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Association of polymorphisms of platelet membrane integrins α IIb β 3 (HPA‐1b/Pl A2 ) and α 2 β 1 (α 2 807TT) with premature myocardial infarction
Author(s) -
ZOTZ R. B.,
WINKELMANN B. R.,
MÜLLER C.,
BOEHM B. O.,
MÄRZ W.,
SCHARF R. E.
Publication year - 2005
Publication title -
journal of thrombosis and haemostasis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.947
H-Index - 178
eISSN - 1538-7836
pISSN - 1538-7933
DOI - 10.1111/j.1538-7836.2005.01432.x
Subject(s) - myocardial infarction , medicine , cardiology , integrin , platelet , receptor
Summary. Conflicting results of an association of the human platelet antigen 1b (HPA‐1b/Pl A2 ), localized on the β ‐subunit of the integrin α IIb β 3 , and the α 2 807TT genotype of the integrin α 2 β 1 with coronary atherosclerosis and myocardial infarction have been reported. Both platelet receptor polymorphisms were genotyped in 3261 patients who had undergone coronary angiography, including 1175 survivors of a myocardial infarction, 1211 individuals with coronary artery disease but no history of myocardial infarction, and 571 control patients without angiographic coronary artery disease, and in 793 blood donors. In a case–control design, the prevalence of HPA‐1b and α 2 807TT genotypes did not differ significantly between the patient groups with coronary artery disease or myocardial infarction and patient controls or blood donors. By contrast, using a multivariate case‐only design, it was found that the median age of onset of myocardial infarction was 5.2 years earlier ( P = 0.006) in carriers of the HPA‐1b allele and 6.3 years earlier ( P = 0.006) in carriers of the α 2 807TT genotype in the 264 survivors of myocardial infarction of recent onset with one‐ or two‐vessel coronary artery disease. A significant interaction with the conventional risk factors hypercholesterolemia, smoking, diabetes, hypertension, and hyperfibrinogenemia was excluded. Human platelet antigen 1b and α 2 807TT are associated with premature myocardial infarction but not with coronary artery disease, suggesting a role of distinct integrin genotypes for increased platelet thrombogenicity. This association requires confirmation in follow‐up studies.