doi: 10.1161/hq0202.102874
© 2002 American Heart Association, Inc.
Thrombosis |
Factor XIIIA Val34Leu Polymorphism Does Not Predict Risk of Coronary Heart Disease
The Atherosclerosis Risk in Communities (ARIC) Study
From the Vascular Biology Research Center and Hematology Division (N.A., C.A., Y.-W.W., H.J., K.K.W.), University of Texas-Houston Medical School; the Division of Epidemiology (A.R.F.), School of Public Health, University of Minnesota, Minneapolis; and the Human Genetics Center (E.B.), University of Texas-Houston Health Science Center.
Reprint requests to Dr Kenneth K. Wu, Professor and Director, Division of Hematology, University of Texas-Houston Medical School, 6431 Fannin, MSB 5.016, Houston, TX 77030. E-mail Kenneth.K.Wu{at}uth.tmc.edu
Factor XIII catalyzes the cross-linking of fibrin. Cross-sectional studies have suggested that a common polymorphism site at residue 34 of the A subunit of factor XIII (FXIIIA) with a substitution of Leu for Val (FXIIIA Val34Leu) was associated with reduced coronary heart disease (CHD). This association has not been examined in prospective studies. Healthy subjects (n=15 792) were recruited from 4 US communities into the Atherosclerosis Risk in Communities (ARIC) study from 1987 to 1989. They were followed, and incident CHD events were identified and verified. For the present study, we included 423 patients with CHD as cases and 479 noncases. FXIIIA Val34Leu polymorphism was determined by the single-strand conformational polymorphism method. There were no significant differences in the genotype frequencies between cases and noncases. The genotypes showed little association with known CHD risk factors. A weighted proportional hazards regression analysis adjusting for other risk factors confirmed no association of the genotypes with risk of CHD. This prospective study did not provide evidence of a reduced CHD risk for the FXIIIA 34Leu allele.
Key Words: factor XIII • factor XIIIA Val34Leu polymorphism • coronary heart disease
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