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The GPIa C807T dimorphism associated with platelet collagen receptor density is not a risk factor for myocardial infarction
Author(s) -
Croft S. A.,
Hampton K. K.,
Sorrell J. A.,
Steeds R. P.,
Channer K. S.,
Samani N. J.,
Daly M. E.
Publication year - 1999
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.1365-2141.1999.01597.x
Subject(s) - medicine , allele , myocardial infarction , odds ratio , genotype , risk factor , gastroenterology , endocrinology , biology , genetics , gene
The platelet collagen receptor, GPIa/IIa, is an important mediator of platelet adhesion to fibrillar collagens at sites of vascular injury. Recently, a dimorphism at nucleotide 807 of the GPIa cDNA (TTC/TTT in codon 224) was shown to be associated with variation in GPIa/IIa receptor density on the platelet surface. We conducted a case–control study to determine if the 807T allele, linked with increased GPIa/IIa density, contributed to risk of myocardial infarction (MI). DNA from 546 acute MI cases and 507 controls, all aged <75 years, was genotyped for the C807T dimorphism using the TaqMan TM system of allelic discrimination. The allelic odds ratio (OR) for MI in the complete cohort was 0.88 (95% CI 0.74–1.05, P = 0.17), indicating that the 807T allele was not associated with an increased risk of MI. There was also no increased risk of MI associated with the homozygous 807TT ( P = 0.22) or heterozygous 807CT ( P = 0.24) genotypes or for carriers of the 807T allele in any cohort subgroup analysed. We conclude that the GPIa 807T allele is not a risk factor for MI in our population either alone or in combination with other major cardiovascular risk factors.