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(Circulation. 1998;98:2815-2821.)
© 1998 American Heart Association, Inc.

Clinical Investigation and Reports*

Correlation of Factor VIIa Values With Factor VII Gene Polymorphism, Fasting and Postprandial Triglyceride Levels, and Subclinical Carotid Atherosclerosis

Habib M. Ghaddar, MD; Aaron R. Folsom, MD; Nena Aleksic, PhD; Leonard B. Hearne, PhD; Lloyd E. Chambless, PhD; James H. Morrissey, PhD; Kenneth K. Wu, MD, PhD; for the Atherosclerosis Risk in Communities Study Investigators

From the Division of Hematology and Vascular Biology Research Center (H.M.G, N.A., K.K.W.), University of Texas, Houston; Department of Biostatistics (L.B.H., L.E.C.), University of North Carolina, Chapel Hill; Division of Epidemiology (A.R.F.), School of Public Health, University of Minnesota, Minneapolis; and Oklahoma Medical Research Foundation (J.H.M.), Oklahoma City.

Correspondence and reprint requests to Kenneth Wu, MD, PhD, Division of Hematology, University of Texas Medical School, 6431 Fannin, MSB 5.016, Houston, TX 77030. E-mail kkwu{at}heart.med.uth.tmc.edu

Background—Factor VII plays a pivotal role in coagulation. Factor VIIc levels were reported to be a risk factor for fatal coronary heart disease (CHD). Factor VIIc and VIIag levels were noted to be positively associated with plasma triglyceride (TG) levels and influenced by a VII gene polymorphism. The purpose of this study is to determine whether these associations are related to activated factor VII (factor VIIa).

Methods and Results—Fasting and 3.5-hour postprandial samples from 216 cases with subclinical atherosclerosis and 341 matched controls selected from the ARIC cohort were assayed for levels of factors VIIa, VIIc, and VIIag and TG, and factor VII codon 353 gene polymorphism. The level of factor VIIa was higher in Arg/Arg than in Arg/Gln+Gln/Gln genotypes, and the difference was in accord with that of factors VIIag and VIIc. However, the factor VIIa difference was statistically insignificant. Factor VIIa values were not correlated with fasting or 3.5-hour postprandial TG levels, nor were they associated with subclinical atherosclerosis.

Conclusions—Factor VIIa levels, like factor VIIag and VIIc levels, are influenced by factor VII gene codon 353 polymorphism. However, unlike factor VIIag or VIIc, factor VIIa is not influenced by TG levels; none of these is associated with subclinical atherosclerosis.

Key Words: factor VIIa • genes • coronary disease • atherosclerosis

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