© 1995 American Heart Association, Inc.
Articles |
Coagulation Factor VII Mass and Activity in Young Men With Myocardial Infarction at a Young Age
Role of Plasma Lipoproteins and Factor VII Genotype
From the Division of Cardiology (E.M.) and the Atherosclerosis Research Unit, King Gustaf V Research Institute (A.S., F. van't H., P.E., A.H.), Department of Medicine, and the Division of Blood Coagulation Research, Department of Laboratory Medicine (A.M.S., M.B.), Karolinska Hospital, Karolinska Institute, Stockholm, Sweden.
Correspondence to Dr Elisabeth Moor, Department of Cardiology, Karolinska Hospital, S-171 76 Stockholm, Sweden.
Abstract Factor VII (FVII) coagulant activity has been proven
to be associated with the risk of future fatal coronary heart disease
(CHD) in middle-aged men. Recent studies have emphasized the role of
triglyceride-rich lipoproteins and FVII genotype in determining plasma
levels of FVII protein and activity. The present study was
undertaken to examine whether FVII activity state and protein
concentration in fasting plasma are altered in young men with proven
myocardial infarction (MI) and examined the relations of FVII to
subfractions of apo B–containing lipoproteins and the Arg
Gln
polymorphism in the FVII gene. Activated FVII (FVIIa) was determined by
a clotting assay using soluble, recombinant, truncated tissue factor. A
total of 94 men with a first MI before the age of 45 (mean age±SD,
39.6±4.5 years) were included in the study along with 99
population-based, age-matched control subjects. In addition to FVIIa
and FVII antigen (FVII:Ag), a panel of FVII activity assays were
included for comparison with previous work in this field. The plasma
level of FVII:Ag was higher in patients than in control subjects when
the entire groups were compared (537±128 versus 479±93 ng/mL,
P<.001), the differences being accounted for by patients
with hypertriglyceridemic lipoprotein phenotypes. In contrast, FVIIa
was similar in patients and control subjects (4.6±1.4 versus 4.3±1.3
ng/mL, NS), which means that the proportion of FVIIa molecules was
unaltered or even lower in the patients. As expected, the ArgGln
polymorphism significantly influenced both FVII mass and activity
levels. In addition, presence of the Gln allele appeared to be
associated with a lower proportion of fully active FVII molecules. The
polymorphism also affected the relation between the plasma
concentration of VLDL and FVII:Ag. The triglyceride content and
particle number of all VLDL subfractions, irrespective of particle
size, correlated fairly strongly with FVII mass determinations but not
at all with FVIIa. HDL cholesterol concentration, on the other hand,
presumably reflecting the efficiency of lipoprotein lipase–mediated
lipolysis of VLDL, related significantly to the FVIIa level. The
ArgGln polymorphism, independent of lipoprotein effects, explained
5% to 10% of the variation in FVII mass and activity. In conclusion,
the present findings speak against a role of FVII as a risk factor
for CHD, because a significantly increased potential for activation of
coagulation (ie, raised basal concentration of FVIIa) was not observed
among young postinfarction patients. Prospective epidemiological
studies including specific determination of FVIIa are needed to resolve
the issue of whether FVII activity is a risk factor for CHD.
Key Words: coagulation factor VII • myocardial infarction • genotype • lipoproteins
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