The −1185 A/G and −1051 G/A dimorphisms in the von Willebrand factor gene promoter and risk of myocardial infarction

Elevated plasma von Willebrand factor (VWF) levels are associated with coronary artery disease, although the precise mechanism for this is unclear. Recently, four linked dimorphisms in the VWF gene promoter were demonstrated to influence plasma VWF level. We conducted a case–control study of 525 acu...

Full description

Saved in:
Bibliographic Details
Published in:British journal of haematology 2001-12, Vol.115 (3), p.701-706
Main Authors: Di Bitondo, Rosa, Cameron, Cherie L., Daly, Martina E., Croft, Stuart A., Steeds, Rick P., Channer, Kevin S., Samani, Nilesh J., Lillicrap, David, Winship, Peter R.
Format: Article
Language:English
Subjects:
Aged
Biological and medical sciences
Cardiology. Vascular system
Case-Control Studies
case–control study
Coronary heart disease
Female
haplotype
Haplotypes
Heart
Humans
Male
Medical sciences
Middle Aged
myocardial infarction
Myocardial Infarction - blood
Myocardial Infarction - genetics
Odds Ratio
Polymorphism, Genetic
promoter polymorphisms
Promoter Regions, Genetic
Risk
Smoking - adverse effects
von Willebrand factor
von Willebrand Factor - genetics
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Elevated plasma von Willebrand factor (VWF) levels are associated with coronary artery disease, although the precise mechanism for this is unclear. Recently, four linked dimorphisms in the VWF gene promoter were demonstrated to influence plasma VWF level. We conducted a case–control study of 525 acute myocardial infarction (MI) cases and 451 control subjects, all aged  75 years, to assess the potential contribution of two of these dimorphisms (−1185 G/A and −1051 A/G) to the risk of MI. The frequency of the −1185A/−1051G haplotype, associated with elevated VWF levels, was similar in the case and control groups, yielding a haplotypic odds ratio for MI of 0·93 (95% CI 0·77, 1·12, P = 0·43), and there was no significant association between the −1185A/−1051G haplotype and the risk of MI in any subgroup analysed. We therefore conclude that possession of the −1185A/−1051G haplotype does not confer an increased risk for MI.
ISSN:0007-1048
1365-2141
DOI:10.1046/j.1365-2141.2001.03176.x