Elevated levels of coagulation factor VII activity (FVIIc) are associated w
ith increased risk of CHD. FVIIc is strongly determined by two polymorphism
s (R353Q and 0/10 base pairs (bp)) and plasma triacylglycerol (TAG) concent
rations. The Q and 10bp polymorphisms show strong linkage disequilibrium an
d have been associated with lower levels of fasting FVII, but there has bee
n little investigation of the effect of these genotypes on the postprandial
FVII metabolism. The present study demonstrated that fasting activated fac
tor VII (FVIIa) and factor VII antigen (FVIIag) levels were significantly l
ower in the heterozygotes carrying the Q and 10bp alleles (n 12), than in t
he R/0 bp homozygotes (n 12) (43.0 (SE 4.8) v. 23.9 (SE 6.5) mU/ml and 85.7
(SE 5.4) v. 71.6 (SE 7.5)% respectively). During postprandial lipaemia the
re was a significant increase in FVIIa in R/0 bp homozygotes but not in the
heterozygotes carrying the Q and 10 bp alleles. The proportion of FVIIa (F
VIIa:FVIIag) increased in the homozygotes but not in the heterozygotes (2.0
4 (SE 0.35) v. 1.20 (SE 0.26) respectively). Therefore possession of the re
latively common Q and 10 bp alleles is not associated with postprandial act
ivation of FVII, which may in turn have a protective effect against CHD.