(Circulation. 1999;99:1005-1010.)
© 1999 American Heart Association, Inc.
Clinical Investigation and Reports |
From Deutsches Herzzentrum and 1. Medizinische Klinik rechts der Isar, Technische Universität München, Munich, Germany.
Correspondence to Dr Adnan Kastrati, Deutsches Herzzentrum, Lazarettstraßr 36, 80636 München, Germany. E-mail kastrati{at}dhm.mhn.de
BackgroundPlatelets play a central role in the process of restenosis after percutaneous coronary interventions. A polymorphism of platelet glycoprotein IIIa (PlA) has been associated with a higher risk of coronary thrombosis. We designed this prospective study to test the hypothesis that PlA polymorphism of glycoprotein IIIa is associated with an increased risk for restenosis after coronary stent placement.
Methods and ResultsThe study included 1150 consecutive patients
with successful coronary stent placement and 6-month follow-up
with coronary angiography. The end point of the study was the
incidence of angiographic restenosis (
50% diameter
stenosis) at follow-up. Of the 1150 patients, 72.5% were
homozygous for PlA1, 24.7% were heterozygous
(PlA1/A2), and 2.8% were homozygous for PlA2.
Patients with the PlA2 allele demonstrated a
significantly higher restenosis rate than did those without
(47% versus 38%; OR, 1.42; 95% CI, 1.09 to 1.84). The risk was
highest in homozygous carriers of PlA2 (53.1%
restenosis rate). After adjustment for several clinical and
angiographic characteristics, the presence of the PlA2
allele remained a significantly independent risk factor for
restenosis (adjusted OR, 1.35; 95% CI, 1.07 to 1.70). The
influence of the PlA2 allele on restenosis was
stronger in women. Women with PlA2 had a restenosis
rate of 52% compared with the 33% incidence among women homozygous
for PlA1 (OR, 2.21; 95% CI, 1.27 to 3.85).
ConclusionsThis study showed a significant association between the PlA polymorphism of glycoprotein IIIa and the risk of restenosis after coronary stent placement. The risk was more pronounced in patients homozygous for PlA2 allele and in female patients.
Key Words: platelets glycoproteins receptors stents genetics
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