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The −1185 A/G and −1051 G/A dimorphisms in the von Willebrand factor gene promoter and risk of myocardial infarction
Author(s) -
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.
Publication year - 2001
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1046/j.1365-2141.2001.03176.x
Subject(s) - haplotype , von willebrand factor , medicine , myocardial infarction , odds ratio , case control study , risk factor , von willebrand disease , gastroenterology , coronary artery disease , cardiology , platelet , endocrinology , genotype , gene , genetics , biology
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.