Polymorphisms of the factor VII gene and circulating FVII:C levels in relation to acute cerebrovascular disease and poststroke mortality.
OBJECTIVE
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 factor VII (FVII) gene polymorphisms in relation to stroke and disease outcome.


METHODS
To examine the association of FVII:C and the Msp I and promoter insertion polymorphisms of the FVII gene in acute stroke, 317 patients and 198 age-matched control subjects were studied.


RESULTS
FVII:C levels were significantly lower in patients at onset than 3 months later (119% versus 135%, respectively; P < .0005). Levels were significantly lower in patients at onset than in control subjects (124% [95% confidence interval, 120% to 129%] versus 141% [95% confidence interval, 135% to 148%], respectively; P < .0005) but were not significantly different at 3 months (135% [95% confidence interval, 128% to 141%] versus 141% [95% confidence interval, 135% to 148%], respectively). We found no difference in genotype distribution for either polymorphism between patients and control subjects, no difference in FVII:C level or genotype distribution between pathological types of stroke, and no relationship with poststroke mortality. Both polymorphisms were significantly associated with FVII:C levels in patients and control subjects. In a multiple regression model for patients, Msp I genotype, cholesterol, and smoking remained as independent predictors of FVII:C levels, accounting for 32% of interindividual variation.


CONCLUSIONS
These results suggest that neither FVII:C levels nor FVII gene polymorphisms are associated with cerebrovascular disease. There were no genotype-specific correlations of environmental factors with FVII:C, but there was evidence of an acute-phase or consumptive fall in FVII:C levels at the time of stroke, whereas levels increased to those similar for healthy age-matched control subjects by 3 months, when the acute phase had presumably subsided.
Heywood
D M
DM
Division of Medicine, School of Medicine, University of Leeds, UK. daniellh@pathology.leeds.ac.uk
Carter
A M
AM
Catto
A J
AJ
Bamford
J M
JM
Grant
P J
PJ
D000208:Acute Disease; D000368:Aged; D000941:Antigens / Q000032:analysis*; D002561:Cerebrovascular Disorders / Q000097:blood* / Q000235:genetics* / Q000401:mortality; D002784:Cholesterol / Q000097:blood; D004251:DNA Transposable Elements; D005167:Factor VII / Q000032:analysis* / Q000235:genetics*; D005260:Female; D005796:Genes; D005838:Genotype; D006801:Humans; D008297:Male; D008875:Middle Aged; D011110:Polymorphism, Genetic; D012727:Sex Characteristics
D000941:Antigens; D004251:DNA Transposable Elements; C042580:factor VII clotting antigen; D005167:Factor VII; D002784:Cholesterol