Dm. Heywood et al., POLYMORPHISMS OF THE FACTOR-VII GENE AND CIRCULATING FVII-C LEVELS INRELATION TO ACUTE CEREBROVASCULAR-DISEASE AND POSTSTROKE MORTALITY, Stroke, 28(4), 1997, pp. 816-821
Background and Purpose FVII:C has been shown to be an independent risk
factor for myocardial infarction and is related to environmental and
genetic factors. This study sought to investigate FVII:C levels and fa
ctor VII (FVII) gene polymorphisms in relation to stroke and disease o
utcome, Methods To examine the association of FVII:C and the Msp I and
promoter insertion polymorphisms of the FVII gene in acute stroke, 31
7 patients and 198 age-matched control subjects were studied. Results
FVII:C levels were significantly lower in patients at onset than 3 mon
ths later (119% versus 135%, respectively; P<.0005), Levels were signi
ficantly lower in patients at onset than in control subjects (124% [95
% confidence interval, 120% to 129%] versus 141% [95% confidence inter
val; 135% to 148%], respectively; P<.0005) but were not significantly
different at 3 months (135% [95% confidence interval, 128% to 141%] ve
rsus 141% [95% confidence interval, 135% to 148%], respectively). We f
ound no difference in genotype distribution for either polymorphism be
tween patients and control subjects, no difference in FVII:C level or
genotype distribution between pathological types of stroke, and no rel
ationship with poststroke mortality, Both polymorphisms were significa
ntly associated with FVII:C levels in patients and control subjects, I
n a multiple regression model for patients, Msp I genotype, cholestero
l, and smoking remained as independent predictors of FVII:C levels, ac
counting for 32% of interindividual variation. Conclusions These resul
ts suggest that neither MI:C levels nor FVII gene polymorphisms are as
sociated with cerebrovascular disease. There were no genotype-specific
correlations of environmental factors with FVII:C, but there was evid
ence of an acute-phase or consumptive fall in FVII:C levels at the tim
e of stroke, whereas levels increased to those similar for healthy age
-matched control subjects by 3 months, when the acute phase had presum
ably subsided.