The GPIa C807T dimorphism associated with platelet collagen receptor density is not a risk factor for myocardial infarction |
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Authors: | S. A. Croft,K. K. Hampton,J. A. Sorrell,R. P. Steeds,K. S. Channer,N. J. Samani,& M. E. Daly |
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Affiliation: | Division of Molecular and Genetic Medicine, University of Sheffield, Royal Hallamshire Hospital, Sheffield. s.a.croft@sheffield.ac.uk |
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Abstract: | 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 TaqManTM 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. |
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Keywords: | platelet GPIa/IIa dimorphism myocardial infarction |
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