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Blood, 1 March 2004, Vol. 103, No. 5, pp. 1735-1740. Prepublished online as a Blood First Edition Paper on November 6, 2003; DOI 10.1182/blood-2003-07-2247. This Article Full Text (PDF) All Versions of this Article: 2003-07-2247v1 103/5/1735    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Dunn, E. J Articles by Grant, P. J Search for Related Content PubMed PubMed Citation Articles by Dunn, E. J Articles by Grant, P. J Social Bookmarking                   What's this? Submitted July 7, 2003 Accepted October 24, 2003 Genetics of fibrin clot structure: a twin study Emma J Dunn, Robert A Ariens, Marlies de Lange, Harold Snieder, John H Turney, Timothy D Spector, and Peter J Grant* Academic Unit of Molecular Vascular Medicine, University of Leeds, Leeds, United Kingdom Twin Research and Genetic Epidemiology Unit, St Thomas' Hospital, London, United Kingdom Georgia Prevention Institute, Department of Pediatrics, Medical College of Georgia, Augusta, GA, USA * Corresponding author; email: p.j.grant{at}leeds.ac.uk. Coronary artery thrombosis following plaque rupture is an important feature of myocardial infarction and studies have highlighted the role of coagulation in this condition. Whilst genetic and environmental influences on the variance in levels of coagulation proteins have been reported, there is no data on the heritability of structure/function of the final phenotype of the coagulation cascade, the fibrin clot. To assess genetic and environmental contributions to fibrin structure, permeation and turbidity studies were performed in 137 twin pairs (66 monozygotic, 71 dizygotic). The environmental influence (e2) on pore size (Ks) (e2 = 0.61 [95%CI: 0.45-0.80]) and fibre size (e2 = 0.54 [95%CI: 0.39-0.73]) was greater than the heritability (h2 = 0.39 [95%CI: 0.20-0.55] and 0.46 [95%CI: 0.27-0.62] respectively). Following correction for fibrinogen levels the environmental effect persisted for Ks (e2=0.61), but genetic influence assumed a greater importance in determining fibre size (h2 =0.73). Multivariate analysis revealed an overlap in the influence of genetic and environmental factors on fibrinogen levels, Ks and fibre size. Factor XIII B-subunit showed environmental and genetic correlation with fibrinogen and fibre size, and a genetic correlation with Ks. The results indicate that both genetic and environmental influences are important in determining fibrin clot structure/function. 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