HPA-1 and HPA-3 polymorphisms of the platelet fibrinogen receptor and coronary artery disease and myocardial infarction

Citation
C. Bottiger et al., HPA-1 and HPA-3 polymorphisms of the platelet fibrinogen receptor and coronary artery disease and myocardial infarction, THROMB HAEM, 83(4), 2000, pp. 559-562
Citations number
39
Categorie Soggetti
Cardiovascular & Hematology Research
Journal title
THROMBOSIS AND HAEMOSTASIS
ISSN journal
03406245 → ACNP
Volume
83
Issue
4
Year of publication
2000
Pages
559 - 562
Database
ISI
SICI code
0340-6245(200004)83:4<559:HAHPOT>2.0.ZU;2-O
Abstract
Platelet fibrinogen receptor (glycoprotein [GP] IIb/IIIa) plays a fundament al role in atherothrombosis. The human platelet antigen (HPA) -1 and the HP A-3 are the most extensively studied polymorphisms of GPIIIa and GPIIb, res pectively. This study was designed to test, in a large population, the hypo thesis that these polymorphisms represent a risk factor for the occurrence of coronary artery disease (CAD) and myocardial infarction (MI). Consecutive. angiographically examined patients with significant coronary s tenoses but without symptoms or signs of old or acute MI constituted the gr oup with CAD (CAD, n = 998) and those with old or acute MI constituted the group with MI (MI, n = 793). As controls served subjects, matched with pati ents for age and sex, with neither angiographic CAD nor symptoms or signs o f MI (matched controls [MC], n = 340) as well as a group of blood donors wi thout cardiac symptoms or signs of CAD (BD, n = 104). Genotype distribution was similar across the groups; HPA-1a/a: HPA-1a/lb: HPA-1b/b was 75.0%: 27 .1%: 2.9% in BD, 72.6%: 24.7%: 2.6% in MC, 70.5%: 26.8%: 2.7% in CAD, and 7 0.7%: 26.4%: 2,9% in MI; HPA-3a/a: HPA-3a/b: HPA-3b/b was 39.4%: 40.4%: 20. 2% in BD,33.5%: 50.0%: 16.5% in MC, 35.0%: 46.3%: 17.0% in CAD, and 37.1%: 48.0%: 16.5% in MI. There was no interaction between these polymorphisms, n or between each of these polymorphisms and other risk factors. Thus, the HPA-1 and HPA-3 polymorphisms are neither separately nor in conce rt associated with any measurable increase of the risk for CAD or MI in ang iographically evaluated subjects.