII Val34Leu polymorphism was determined by polymerase chain reaction–allelic specific restriction assay (PCR–ASRA). Prevalence of Val34Leu polymorphism of patients was compared to 585 unrelated subjects from the same geographical area. Plasma fibrinogen (Clauss), TF, IL6 and sPsel (all ELISA) were quantified in patient group. Research indices were compared to 74 controls in sinus rhythm with similar clinical characteristics. Results. – There were no statistical differences in FXIII polymorphism prevalence between AF patients and controls. Patients carrying the Leu34 allele had higher plasma levels of TF, IL6 and sPsel (all P 
ISSN:0022-2828
1095-8584
DOI:10.1016/j.yjmcc.2004.06.001