PlA polymorphism of glycoprotein IIIa and risk of adverse events after coronary stent placement.
OBJECTIVE
We designed this prospective study to test the hypothesis that platelet antigen (PlA) polymorphism of glycoprotein (GP) IIIa is associated with an increased risk for adverse events after coronary stent placement.


BACKGROUND
Platelets play a central role in arterial thrombosis. The PlA polymorphism of GP IIIa, a constituent of the fibrinogen receptor, may influence the platelet function and, thereby, the early outcome of patients after coronary stent placement.


METHODS
The study included 1,759 consecutive patients with stable or unstable angina and successful coronary stent placement. Platelet antigen genotypes were determined by allele-specific restriction enzyme analysis. The end point of the study was a composite of death, myocardial infarction and urgent revascularization during the first 30 days after stent placement.


RESULTS
The PlA1 genotype of the patients included was: 70.2% were homozygous for platelet antigen 1 (PlA1), 2.6% homozygous for platelet antigen 2 (PlA1), and 27.2% were heterozygous (PlA1/A2). The incidence of the composite end point was 5.5% among PlA2 carriers and 5.4% in homozygous PlA1 subjects (p = 0.94). It was 5.4% in PlA1/A1 patients, 4.8% in PlA1/A2 patients and 13.0% in PlA2A2 patients (p = 0.06). The combined incidence of death or myocardial infarction was 4.3% in PlA1/A1 patients, 4.2% in PlA1/A2 patients and 13.0% in PlA2/A2 patients (p = 0.02).


CONCLUSIONS
The isolated presence of the PlA2 allele in heterozygous patients is not associated with any detectable increase in the risk for an adverse 30-day outcome after coronary stenting. This study suggests also that an increased risk is likely to be present in homozygous carriers of the PlA2 allele, but this should be confirmed in a much larger series of patients.
Kastrati
A
A
Deutsches Herzzentrum and 1. Medizinische Klinik rechts der Isar, Technische Universität München, Munich, Germany. kastrati@dhm.mhn.de
Koch
W
W
Gawaz
M
M
Mehilli
J
J
Böttiger
C
C
Schömig
K
K
von Beckerath
N
N
Schömig
A
A
D000368:Aged; D000483:Alleles; D000787:Angina Pectoris / Q000601:surgery; D015703:Antigens, CD / Q000235:genetics* / Q000378:metabolism; D016824:Antigens, Human Platelet / Q000097:blood / Q000235:genetics*; D017023:Coronary Angiography; D003328:Coronary Thrombosis / Q000097:blood / Q000150:complications / Q000000981:diagnostic imaging / Q000235:genetics*; D004247:DNA / Q000032:analysis; D017931:DNA Primers / Q000737:chemistry; D000939:Epitopes / Q000097:blood / Q000235:genetics; D005260:Female; D005819:Genetic Markers; D005838:Genotype; D006801:Humans; D039661:Integrin beta3; D016023:Integrins / Q000097:blood / Q000235:genetics; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood / Q000000981:diagnostic imaging / Q000209:etiology; D016017:Odds Ratio; D010980:Platelet Membrane Glycoproteins / Q000235:genetics* / Q000378:metabolism; D016133:Polymerase Chain Reaction; D011110:Polymorphism, Genetic; D011379:Prognosis; D011446:Prospective Studies; D012307:Risk Factors; D015607:Stents / Q000009:adverse effects*
D015703:Antigens, CD; D016824:Antigens, Human Platelet; D017931:DNA Primers; D000939:Epitopes; D005819:Genetic Markers; C061248:ITGB3 protein, human; D039661:Integrin beta3; D016023:Integrins; D010980:Platelet Membrane Glycoproteins; C083451:human platelet antigen 1b; D004247:DNA