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Correlation of factor VIIa values with factor VII gene polymorphism, fasting and postprandial triglyceride levels, and subclinical carotid atherosclerosis.

TitleCorrelation of factor VIIa values with factor VII gene polymorphism, fasting and postprandial triglyceride levels, and subclinical carotid atherosclerosis.
Publication TypeJournal Article
Year of Publication1998
AuthorsGhaddar HM, Folsom AR, Aleksic N, Hearne LB, Chambless LE, Morrissey JH, Wu KK
JournalCirculation
Volume98
Issue25
Pagination2815-21
Date Published1998 Dec 22-29
ISSN0009-7322
KeywordsArteriosclerosis, Carotid Artery Diseases, Coronary Artery Disease, Factor VII, Factor VIIa, Fasting, Female, Genotype, Humans, Hypertriglyceridemia, Male, Middle Aged, Polymorphism, Genetic, Postprandial Period, Triglycerides
Abstract

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.

DOI10.1161/01.cir.98.25.2815
Alternate JournalCirculation
PubMed ID9860781
Grant ListN01-HL-55015 / HL / NHLBI NIH HHS / United States
N01-HL-55016 / HL / NHLBI NIH HHS / United States
U01-HL45467 / HL / NHLBI NIH HHS / United States