Title of article :
Polymorphism of platelet glycoprotein IIb and risk of thrombosis and restenosis after coronary stent placement
Author/Authors :
Bِttiger، نويسنده , , Corinna and Kastrati، نويسنده , , Adnan and Koch، نويسنده , , Werner and Mehilli، نويسنده , , Julinda and von Beckerath، نويسنده , , Nicolas and Dirschinger، نويسنده , , Josef and Gawaz، نويسنده , , Meinrad and Schِmig، نويسنده , , Albert، نويسنده ,
Issue Information :
روزنامه با شماره پیاپی سال 1999
Pages :
5
From page :
987
To page :
991
Abstract :
Both glycoprotein (GP) IIb and IIIa of platelet fibrinogen receptor are polymorphic proteins. Unlike GPIIIa, there is little information about the clinical significance of the GPIIb polymorphism. We designed this prospective study to assess whether patients with the human platelet antigen (HPA)-3 polymorphism of GPIIb are more susceptible to developing thrombosis and restenosis after coronary stent placement. We included 2,178 consecutive patients with coronary artery disease who underwent intracoronary stent implantation, 789 (36.2%) with HPA-3a/a, 1,023 (47.0%) with HPA-3a/b, and 366 (16.8%) with HPA-3b/b genotype. The incidence of stent thrombosis was 1.7% in HPA-3a/a, 1.7% in HPA-3a/b, and 1.6% in HPA-3b/b patients (p = 0.999). The incidence of stent restenosis was 37.3% in HPA-3a/a, 36.2% in HPA-3a/b, and 34.6% in HPA-3b/b patients (p = 0.724). Event-free survival 1 year after stent placement was 76.1% for HPA-3a/a, 76.5% for HPA-3a/b, and 76.4% for HPA-3b/b patients (p = 0.968). We conclude that the HPA-3 polymorphism of platelet GPIIb is not associated with an increase in the risk of thrombosis and restenosis over 1 year after coronary stent placement. These data indicate that unlike the HPA-1 polymorphism of GPIIIa, the HPA-3 polymorphism of GPIIb may not serve as a useful genetic marker for the risk assessment of patients treated with intracoronary stenting.
Journal title :
American Journal of Cardiology
Serial Year :
1999
Journal title :
American Journal of Cardiology
Record number :
1891539
Link To Document :
بازگشت